CARDIOVASCULAR BIOMARKERS FOR SYSTEMIC LUPUS ERYTHEMATOSUS CROSS-REFERENCE TO RELATED APPLICATIONS [0001] This application claims priority to US Application No.63/002,299 filed March 30, 2020, the disclosure of which is incorporated by reference herein in its entirety. BACKGROUND [0002] Patients with systemic lupus erythematosus (SLE) are at increased risk of cardiovascular events compared to the general population. Cardiovascular events include arterial events, such as myocardial Infarction (MI) and cerebrovascular events (CVA), and venous events, the most common of which are pulmonary embolism (PE) and deep vein thrombosis (DVT). In addition to traditional risk factors (obesity, smoking, diabetes, high blood pressure, or hyperlipidemia) that contribute to thrombosis in SLE, additional risk factors include hypocomplementemia, presence of antiphospholipid (aPL) antibodies (in particular, lupus anticoagulant (LAC)), and use of certain medications. [0003] Cell-bound complement activation products (CB-CAPs) and deposition of C4d split fragments on hematopoietic cells such as B lymphocytes (BC4d) and erythrocyte (EC4d) are commonly present in SLE. In contrast, deposition of C4d on platelets (PC4d) is generally uncommon (20% SLE) but highly specific. (Magder et al, Am J Epidemiol.2012;176(8):708- 719; Girolami et al, Clin. Appl. Thromb. Hemost.2013;19:613-618). [0004] There is a need in the art to identify cardiovascular biomarkers and risks, such as arterial thrombosis and myocardial infarction, in patients having systemic lupus erythematosus BRIEF SUMMARY [0005] Provided herein are methods for diagnosing arterial thrombosis in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing arterial thrombosis in a subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti- thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0006] In an aspect, provided herein are methods for prognosing development of arterial thrombosis in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing the development of arterial thrombosis in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0007] Provided herein are methods for diagnosing myocardial infarction or a history of myocardial infarction in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing myocardial infarction or the history of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0008] Provided herein are methods for prognosing development of myocardial infarction in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing development of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0009] Provided herein are methods of detecting an arterial thrombosis marker and/or a myocardial infarction marker in a systemic lupus erythematosus subject that has or is suspected of having had arterial thrombosis and/or myocardial infarction, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and detecting the arterial thrombosis marker and/or the myocardial infarction marker in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0010] Provided herein are methods of treating arterial thrombosis in a systemic lupus erythematosus subject, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying arterial thrombosis in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject (C1) an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, and/or (C2) an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat arterial thrombosis. [0011] Provided herein are methods of treating arterial thrombosis in a systemic lupus erythematosus subject in need thereof, the method comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof to treat arterial thrombosis; wherein: (i) a level of PC4d in a biological sample obtained from the subject is ≥10 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. [0012] Provided herein are methods of treating myocardial infarction in a systemic lupus erythematosus subject, the method comprising: measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying myocardial infarction in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject: (C1) an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat myocardial infarction, and/or (C2) an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat myocardial infarction. [0013] Provided herein are methods of treating myocardial infarction in a systemic lupus erythematosus subject in need thereof, the method comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof; wherein:(i) a level of PC4d in a biological sample obtained from the subject is ≥10 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. [0014] Provided herein are methods for preparing a sample from a systemic lupus erythematosus subject useful for analyzing a plurality of markers involved in arterial thrombosis and/or myocardial infarction, including: (a) collecting whole blood from the subject; (b) producing a platelet fraction derived from whole blood from said subject comprising lysing red blood cells, and measuring a level of PC4d in said platelet fraction using a methodology configured to identify whether the PC4d level is ≥10 mean fluorescence intensity units; and (c) producing a first serum fraction or a first plasma fraction from the whole blood from said subject and measuring a level of C3 in said fractions; and (d) producing a second serum fraction or a second plasma fraction from the whole blood from said subject and measuring a level of PS/PT complex antibody in said fraction. BRIEF DESCRIPTION OF THE DRAWING [0015] The figure shows vascular events in systemic lupus erythematosus subjects stratified by antiphospholipid antibody (aPL) status and PC4d. The percent of subjects with a history of vascular events within five years of study enrollment stratified by aPL presence (NEG = negative; POS = positive) and PC4d status (NEG=PC4d<10, POS=PC4d≥10). Results are percent patients with events ± 95% confidence interval (CI). *p=0.02, **p<0.0001, ns not significant at α = 0.05. DETAILED DESCRIPTION [0016] Definitions [0017] Unless defined otherwise, technical and scientific terms used herein have the same meaning as commonly understood by a person of ordinary skill in the art. Any methods, devices and materials similar or equivalent to those described herein can be used. The following definitions are provided to facilitate understanding of certain terms used frequently herein and are not meant to limit the scope of the disclosure. [0018] The singular terms "a," "an," and "the" include the plural reference unless the context clearly indicates otherwise. [0019] The term "about" refers to a quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length that varies by as much as 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1% to a reference quantity, level, value, concentration, measurement, number, frequency, percentage, dimension, size, amount, weight or length. In embodiments, the terms "about" when preceding a numerical value indicates the value plus or minus a range of 10%, 5%, or 1%. In embodiments, the terms "about" when preceding a numerical value indicates ± 10% [0020] The terms “disease” or “condition” are used in accordance with their plain and ordinary meaning and refer to a state of being or health status of a patient or subject capable of being treated with the compounds or methods provided herein. In embodiments, the disease is an autoimmune disease. In embodiments, the disease is systemic lupus erythematosus. In embodiments, the disease is an inflammatory disease. In embodiments, the disease is a cardiovascular disease. In embodiments, the disease is thrombosis. In embodiments, the disease is arterial thrombosis. In embodiments, the disease is myocardial infarction. [0021] The term “systemic lupus erythematosus” or “SLE” are used in accordance with its plain and ordinary meaning and refer to an autoimmune disease, characterized by the production of unusual autoantibodies in the blood. These autoantibodies bind to their respective antigens, forming immune complexes which circulate and eventually deposit in tissues. This immune complex deposition causes chronic inflammation and tissue damage. [0022] The term “cardiovascular disease” or “cardiovascular event” is used in accordance with its plain and ordinary meaning and refers to a class of diseases that involve the heart or blood vessels. Cardiovascular disease includes, but is not limited to, coronary artery diseases, thrombosis (e.g., arterial thrombosis, venous thrombosis), myocardial infarction (commonly known as a heart attack), stroke, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, congestive heart failure, cardiac arrhythmias (e.g., atrial fibrillation, ventricular tachycardia, etc.), cerebrovascular disease, peripheral arterial disease, aortic valve stenosis, other cardiac valvular disease, and thrombosis. [0023] The term “thrombosis” is used in accordance with its plain and ordinary meaning and refers to the formation of a blood clot inside a blood vessel which obstructs the flow of blood through the circulatory system. When a blood vessel (a vein or an artery) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot, or a piece of the clot, that breaks free and begins to travel around the body is known as an embolus. Thrombosis may occur in veins (venous thrombosis) or in arteries (arterial thrombosis). Venous thrombosis leads to congestion of the affected part of the body, while arterial thrombosis (and rarely severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. [0024] The term “myocardial infarction” or “MI” or “heart attack” is used in accordance with its plain and ordinary meaning and occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. [0025] The term “diagnosis” is used in accordance with its plain and ordinary meaning and refers to an identification or likelihood of the presence of a cardiovascular disease (e.g., thrombosis, myocardial infarction) or outcome in a subject. [0026] The term “prognosis” is used in accordance with its plain and ordinary meaning and refers to the likelihood or risk of a subject developing a particular outcome or particular event, such as thrombosis or myocardial infarction. [0027] “Biological sample” is used in accordance with its plain and ordinary meaning and encompasses any sample type that can be used in a diagnostic, prognostic, or treatment method described herein. The biological sample may be any bodily fluid, tissue or any other sample obtained from a subject or subject’s body from which clinically relevant protein marker levels or antibody levels may be determined. The definition encompasses blood and other liquid samples of biological origin, solid tissue samples such as a biopsy specimen or tissue cultures or cells derived therefrom and the progeny thereof. The definition also includes samples that have been manipulated in any way after their procurement, such as by treatment with reagents, solubilization, or enrichment for certain components, such as polypeptides or proteins. The term "biological sample" encompasses a clinical sample, but also, In embodiments, includes cells in culture, cell supernatants, cell lysates, blood, serum, plasma, urine, cerebral spinal fluid, biological fluid, and tissue samples. The sample may be pretreated as necessary by dilution in an appropriate buffer solution or concentrated, if desired. In embodiments, the biological sample is a blood sample. In embodiments, the biological sample is whole blood, plasma, or serum. In embodiments, the biological sample is whole blood. In embodiments, the biological sample is plasma. In embodiments, the biological sample is serum. [0028] The term “whole blood” is used in accordance with its plain and ordinary meaning and refers to blood drawn directly from the body from which none of the components, such as plasma or platelets, have been removed. [0029] The terms “plasma” and “blood plasma” are used in accordance with their plain and ordinary meaning and refers to the yellowish liquid component of blood that holds the blood cells in whole blood in suspension. It is the liquid part of the blood that carries cells and proteins throughout the body. It makes up about 55% of the body's total blood volume. Blood plasma is separated from the blood by spinning a tube of fresh blood containing an anticoagulant in a centrifuge until the blood cells fall to the bottom of the tube. The blood plasma is then poured or drawn off. [0030] The term “serum” is used in accordance with its plain and ordinary meaning and refers to the fluid and solute component of blood which does not play a role in clotting. It may be defined as blood plasma without fibrinogens. Serum includes all proteins not used in blood clotting; all electrolytes, antibodies, antigens, hormones; and any exogenous substances (e.g., drugs or microorganisms). Serum does not contain white blood cells (leukocytes), red blood cells (erythrocytes), platelets, or clotting factors. [0031] The terms “treating” or “treatment” are used in accordance with their plain and ordinary meaning and broadly includes any approach for obtaining beneficial or desired results in a subject’s condition, including clinical results. Beneficial or desired clinical results can include, but are not limited to, alleviation or amelioration of one or more symptoms or conditions, diminishment of the extent of a disease, stabilizing (i.e., not worsening) the state of disease, prevention of a disease’s transmission or spread, delay or slowing of disease progression, amelioration or palliation of the disease state, diminishment of the reoccurrence of disease, and remission, whether partial or total and whether detectable or undetectable. In other words, "treatment" as used herein includes any cure, amelioration, or prevention of a disease. Treatment may prevent the disease from occurring; inhibit the disease’s spread; relieve the disease’s symptoms, fully or partially remove the disease’s underlying cause, shorten a disease’s duration, or do a combination of these things. [0032] The terms "treating" and "treatment" may include prophylactic treatment. Treatment methods include administering to a subject a therapeutically effective amount of an active agent. The administering step may consist of a single administration or may include a series of administrations. The length of the treatment period depends on a variety of factors, such as the severity of the risk or condition, the age of the patient, the concentration of active agent, the activity of the compositions used in the treatment, or a combination thereof. It will also be appreciated that the effective dosage of an agent used for the treatment or prophylaxis may increase or decrease over the course of a particular treatment or prophylaxis regime. Changes in dosage may result and become apparent by standard diagnostic assays known in the art. In embodiments, chronic administration is required. For example, the therapeutic agents are administered to the subject in an amount and for a duration sufficient to treat the patient. [0033] The term “prevent” is used in accordance with its plain and ordinary meaning and refers to a decrease in the occurrence of disease symptoms in a patient. The prevention may be complete (no detectable symptoms) or partial, such that fewer symptoms are observed than would likely occur absent treatment. [0034] The terms “patient” or “subject in need thereof” or “subject” are used in accordance with their plain and ordinary meaning and refer to a living organism suffering from or prone to a disease or condition that can be treated by administration of a pharmaceutical composition. Non-limiting examples include humans, other mammals, bovines, rats, mice, dogs, cats, monkeys, goat, sheep, cows, and other non-mammalian animals. In embodiments, a subject is human. In embodiments, the subject is a human with systemic lupus erythematosus. [0035] The term “control” or “control experiment” are used in accordance with their plain and ordinary meaning and refer to an experiment in which the subjects or reagents of the experiment are treated as in a parallel experiment except for omission of a procedure, reagent, or variable of the experiment. In embodiments, the control is used as a standard of comparison in evaluating experimental effects. In embodiments, a control is the measurement of the activity of a protein in the absence of a compound as described herein (including embodiments and examples). In embodiments, the control is a quantification standard used as a reference for assay measurements. The quantification standard may be a synthetic protein, a recombinantly expressed purified protein, a purified protein isolated from its natural environment, a protein fragment, a synthesized polypeptide, or the like. [0036] The terms "marker," "protein marker," “polypeptide marker,” and “biomarker” are used interchangeably throughout the disclosure, and are used in accordance with their plain and ordinary meaning. A protein marker refers generally to a protein or polypeptide, the level or concentration of which is associated with a particular biological state, particularly a state associated with a cardiovascular disease, event or outcome. Panels, assays, kits and methods described herein may comprise antibodies, binding fragments thereof or other types of target- binding agents, which are specific for the protein marker described herein. In embodiments, the marker is PC4d, complement C3, or anti-PS/PT antibodies. [0037] The terms "polypeptide" and "protein", may be used interchangeably, are used in accordance with their plain and ordinary meaning, and refer to a polymeric form of amino acids of any length, which can include coded and non-coded amino acids, chemically or biochemically modified or derivatized amino acids, and polypeptides having modified peptide backbones. In embodiments, detecting the levels of naturally occurring protein marker proteins in a biological sample is contemplated for use within diagnostic, prognostic, or monitoring methods disclosed herein. The term also includes fusion proteins, including, but not limited to, naturally occurring fusion proteins with a heterologous amino acid sequence, fusions with heterologous and homologous leader sequences, with or without N-terminal methionine residues; immunologically tagged proteins; and the like. [0038] The term "antibody" is used in accordance with its plain and ordinary meaning and in the broadest sense. The term specifically covers, but is not limited to, monoclonal antibodies, polyclonal antibodies, multi-specific antibodies (e.g., bispecific antibodies) formed from at least two intact antibodies, single chain antibodies (e.g., scFv), and antibody fragments or other derivatives, so long as they exhibit the desired biological specificity. The term "antibody" refers to a polypeptide encoded by an immunoglobulin gene or functional fragments thereof that specifically binds and recognizes an antigen. The recognized immunoglobulin genes include the kappa, lambda, alpha, gamma, delta, epsilon, and mu constant region genes, as well as the myriad immunoglobulin variable region genes. Light chains are classified as either kappa or lambda. Heavy chains are classified as gamma, mu, alpha, delta, or epsilon, which in turn define the immunoglobulin classes, IgG, IgM, IgA, IgD and IgE, respectively. [0039] The term "monoclonal antibody" is used in accordance with its plain and ordinary meaning and refers to an antibody obtained from a population of substantially homogeneous antibodies, i.e., the individual antibodies comprising the population are identical except for possible naturally occurring mutations that can be present in minor amounts. In embodiments, the monoclonal antibody is an antibody specific for a protein marker described herein. [0040] The term "detectably labeled antibody" is used in accordance with its plain and ordinary meaning and refers to an antibody (or antibody fragment) which retains binding specificity for a protein marker described herein, and which has an attached detectable label. The detectable label can be attached by any suitable means, e.g., by chemical conjugation or genetic engineering techniques. Methods for production of detectably labeled proteins are well known in the art. Detectable labels may be selected from a variety of such labels known in the art, including, but not limited to, haptens, radioisotopes, fluorophores, paramagnetic labels, enzymes (e.g., horseradish peroxidase), or other moieties or compounds which either emit a detectable signal (e.g., radioactivity, fluorescence, color) or emit a detectable signal after exposure of the label to its substrate. Various detectable label/substrate pairs (e.g., horseradish peroxidase/diaminobenzidine, avidin/streptavidin, and luciferase/luciferin)), methods for labeling antibodies, and methods for using labeled antibodies are known in the art. [0041] The term “specifically (or selectively) binds” to an antibody or “specifically (or selectively) immunoreactive with,” when referring to a protein or peptide, is used in accordance with its plain and ordinary meaning and refers to a binding reaction that is determinative of the presence of the protein, often in a heterogeneous population of proteins and other biologics. Thus, under designated immunoassay conditions, the specified antibodies bind to a particular protein at least two times the background and more typically more than 10 to 100 times background. Specific binding to an antibody under such conditions requires an antibody that is selected for its specificity for a particular protein. For example, polyclonal antibodies can be selected to obtain only a subset of antibodies that are specifically immunoreactive with the selected antigen and not with other proteins. This selection may be achieved by subtracting out antibodies that cross-react with other molecules. A variety of immunoassay formats may be used to select antibodies specifically immunoreactive with a particular protein. For example, immunoassays are routinely used to select antibodies specifically immunoreactive with a protein. [0042] An example immunoglobulin (antibody) structural unit comprises a tetramer. Each tetramer is composed of two identical pairs of polypeptide chains, each pair having one “light” (about 25 kDa) and one “heavy” chain (about 50-70 kDa). The N-terminus of each chain defines a variable region of about 100 to 110 or more amino acids primarily responsible for antigen recognition. The terms “variable heavy chain,” “V _H ,” or “VH” refer to the variable region of an immunoglobulin heavy chain, including an Fv, scFv, dsFv or Fab, while the terms “variable light chain,” “V _L ” or “VL” refer to the variable region of an immunoglobulin light chain, including of an Fv, scFv, dsFv or Fab. [0043] The term "functional fragments" is used in accordance with its plain and ordinary meaning and in the context of antibodies, refers to those fragments that retain sufficient binding affinity and specificity for a protein marker to permit a determination of the level of the protein marker in a biological sample. In embodiments, a functional fragment will bind to a protein marker with substantially the same affinity and/or specificity as an intact full chain molecule from which it may have been derived. Examples of antibody functional fragments include, but are not limited to, complete antibody molecules, antibody fragments, such as Fv, single chain Fv (scFv), complementarity determining regions (CDRs), VL (light chain variable region), VH (heavy chain variable region), Fab, F(ab)2' and any combination of those or any other functional portion of an immunoglobulin peptide capable of binding to target antigen. As appreciated by one of skill in the art, various antibody fragments can be obtained by a variety of methods, for example, digestion of an intact antibody with an enzyme, such as pepsin, or de novo synthesis. Antibody fragments are often synthesized de novo either chemically or by using recombinant DNA methodology. Thus, the term antibody includes antibody fragments either produced by the modification of whole antibodies, or those synthesized de novo using recombinant DNA methodologies (e.g., single chain Fv) or those identified using phage display libraries. [0044] For specific proteins described herein, the named protein includes any of the protein’s naturally occurring forms, variants or homologs that maintain the protein transcription factor activity (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99% or 100% activity compared to the native protein). In embodiments, variants or homologs have at least 90%, 95%, 96%, 97%, 98%, 99% or 100% amino acid sequence identity across the whole sequence or a portion of the sequence (e.g. a 50, 100, 150 or 200 continuous amino acid portion) compared to a naturally occurring form. [0045] The term “complement system” also known as “complement cascade” is used in accordance with its plain and ordinary meaning and refers to a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. The complement system consists of a number of small proteins that are synthesized by the liver, and circulate in the blood as inactive precursors. When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end result of this complement activation or complement fixation cascade is stimulation of phagocytes to clear foreign and damaged material, inflammation to attract additional phagocytes, and activation of the cell- killing membrane attack complex. Over 30 proteins and protein fragments make up the complement system, including serum proteins, and cell membrane receptors. [0046] The term “classical pathway” or “classical complement pathway” are used in accordance with their plain and ordinary meaning and refer to one of three biochemical pathways activate the complement system. The classical pathway is triggered by activation of the C1-complex. The C1-complex is composed of 1 molecule of C1q, 2 molecules of C1r and 2 molecules of C1s, or C1qr ² s ² . This occurs when C1q binds to IgM or IgG complexed with antigens. A single pentameric IgM can initiate the pathway, while several, ideally six, IgGs are needed. This also occurs when C1q binds directly to the surface of the pathogen. Such binding leads to conformational changes in the C1q molecule, which leads to the activation of two C1r molecules. C1r is a serine protease. They then cleave C1s (another serine protease). The C1r ² s ² component now splits C4 and then C2, producing C4a, C4b, C2a, and C2b (historically, the larger fragment of C2 was called C2a but is now referred to as C2b). C4b and C2a bind to form the classical pathway C3-convertase (C4b2a complex), which promotes cleavage of C3 into C3a and C3b. C3b later joins with C4b2a to make C5 convertase (C4b2a3b complex). [0047] The term “cell-bound complement activation products” or “CB-CAPS” refers to hydrolyzed complement activation products bound to circulating cells such as erythrocytes, platelets, B and T lymphocytes. [0048] The term “platelet-bound C4d” or “PC4d” refers to C4d products of complement activation deposited on platelets. [0049] The terms “complement component 3” and “C3” are used in accordance with their plain and ordinary meaning and refer to a protein of the immune system of the same name. C3 plays a central role in the activation of the complement system and contributes to innate immunity. Its activation is required for both classical and alternative complement activation pathways. [0050] The terms “anti-phosphatidylserine/prothrombin complex” and “anti-PS/PT” are used in accordance with their plain and ordinary meaning and refer to an antiphospholipid antibody. In embodiments, antibodies to phosphatidylserine/prothrombin complex include IgG and IgM. [0051] The terms “enzyme-linked immunosorbent assay” and “ELISA” are used in accordance with their plain and ordinary meaning and refer to a commonly used analytical biochemistry assay. The assay uses a solid-phase enzyme immunoassay (EIA) to detect the presence of a ligand (commonly a protein) in a liquid sample using antibodies directed against the protein to be measured. ELISA has been used as a diagnostic tool in medicine, plant pathology, and biotechnology, as well as a quality control check in various industries. In the most simple form of an ELISA, antigens from the sample are attached to a surface. Then, a matching antibody is applied over the surface so it can bind to the antigen. This antibody is linked to an enzyme, and in the final step, a substance containing the enzyme's substrate is added. The subsequent reaction produces a detectable signal, most commonly a color change. [0052] The terms “luminescent enzyme-linked immunosorbent assay” and “luminescent ELISA” and “luminescent immunoassay” are variations of the standard ELISA where an enzyme converts a substrate to a reaction product that emits photons of light instead. Luminescence is the emission of light from a substance as it returns from an electronically excited state to ground state. The various forms of luminescence (bioluminescence, chemiluminescence, photoluminescence) differ in the way the excited state is reached. For example, photoluminescence is simply fluorescence; the excitation is initiated by light at a particular wavelength. Bioluminescence is characterized by the use of a bioluminescent compound, such as luciferin and firefly luciferase. Chemiluminescence is light produced by a chemical reaction. The chemiluminescent substance is excited by the oxidation and catalysis forming intermediates. When the excited intermediates return back to their stable ground state, a photon is released, which is detected by the luminescent signal instrument. A luminescent ELISA can be direct (e.g., using luminophore markers) or indirect (e.g., using enzyme markers), and either method may be competitive or non-competitive. In embodiments of the methods described herein, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. In embodiments, the ELISA is a bioluminescent ELISA. In embodiments, the ELISA is a photoluminescent ELISA. [0053] The term “immunoturbidimetry” is used in accordance with its plain and ordinary meaning and refers to a technique which relies upon the light scattering characteristics of antigen/antibody complexes. For example, when a patient specimen, containing an antigen (such as C3, C3c or C4), is combined with antiserum, a complex between the antigen and the antiserum will form. When light is directed through this suspension, a portion of the light will be transmitted and focused onto an optic device (photodiode via an optical lens system). The amount of transmitted light observed by the optic device is indirectly proportional to the protein concentration (C3, C3c or C4) in the patient specimen. Therefore, a specimen that contains a high concentration of C3 or C3c or C4 would transmit less light than a specimen that contains a low concentration of C3 or C3c or C4. [0054] The term “transformed” refers to a mathematical process applied to a numerical value, regardless of the input or output value. It may include taking protein concentrations and calculating the natural log base from original values, reflecting a "log-transformation." [0055] The term “transformation analysis” can be any suitable mathematical operation, including but not limited to generalized models (e.g. logistic regression, generalized additive models) and multivariate analysis (e.g. discriminant analysis, principal components analysis, factor analysis). In embodiments, the transformation analysis can include the use of weighting coefficients, which can be determined by a variety of techniques. In one example of determining appropriate weighting coefficients, multivariable logistic regression (MLR) is performed using the maker levels found within two groups of patients, for example, one with and one without SLE. There are several methods for variable (marker) selection that can be used with MLR, whereby the markers not selected are eliminated from the model and the weighting coefficients for each predictive marker remaining in the model are determined. These weighting coefficients can then be, for example, multiplied by the marker level in the sample (expressed in any suitable units, including but not limited weight/volume, weight/weight, weight/number packed cells, etc.) and then, for example, summed to calculate a risk score. In embodiments, some components constituting the index score may be associated with predetermined threshold/cutoff values (for example, a component might have a value of 0, 1, or 2). In such a scenario, the index can potentially change from positive to negative (or vice versa) based on the analytical error at the threshold decision limit for the marker. In embodiments, equivocal results can be defined when components use to determine the index score are assessed using a threshold/cutoff value and are within 20% or less of the threshold value (and therefore potentially able to affect the positivity or negativity of the index). In this embodiment, the score may be noted as equivocal. [0056] As used herein, “combining” includes any mathematical operation to use markers in combination to arrive at a single score that can be compared to a threshold (adding, subtracting, dividing, multiplying, and combinations thereof). In these methods, the level of the markers may be adjusted using an appropriate weighting coefficient. [0057] The methods may employ comparisons between a measured risk score and a standard risk score. Any suitable standard for comparison can be used, including but not limited to a pre-determined level or range of risk scores from a normal individual or population of subjects having SLE. As used herein, a “pre-determined level” or “pre-determined range” refers to a value or range of values that can be determined from the quantity or amount (e.g., absolute value or concentration) of a particular SLE risk score measured in a population of control subjects (i.e. healthy subjects) or a population of subjects afflicted with SLE. A pre-determined level or pre-determined range of risk scores can be selected by calculating the value or range of risk score values that achieves the greatest statistical significance. [0058] The term “score” refers to a numerical values assigned to a result as it relates diagnostic, prognostic, or treatment determinations. A score can be a positive, intermediate, or negative diagnostic, prognostic, or treatment score. One or multiple cutoffs can be used with the score to determine specific levels of risk. In embodiments, a score is algorithmically derived based on normalized and/or mathematically transformed values, such as protein concentrations, the presence/absence of clinical factors, vital statistics, or ratios of different factors. The algorithm which generates the score can be ratio-based, cut-off-based, linear or non-linear, including decision tree or rule-based models. In embodiments, a thrombotic risk score assigns 1 point for every abnormality, so it can be 0, 1, 2, or 3. It may not be less than 0. A score of 0 can be considered negative in terms of risk of thrombosis. [0059] As further described herein, the “training set” is the set of patients or patient samples that are used in the process of training (i.e., developing, evaluating and building) the final diagnostic or prognostic model. The “validation set” is a set of patients or patient samples that are withheld from the training process, and are only used to validate the performance of the final diagnostic or prognostic model. If the set of patients or patient samples are limited in number, all available data may be used as a training set, or as an "in-sample" validation set. [0060] The term “normalized” refers to a type of transformation where the values are designed to fit a specific distribution, typically so that they are similar to the distributions of other variables. For example, for hypothetical proteins A and B, the raw concentration of protein A ranges from 0 to 500 and the raw concentration of Protein B ranges from 0 to 20,000, it is not trivial looking at thee raw values to determine which one is “higher.” For instance, is 400 of Protein A higher than 15,000 of Protein B. By conducting a normalization process, the concentrations are rescaled so that they are on the same scale: centered at zero, with a variance of 1. Thus, it becomes a routine exercise to determine which one is higher because the normalized concentrations are comparable. Many learning algorithms work better on data that are normalized; otherwise, in this example for instance, Protein B might get more weight in the algorithm because it has higher values even if it were not empirically “higher.” [0061] The term “prescribed” with reference to a therapeutic agent (e.g., prescribed anti- thrombotic agent, prescribed anti-platelet agent, prescribed beta-blocker, prescribed ACE inhibitor, prescribed statin) refers to a therapeutic agent that is being administered to the subject at the time the assays described herein are conducted and/or at the time a diagnosis, prognosis, or treatment decision is being made. [0062] The phrase “increased dose” with reference to a “prescribed” therapeutic agent refers to a dose that is higher than the dose of a prescribed therapeutic agent. For example, if a subject is being administered 5 mg/day of an anti-thrombotic agent (e.g., a prescribed anti- thrombotic agent), administering an increased dose of the prescribed anti-thrombotic agent would be administering any amount that is greater than 5 mg per day, such as 5 mg twice per day, 10 mg per day, 2.5 mg three times per day, and the like. [0063] Methods [0064] Provided herein are methods for diagnosing thrombosis in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had thrombosis or may be at risk for thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. [0065] In embodiments, the disclosure provides methods for diagnosing thrombosis in a subject having systemic lupus erythematosus by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing thrombosis in a subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the method for diagnosing thrombosis is a method for diagnosing a risk of thrombosis. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. In embodiments, the methods further comprise administering to the subject an effective amount of an anti-thrombotic agent. In embodiments, the methods further comprise administering to the subject an increased dose of a prescribed anti-thrombotic agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0066] Provided herein are methods for prognosing development of thrombosis in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥5 net mean fluorescence intensity units (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject is at risk of developing thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. [0067] In embodiments, the disclosure provides methods for prognosing development of thrombosis in a subject having systemic lupus erythematosus by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing the development of thrombosis in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. In embodiments, the methods further comprise administering to the subject an effective amount of an anti-thrombotic agent. In embodiments, the methods further comprise administering to the subject an increased dose of a prescribed anti-thrombotic agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. [0068] Provided herein are methods for diagnosing a history of myocardial infarction (MI) in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet- bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level where the threshold PC4d level is ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had a myocardial infarction. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0069] In embodiments, the disclosure provides methods for diagnosing myocardial infarction or a history of myocardial infarction in a subject having systemic lupus erythematous by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing myocardial infarction or the history of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. In embodiments, the methods further comprise administering to the subject an effective amount of an anti- platelet agent. In embodiments, the methods further comprise administering to the subject an increased dose of a prescribed anti-platelet agent. In embodiments, the methods comprise diagnosing a history of myocardial infarction, e.g., diagnosing that the subject has had one or more myocardial infarctions in the past). In embodiments, the methods comprise diagnosing a myocardial infarction, e.g., diagnosing a risk of the subject having a myocardial infarction in the future). In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0070] Provided herein are methods for prognosing development of myocardial infarction in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet- bound C4d (PC4d) protein in a biological sample from the subject; (b)a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥5 net mean fluorescence intensity units (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject is at risk of developing myocardial infarction. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0071] In embodiments, the disclosure provides methods for prognosing development of myocardial infarction in a subject having systemic lupus erythematosus by comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing development of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. In embodiments, the methods further comprise administering to the subject an effective amount of an anti-platelet agent. In embodiments, the methods further comprise administering to the subject an increased dose of a prescribed anti- platelet agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0072] Provided herein are methods of detecting a marker in a systemic lupus erythematosus, subject that has or is suspected of having had thrombosis and/or myocardial infarction, the method including measuring: (a) a level of platelet C4d (PC4d) protein in a biological sample from the subject using a methodology configured to identify whether the PC4d level is ≥5 net mean fluorescence intensity units; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. [0073] In embodiments, the disclosure provides methods of detecting a thrombosis marker and/or a myocardial infarction marker in a systemic lupus erythematosus subject that has, is suspected of having, or is at risk of having thrombosis and/or myocardial infarction by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and detecting the thrombosis marker and/or the myocardial infarction marker in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods further comprise: (i) administering to the subject an effective amount of an anti- thrombotic agent, an antiplatelet agent, or a combination thereof; and/or (ii) administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. In embodiments, the methods comprise detecting a thrombosis marker. In embodiments, the methods comprise detecting a myocardial infarction marker. In embodiments, the methods comprise detecting a thrombosis marker and a myocardial infarction marker. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0074] Provided herein are methods of diagnosing thrombosis in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥10 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had thrombosis. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. In embodiments, the threshold PC4d level is ≥5 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0075] Provided herein are methods for prognosing development of thrombosis in a subject having systemic lupus erythematosus, including measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had thrombosis. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0076] Provided herein are methods for monitoring treatment for thrombosis in a subject having systemic lupus erythematosus and being treated for thrombosis, including measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; where a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, where the threshold PC4d level is ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level. In embodiments, a combination of (i) a level of PC4d in the biological sample above ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the treatment for thrombosis has not been effective. In embodiments, a combination of (i) a level of PC4d in the biological sample at or below ≥5 net mean fluorescence intensity units, (ii) a level of complement C3 at or above a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody at or below a threshold anti- PS/PT IgG antibody level, indicates that the treatment for thrombosis has been effective. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0077] Provided herein are methods of treating thrombosis in a systemic lupus erythematosus subject comprising measuring: (a) a level of PC4d ≥5 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein < 81.1 mg/dl in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody ≥ 30 units in a third blood sample from the subject measured using ELISA; and (d) treating thrombosis with an effective amount of one or more therapeutic agents. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the methods of treating thrombosis are methods of reducing the risk of the occurrence of thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0078] Provided herein are methods of treating thrombosis in a systemic lupus erythematosus subject in need thereof comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof to treat thrombosis; wherein: (i) a level of PC4d in a biological sample obtained from the subject is ≥ 5 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods comprise administering to the subject an effective amount of an anti-thrombotic agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti-thrombotic agent. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the methods of treating thrombosis are methods of reducing the risk of the occurrence of thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3- specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0079] In embodiments, the disclosure provides methods of treating thrombosis in a systemic lupus erythematosus subject by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying thrombosis in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject (C1) an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, and/or (C2) an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat thrombosis. In embodiments, the methods comprise administering to the subject an effective amount of an anti-thrombotic agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti-thrombotic agent. In embodiments “identifying arterial thrombosis” refers to identifying a subject who is at risk (e.g., has an increased probability) of having thrombosis and/or identifying a previous thrombosis in the subject. In embodiments, “identifying arterial thrombosis” refers to identifying a subject who is at risk (e.g., has an increased probability) of having a thrombosis. In embodiments “identifying arterial thrombosis” refers to identifying a previous thrombosis in the subject. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the thrombosis is venous thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0080] Provided herein are methods of treating myocardial infarction in a systemic lupus erythematosus, subject including measuring: (a) a level of PC4d ≥5 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein < 81.1 mg/dl in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody > 30 units in a third blood sample from the subject measured using ELISA; and (d) treating the subject likely to have had myocardial infarction or at increased risk of having a myocardial infarction with an effective amount of one or more therapeutic agents. In embodiments, the therapeutic agent is an anti-thrombotic agent, an antiplatelet agent, or a combination thereof. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0081] In embodiments, the disclosure provides methods of treating myocardial infarction in a systemic lupus erythematosus subject by measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying myocardial infarction in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥5 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject: (C1) an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat myocardial infarction, and/or (C2) an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat myocardial infarction. In embodiments, the methods comprise administering to the subject an effective amount of an anti-platelet agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti-platelet agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3- specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. In embodiments “identifying myocardial infarction” refers to identifying a subject who is at risk (e.g., has an increased probability) of having a myocardial infarction and/or identifying a previous myocardial infarction in the subject and/or identifying a subject who is having a myocardial infarction. In embodiments, “identifying myocardial infarction” refers to identifying a subject who is at risk (e.g., has an increased probability) of having a myocardial infarction. In embodiments “identifying myocardial infarction” refers to identifying a previous myocardial infarction in the subject. In embodiments “identifying myocardial infarction” refers to identifying a subject who is having a myocardial infarction. [0082] Provided herein are methods of treating myocardial infarction in a systemic lupus erythematosus subject in need thereof comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof; wherein: (i) a level of PC4d in a biological sample obtained from the subject is ≥5 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. In embodiments, the methods comprise administering to the subject an effective amount of an anti-platelet agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti-platelet agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3- specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0083] In embodiments, methods of treating thrombosis in an SLE subject include measuring: (a) a level of PC4d ≥5 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a third blood sample from the subject, where the first, second, and third blood samples may be the same or different; and (d) treating the subject with an effective amount of one or more therapeutic agents. In embodiments, the methods comprise administering to the subject an effective amount of an anti-thrombotic agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti- thrombotic agent. In embodiments, the thrombosis is arterial thrombosis. In embodiments, the methods of treating thrombosis are methods of reducing the risk of the occurrence of thrombosis. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0084] In embodiments, methods of treating myocardial infarction in an SLE subject include measuring: (a) a level of PC4d ≥5 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a third blood sample from the subject, where the first, second, and third blood samples may be the same or different; and (d) treating the subject with an effective amount of one or more therapeutic agents. In embodiments, the methods comprise administering to the subject an effective amount of an anti-platelet agent. In embodiments, the methods comprise administering to the subject an increased dose of a prescribed anti-platelet agent. In embodiments, the threshold PC4d level is ≥10 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the level of PC4d in the biological sample is ≥ 5 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the level of PC4d in the biological sample is ≥ 10 net mean fluorescence intensity units; the level of complement C3 in the biological sample is < 81.1 mg protein per deciliter serum or plasma measured using a C3-specific antibody; and the level of anti-PS/PT IgG level is > 30 units measured using an ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0085] In embodiments of the methods provided, the subject is a human. In embodiments, the subject has systemic lupus erythematosus. In embodiments, the subject is a human with systemic lupus erythematosus. In embodiments, the subject is suspected of having systemic lupus erythematosus. In embodiments, the subject has systemic lupus erythematosus and has had a thrombosis. In embodiments, the subject has systemic lupus erythematosus and is at risk of having thrombosis. In embodiments, the subject has systemic lupus erythematosus and has had arterial thrombosis. In embodiments, the subject has systemic lupus erythematosus and is at risk of having arterial thrombosis. In embodiments, the subject has systemic lupus erythematosus and has had myocardial infarction. In embodiments, the subject has systemic lupus erythematosus and is at risk of having myocardial infarction. [0086] Any suitable biological sample from the subject may be used. In embodiments, the biological sample is a blood, whole blood, serum, or plasma sample from a subject. In embodiments, the biological sample is a blood sample from a subject. In embodiments, the biological sample is a whole blood sample from a subject. In embodiments, the biological sample is a serum sample from a subject. In embodiments, the biological sample is a plasma sample from a subject. [0087] In embodiments, the biological samples in the different assays (e.g., PC4d, C3, anti- PS/PT) may be the same biological sample or different biological samples. In embodiments, the biological samples are different fractions of a biological sample derived from a subject. In embodiments, the biological samples in the different assays are different samples and are referred to as a first biological sample, second biological sample, etc. [0088] In embodiments, a blood sample is treated with ethylenediaminetetraacetic acid (EDTA) to inhibit complement activation. In embodiments, samples are maintained at room temperature. In embodiments, samples are stored at about 4 °C. The collected blood may separated into components methods known in the art. For example, centrifugation may be used to separate whole blood into plasma and red cells or under a lower centrifugal force, to separate it into plasma, buffy coat (used to make platelets), and red blood cells. [0089] In embodiments, a whole blood sample may be fractionated into different components. In embodiments, a whole blood sample is centrifuged to isolate plasma. In embodiments, the whole blood is treated with a coagulant, centrifuged to remove clots and blood cells, and the resulting liquid supernatant is serum. [0090] In embodiments, red blood cells are separated from other cell types in the sample by differential centrifugation. In embodiments, the whole blood is treated with a lysing agent to lyse red blood cells and obtain a platelet fraction. Platelet isolation can be performed with methods known in the art, including differential centrifugation or immunoprecipitation using antibodies specific for platelets (e.g., CD42b). [0091] The level (e.g., quantity or amount) of a particular biomarker or protein marker or component can be measured in a sample using a variety of methods known to those of skill in the art. Such methods include, but are not limited to, flow cytometry, ELISA, and the like. In embodiments, the measurement of the level of PC4d and C3 is made using flow cytometric methods, with measurements taken by direct or indirect immunofluorescence using polyclonal or monoclonal antibodies specific for each of the molecules. Each of these molecules can be measured with a separate sample (e.g., platelet-specific fractions) or using a single sample (e.g., whole blood). In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0092] In embodiments, measuring a level includes processing a biological sample from a subject and detecting amounts of a particular component of the sample. In embodiments, measuring a level includes processing a biological sample and detecting a levels of PC4d in the sample. [0093] In embodiments, the biological sample is a platelet fraction of whole blood. In embodiments, the platelet fraction can be processed for analysis of platelet-bound complement activation products, such as PC4d. In embodiments, the platelet-bound complement activation products are measured by fluorescence-activated cell sorting (FACS). In embodiments, the platelet-bound complement activation product is PC4d. [0094] In embodiments, PC4d levels are measured by FACS as follows: red blood cells from an EDTA-anticoagulated whole blood sample are lysed and platelets are stained using a mouse monoclonal antibody against human C4d or a mouse IgG1 kappa monoclonal antibody (MOPC-21) as the isotype control. After incubation, samples are stained using a goat anti- mouse antibody conjugated to fluorescein isothiocyanate (FITC). A monoclonal antibody against human CD42b conjugated to phycoerythrin (PE) (platelet-specific marker) is used to identify C4d complement activation fragment covalently bound to the platelets. FACS analysis is performed using a flow cytometer equipped with a software to measure fluorescent staining intensity. Light scatter (forward and side) gating parameters are used during acquisition to isolate the platelet population, followed by secondary gating based on positive CD42b PE staining. Quantification of the non-specific (isotype control) and specific (C4d) fluorescence in the FL1 (fluorescein isothiocyanate) channel is used to measure the CD42b PE gated platelet cells (5000 events). Net mean fluorescence intensity is determined by subtraction of isotype control background MFI results from the specific C4d MFI results on gated platelet cells. [0095] In embodiments, measuring a level includes processing a biological sample from a subject and detecting a level of complement C3 in the sample. Low complement C3 status is established using any suitable method, including but not limited to immunoturbidity, chemiluminescence, and the like. In embodiments, the biological sample is serum and C3 levels are measured using immunoturbidimetry. [0096] In embodiments, immunoturbidimetry includes in vitro measurement of serum C3c and C4. In embodiments, immunoturbidimetry includes in vitro measurement of serum C3. In embodiments, immunoturbidity assays are performed on a device or instrument, for example the Optilite Clinical Chemistry Analyzer. In embodiments, measurements of C3 concentrations are reported in milligrams per deciliter (mg/dL), and are calculated by reference to a calibration curve that is maintained within the instrument operating software. [0097] In embodiments, measuring a level includes processing a biological sample from a subject and measuring a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody and/or IgM antibody. In embodiments, the biological sample is whole blood. In embodiments, the biological sample is serum. In embodiments, the biological sample is plasma. Anti-PS/PT complex antibodies is measured using any suitable means, including but not limited to immunoassays. In embodiments, a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG and/or IgM antibody is measured by ELISA. In embodiments, ELISA for the detection of IgG and IgM class antibodies to phosphatidylserine/prothrombin complex (PS/PT) in serum or plasma is semi-quantitative and qualitative. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0098] In embodiments, microwell plate wells are coated with purified PS/PT complex and then stabilized. Upon incubation, serum containing PS/PT IgG or PS/PT IgM antibodies bind with the PS/PT. Unbound protein is removed by washing and anti-human IgG or IgM horseradish peroxidase (HRP) labeled conjugate is added to the wells. After incubation, the unbound conjugate is removed by washing. A peroxidase substrate is then added, which undergoes a color change in the presence of the conjugated enzyme. After stopping the enzymatic production of colored product, the presence or absence of prothrombin antibody is determined spectrophotometrically by measuring and comparing the color intensity that develops in the patient wells with that of a five point calibration curve. units as defined by the device or instrument (for example Inova ELISA: QUANTA Lite™ aPS/PT IgG and/or QUANTA Lite™ aPS/PT IgM kits). [0099] In embodiments, the methods described herein comprise measuring a level of PC4d protein in a whole blood biological sample from a subject. In embodiments, the methods comprise measuring the level of PC4d protein in a platelet fraction derived from a whole blood biological sample from a subject. In embodiments, measuring the level of PC4d is determined using an antibody specific for C4d in flow cytometry. In embodiments described herein, a threshold PC4d level is ≥ 10 net mean fluorescence intensity units measured using flow cytometry. In embodiments, the threshold PC4d level is ≥5 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. [0100] In embodiments, the methods include measuring a level of complement C3 protein in a serum sample from a subject. In embodiments, a level of C3 is determined using an antibody specific for C3 in an immunoturbidity assay. In the various embodiments described herein, a threshold C3 marker level is < 81 mg protein per deciliter (mg/dl) serum measured using a C3- specific antibody. [0101] In embodiments, the methods include measuring a level of anti-PS/PT antibody is in a serum, plasma, or whole blood sample. In embodiments, a level of anti-PS/PT IgG is determined using an enzyme-linked immunosorbent assay (ELISA). In embodiments, a level of anti-PS/PT IgM is determined using an enzyme-linked immunosorbent assay (ELISA). In embodiments described herein, a threshold anti-PS/PT IgG level is > 30 units measured using ELISA. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0102] In embodiments, the methods provided herein include where the PC4d level, C3 level, and anti-PS/PT IgG antibody level is determined 2, 3, 4 or more times. In embodiments, the methods provided herein include where the PC4d level, C3 level, and anti-PS/PT IgG antibody level is determined twice. In embodiments, the methods provided herein include where the PC4d level, C3 level, and anti-PS/PT IgG antibody level is determined 3 times. In embodiments, the methods provided herein include where the PC4d level, C3 level, and anti- PS/PT IgG antibody level is determined 4 times. In embodiments, the methods provided herein include where the PC4d level, C3 level, and anti-PS/PT IgG antibody level is determined more than 4 times [0103] In embodiments, the methods provided herein include where the subject is being treated with hydroxychloroquine (HCQ), and where the method further includes measuring a level of HCQ in a whole blood sample from the subject. In embodiments, an HCQ level below a threshold HCQ whole blood level indicates that the subject, is at risk of venous thrombosis, and/or indicates efficacy of HCQ and any other anti-thrombotic therapy. In embodiments, the threshold HCQ whole blood level is 500 ng/ml. [0104] In embodiments, the various methods described herein further include communication of the diagnosis, prognosis, or indication of treatment effect via a remote patient monitoring (RPM) internet-based devices to a medical professional, including but not limited to the subject’s doctor and/or the subject’s pharmacy for automated ordering of an anti- thrombotic agent and/or anti-platelet agent, including but not limited to an oral anti-coagulant. [0105] In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as having thrombosis and/or is identified as being at risk for thrombosis. In embodiments, the methods provided herein comprise administering an increased dose of a prescribed therapeutic agent to a subject when the subject is identified as having thrombosis and/or is identified as being at risk for thrombosis. In embodiments, the methods provided herein comprise: (i) administering an effective amount of a therapeutic agent to a subject when the subject is identified as having thrombosis and/or is identified as being at risk for thrombosis; and/or (ii) administering an increased dose of a prescribed therapeutic agent to a subject when the subject is identified as having thrombosis and/or is identified as being at risk for thrombosis; wherein the therapeutic agent and the prescribed therapeutic agent are different. For example, the subject can be administered an effective amount of an anti-thrombotic agent and administered an increased dose of a prescribed anti-platelet agent (e.g., the anti-thrombotic agent is a new drug for the subject and the patient was previously taking an anti-platelet agent but will be taking an increased dose of the anti-platelet agent going forward). In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an anti-thrombotic agent. In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an anti-thrombotic agent, an antiplatelet agent, or a combination thereof. In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an anti-thrombotic agent, an antiplatelet agent, a beta-blocker, an ACE inhibitor, a statin, or a combination of two or more thereof. In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as having thrombosis. In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as being at risk for thrombosis. [0106] In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as having myocardial infarction and/or is identified as being at risk for myocardial infarction. In embodiments, the methods provided herein comprise administering an increased dose of a prescribed therapeutic agent to a subject when the subject is identified as having myocardial infarction and/or is identified as being at risk for myocardial infarction. In embodiments, the methods provided herein comprise: (i) administering an effective amount of a therapeutic agent to a subject when the subject is identified as having myocardial infarction and/or is identified as being at risk for myocardial infarction; and/or (ii) administering an increased dose of a prescribed therapeutic agent to a subject when the subject is identified as having myocardial infarction and/or is identified as being at risk for myocardial infarction; wherein the therapeutic agent and the prescribed therapeutic agent are different. For example, the subject can be administered an effective amount of an anti-thrombotic agent and administered an increased dose of a prescribed anti-platelet agent (e.g., the anti-thrombotic agent is a new drug for the subject and the patient was previously taking an anti-platelet agent but will be taking an increased dose of the anti-platelet agent going forward). In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an antiplatelet agent. In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an anti-thrombotic agent, an antiplatelet agent, or a combination thereof. In embodiments, the therapeutic agent and/or prescribed therapeutic agent is an anti- thrombotic agent, an antiplatelet agent, a beta-blocker, an ACE inhibitor, a statin, or a combination of two or more thereof. In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as having myocardial infarction. In embodiments, the methods provided herein comprise administering an effective amount of a therapeutic agent to a subject when the subject is identified as being at risk for myocardial infarction. [0107] In embodiments, the anti-thrombotic agent or the prescribed anti-thrombotic agent is hydroxychloroquine, heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban, edoxaban, or a combination of two or more thereof. In embodiments, the anti-thrombotic agent is hydroxychloroquine. In embodiments, the anti- thrombotic agent is heparin. In embodiments, the anti-thrombotic agent is dalteparin. In embodiments, the anti-thrombotic agent is fondaparinux. In embodiments, the anti-thrombotic agent is enoxaparin. In embodiments, the anti-thrombotic agent is warfarin. In embodiments, the anti-thrombotic agent is dabigatran. In embodiments, an anti-thrombotic agent is rivaroxaban. In embodiments, the anti-thrombotic agent is apixaban. In embodiments, the anti- thrombotic agent is betrixaban. In embodiments, the anti-thrombotic agent is edoxaban. [0108] In embodiments, the anti-platelet agent or the prescribed anti-platelet agent is abciximab, eptifibatide, tirofiban, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, vorapaxar, aspirin, or a combination of two or more thereof. In embodiments, the anti-platelet agent is abciximab. In embodiments, the anti-platelet agent is eptifibatide. In embodiments, the anti-platelet agent is tirofiban. In embodiments, the anti- platelet agent is aspirin. In embodiments, the anti-platelet agent is cangrelor. In embodiments, the anti-platelet agent is cilostazol. In embodiments, the anti-platelet agent is clopidogrel. In embodiments, the anti-platelet agent is dipyridamole. In embodiments, the anti-platelet agent is prasugrel. In embodiments, the anti-platelet agent is ticlopidine. In embodiments, the anti- platelet agent is ticagrelor. In embodiments, the anti-platelet agent is vorapaxar. [0109] In embodiments, the beta-blocker or the prescribed beta-blocker is acebutolol, atenolol, betaxolol, bisoprolol, carteolol, carvedilol, labetalol, metoprolol, nadolol, nebivolol, penbutolol, pindolol, propranolol, sotalol, or timolol. [0110] In embodiments, the ACE inhibitor or the prescribed ACE inhibitor is benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, or trandolapril. [0111] In embodiments, the statin or the prescribed statin is atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, or simvastatin. [0112] In embodiments, measuring a level of PC4d in a first blood sample from the subject includes any one of the various methods described herein. In embodiments, measuring a level of a level of complement C3 protein in a second blood sample from the subject includes any of the various methods described herein. In embodiments, measuring a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody includes any of the various methods described herein. In embodiments, measuring a level of PC4d above a threshold of ≥10 net mean fluorescence intensity units measured using flow cytometry; measuring a level of C3 below a threshold of <81.1 mg protein per deciliter (mg/dl) serum measured using a C3-specific antibody, and measuring a level of anti-PS/PT IgG above a threshold of >30 units measured using ELISA provides a determination of risk of arterial thrombosis in the subject. In embodiments, the threshold PC4d level is ≥5 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥5 and less than 20 net mean fluorescence intensity units. In embodiments, the threshold PC4d level is ≥10 and less than 20 net mean fluorescence intensity units. In embodiments, the ELISA is a luminescent ELISA. In embodiments, the ELISA is a chemiluminescent ELISA. [0113] Provided herein are methods for preparing a sample from a systemic lupus erythematosus subject useful for analyzing a plurality of markers involved in arterial thrombosis and/or myocardial infarction, including: (a) collecting whole blood from the subject; (b) producing a platelet fraction derived from whole blood from said subject comprising lysing red blood cells, and measuring a level of PC4d in said platelet fraction using a methodology configured to identify whether the PC4d level is ≥10 mean fluorescence intensity units; and (c) producing a first serum fraction or a first plasma fraction from the whole blood from said subject and measuring a level of C3 in said fractions; and (d) producing a second serum fraction or a second plasma fraction from the whole blood from said subject and measuring a level of PS/PT complex antibody in said fraction. The term “markers” refers to PC4d, C3, and PS/PT. [0114] In embodiments, the methods for preparing a sample include collecting whole blood from a subject and producing a platelet fraction. Producing a platelet fraction may be accomplished by any method known in the art. In embodiments, producing a platelet fraction includes lying red blood cells and using a platelet specific antibody. In embodiments, measuring a level of PC4d includes any of the various embodiments described herein. In embodiments, measuring a level of PC4d includes using a platelet specific antibody and a C4d antibody includes fluorescence activated cell sorting. [0115] In embodiments, the methods for preparing a sample include producing a first serum or plasma fraction from the whole blood of a subject and measuring a level of C3 in the first serum or plasma fraction. In embodiments, measuring a level of C3 includes any of the various embodiments described herein. In embodiments, measuring the level of C3 includes an immunoturbidity assay. [0116] In embodiments, the methods for preparing a sample include producing a first serum or plasma fraction from the whole blood of a subject and measuring a level of anti-PS/PT complex antibody. In embodiments, measuring a level of anti-PS/PT complex antibody includes any of the various embodiments described herein. In embodiments, measuring a level of anti-PS/PT complex antibody an immunoassay. [0117] Embodiments 1 to 31 [0118] Embodiment 1. A method for diagnosing arterial thrombosis in a subject having systemic lupus erythematosus, the method comprising: measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing arterial thrombosis in a subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. [0119] Embodiment 2. A method for prognosing development of arterial thrombosis in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing the development of arterial thrombosis in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. [0120] Embodiment 3. A method for diagnosing myocardial infarction or a history of myocardial infarction in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and diagnosing myocardial infarction or the history of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. [0121] Embodiment 4. A method for prognosing development of myocardial infarction in a subject having systemic lupus erythematosus, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and prognosing development of myocardial infarction in the subject having systemic lupus erythematosus when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. [0122] Embodiment 5. A method of detecting an arterial thrombosis marker and/or a myocardial infarction marker in a systemic lupus erythematosus subject that has or is suspected of having had arterial thrombosis and/or myocardial infarction, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; and detecting the arterial thrombosis marker and/or the myocardial infarction marker in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level. [0123] Embodiment 6. The method of any one of Embodiments 1 to 5, further comprising administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof. [0124] Embodiment 7. The method of any one of Embodiments 1 to 6, further comprising administering to the subject an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof. [0125] Embodiment 8. A method of treating arterial thrombosis in a systemic lupus erythematosus subject in need thereof, the method comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof to treat arterial thrombosis; wherein: (i) a level of PC4d in a biological sample obtained from the subject is ≥10 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. [0126] Embodiment 9. A method of treating arterial thrombosis in a systemic lupus erythematosus subject, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying arterial thrombosis in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat arterial thrombosis, and/or an increased dose of a prescribed anti- thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat arterial thrombosis. [0127] Embodiment 10. A method of treating myocardial infarction in a systemic lupus erythematosus subject in need thereof, the method comprising: (a) administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof, or (b) administering to the subject an increased amount of a prescribed anti-thrombotic agent, a prescribed antiplatelet agent, or a combination thereof; wherein: (i) a level of PC4d in a biological sample obtained from the subject is ≥10 net mean fluorescence intensity units; (ii) a level of complement C3 in the biological sample obtained from the patient is below a threshold C3 level; and (iii) a level of anti-PS/PT IgG antibody in the biological sample obtained from the patient is above a threshold anti-PS/PT IgG antibody level. [0128] Embodiment 11. A method of treating myocardial infarction in a systemic lupus erythematosus subject, the method comprising measuring: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; identifying myocardial infarction in the systemic lupus erythematosus subject when: (i) the level of PC4d in the biological sample is ≥10 net mean fluorescence intensity units; (ii) the level of complement C3 in the biological sample is below a threshold C3 level; and (iii) the level of anti-PS/PT IgG antibody in the biological sample is above a threshold anti-PS/PT IgG antibody level; and administering to the subject an effective amount of an anti-thrombotic agent, an antiplatelet agent, or a combination thereof to treat myocardial infarction, and/or an increased dose of a prescribed anti-thrombotic agent, an increased dose of a prescribed antiplatelet agent, or a combination thereof to treat myocardial infarction. [0129] Embodiment 12. The method of any one of Embodiments 6 to 11, wherein the anti- thrombotic agent or the prescribed anti-thrombotic agent is hydroxychloroquine, heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban, edoxaban, or a combination of two or more thereof; and wherein the anti-platelet agent or the prescribed anti-platelet agent is abciximab, eptifibatide, tirofiban, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, vorapaxar, aspirin, or a combination of two or more thereof. [0130] Embodiment 13. The method of any one of Embodiments 6 to 12, further comprising administering to the subject an effective amount of a beta-blocker, an ACE inhibitor, a statin, or a combination of two or more thereof; and/or increasing the dose of a prescribed beta- blocker, a prescribed ACE inhibitor, a prescribed statin, or a combination of two or more thereof. [0131] Embodiment 14. The method of Embodiment 13, wherein the beta-blocker or the prescribed beta-blocker is acebutolol, atenolol, betaxolol, bisoprolol, carteolol, carvedilol, labetalol, metoprolol, nadolol, nebivolol, penbutolol, pindolol, propranolol, sotalol, or timolol; wherein the ACE inhibitor or the prescribed ACE inhibitor is benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, or trandolapril; and wherein the statin or the prescribed statin is atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, or simvastatin. [0132] Embodiment 15. The method of any one of Embodiments 1 to 14, wherein the biological sample is a blood sample. [0133] Embodiment 16. The method of any one of Embodiments 1 to 15, comprising measuring the level of PC4d protein in the biological sample, wherein the biological sample is a whole blood sample. [0134] Embodiment 17. The method of any one of Embodiments 1 to 16, comprising measuring the level of complement C3 protein in the biological sample, wherein the biological sample is a serum sample or a plasma sample. [0135] Embodiment 18. The method of any one of Embodiments 1 to 17, comprising measuring the level of anti-PS/PT antibody in the biological sample, wherein the biological sample is a serum sample, a plasma sample, or a whole blood sample. [0136] Embodiment 19. The method of any one of Embodiments 1 to 18, comprising (a) measuring the level of PC4d using an antibody specific for C4d; (b) measuring the level of C3 using an antibody specific for C3; and (c) measuring the level of anti-PS/PT IgG antibody using an enzyme-linked immunosorbent assay which comprises plates coated with PS/PT. [0137] Embodiment 20. The method of any one of Embodiments 1 to 19, wherein the threshold C3 level is < 81.1 mg protein per deciliter serum measured using a C3-specific antibody. [0138] Embodiment 21. The method of any one of Embodiments 1 to 20, wherein the threshold anti-PS/PT IgG level is > 30 units measured using an enzyme-linked immunosorbent assay. [0139] Embodiment 22. The method of any one of Embodiments 1 to 21, wherein the subject is a human subject. [0140] Embodiment 23. The method of any one of Embodiments 1 to 22, wherein the subject is being treated with hydroxychloroquine; and wherein the method further comprises measuring a level of hydroxychloroquine in a whole blood sample from the subject; identifying the subject as being at risk of arterial thrombosis when the hydroxychloroquine level is below a threshold hydroxychloroquine level; and administering to the subject an increased dose of hydroxychloroquine. [0141] Embodiment 24. The method of Embodiment 23, wherein the threshold hydroxychloroquine level is 500 ng/ml. [0142] Embodiment 25. The method of Embodiment 1, 2, 5, 8, or 9 further comprising: (i) calculating an arterial thrombosis risk score by adjusting the level of the level of platelet-bound C4d (PC4d) protein, the level of complement C3 protein, and the level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody by one or more transformation analyses; and (ii) comparing the arterial thrombosis risk score to a standard arterial thrombosis risk score. [0143] Embodiment 26. The method of Embodiment 3, 4, 5, 10, or 11, further comprising: (i) calculating a myocardial infarction risk score by adjusting the level of the level of platelet- bound C4d (PC4d) protein, the level of complement C3 protein, and the level of anti- phosphatidyl serine/prothrombin (PS/PT) IgG antibody by one or more transformation analyses; and (ii) comparing the arterial thrombosis risk score to a standard myocardial infarction risk score. [0144] Embodiment 27. A method for preparing a sample from a systemic lupus erythematosus subject to analyzing a plurality of markers involved in arterial thrombosis and/or myocardial infarction, the method comprising: (a) producing a platelet fraction derived from whole blood obtained from the subject comprising lysing red blood cells, and measuring a level of PC4d in the platelet fraction using a methodology configured to identify whether the PC4d level is > 10 mean fluorescence intensity units; and (b) producing a first serum fraction or a first plasma fraction from the whole blood from obtained from the subject and measuring a level of C3 in the first serum fraction or first plasma fraction; and (c) producing a second serum fraction or a second plasma fraction from the whole blood obtained from the subject and measuring a level of PS/PT complex antibody in the second serum fraction or second plasma fraction. [0145] Embodiment 28. The method of Embodiment 27, wherein measuring the level of PC4d further comprises binding platelets using a platelet specific antibody. [0146] Embodiment 29. The method of Embodiment 27 or 28, wherein measuring the level of PC4d further comprises fluorescence-activated cell sorting. [0147] Embodiment 30. The method of one of Embodiments 27 to 29, wherein measuring the level of C3 comprises an immunoturbidity assay. [0148] Embodiment 31. The method of one of Embodiments 27 to 30, wherein measuring the level of PS/PT complex antibodies comprises an immunoassay. [0149] Embodiments P1 to P43 [0150] Embodiment P1. A method for diagnosing arterial thrombosis in a subject having systemic lupus erythematosus, comprising determining: (a) a level of platelet-bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; wherein a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, wherein the threshold PC4d level is ≥10 net mean fluorescence intensity units (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had an arterial thrombosis. [0151] Embodiment P2. A method for prognosing development of arterial thrombosis in a subject having systemic lupus erythematosus, comprising determining: (a) a level of platelet- bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; wherein a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, wherein the threshold PC4d level is ≥10 net mean fluorescence intensity units (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject is at risk of developing arterial thrombosis. [0152] Embodiment P3. A method for diagnosing a history of myocardial infarction (MI) in a subject having systemic lupus erythematosus, comprising determining: (a) a level of platelet- bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; wherein a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level wherein the threshold PC4d level is ≥10 net mean fluorescence intensity units, (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject has had a myocardial infarction. [0153] Embodiment P4. A method for prognosing development of myocardial infarction in a subject having systemic lupus erythematosus, comprising determining: (a) a level of platelet- bound C4d (PC4d) protein in a biological sample from the subject; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject; wherein a combination of (i) a level of PC4d in the biological sample above a threshold PC4d level, wherein the threshold PC4d level is ≥10 net mean fluorescence intensity units (ii) a level of complement C3 below a threshold C3 level, and (iii) a level of anti-PS/PT IgG antibody above a threshold anti-PS/PT IgG antibody level, indicates that the subject is at risk of developing myocardial infarction. [0154] Embodiment P5. The method of any one of Embodiments P1 to P3, wherein the level of PC4d protein is in a whole blood biological sample. [0155] Embodiment P6. The method of any one of Embodiments P1 to P4, wherein the level of complement C3 protein is in a serum or plasma sample. [0156] Embodiment P7. The method of any one of Embodiments P1 to P5, wherein the level of anti-PS/PT antibody is in a serum, plasma, or whole blood sample. [0157] Embodiment P8. The method of any one of Embodiments P1 to P6, wherein the level of PC4d is determined using an antibody specific for C4d, and the level of C3 is determined using an antibody specific for C3. [0158] Embodiment P9. The method of any one of Embodiments P1 to P7, wherein the level of anti-PS/PT IgG antibody is determined using an enzyme-linked immunosorbent assay (ELISA) comprising ELISA plates, wherein the ELISA plates are coated with PS/PT. [0159] Embodiment P10. The method of any one of Embodiments P1 to P9, wherein the threshold C3 marker level is <81.1 mg protein per deciliter (mg/dl) serum measured using a C3-specific antibody. [0160] Embodiment P11. The method of any one of Embodiments P1 to P10, wherein the threshold anti-PS/PT IgG level is >30 units measured using ELISA. [0161] Embodiment P12. The method of any one of Embodiments P1 to P11, wherein the subject is a human subject. [0162] Embodiment P13. The method of any one of Embodiments P1 to P12, wherein the PC4d level, C3 level, and the level of anti-PS/PT IgG antibody are determined 2, 3, 4, or more times. [0163] Embodiment P14. The method of any one of Embodiments P1 to P13, wherein the subject is being treated with hydroxychloroquine (HCQ), and wherein the method further comprises determining a level of HCQ in a whole blood sample from the subject, wherein an HCQ level below a threshold HCQ whole blood level indicates that the subject is at risk of arterial thrombosis, and/or indicates reduced efficacy of HCQ. [0164] Embodiment P15. The method of Embodiment P14, wherein the threshold HCQ whole blood level is 500 ng/ml. [0165] Embodiment P16. The method of any one of Embodiments P1 to P15, wherein the method further comprises communication of the diagnosis, prognosis, or indication of treatment effect via a remote patient monitoring (RPM) internet-based devices to a medical professional, including but not limited to the subject’s doctor and/or the subject’s pharmacy for automated ordering of an anti-thrombotic agent, including but not limited to an oral anti- coagulant. [0166] Embodiment P17. The method of any one of Embodiments P1 to P16, wherein the subject is identified as having arterial thrombosis, at risk of arterial thrombosis, or in need of modified therapy for arterial thrombosis, wherein the method further comprises treating the subject with an anti-thrombotic agent, or increasing the dosage of an anti-thrombotic agent, wherein the anti-thrombotic is selected from heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban and edoxaban. [0167] Embodiment P18. The method of Embodiment P17, further comprising treating the subject with an anti-platelet agent or increasing the dosage of an anti-platelet agent, wherein the anti-platelet agent is selected from abciximab, eptifibatide, tirofiban, aspirin, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, and vorapaxar. [0168] Embodiment P19. A method of detecting a marker in a systemic lupus erythematosus, subject that has or is suspected of having had arterial thrombosis, the method comprising determining: (a) a level of platelet C4d (PC4d) protein in a biological sample from the subject using a methodology configured to identify whether the PC4d level is ≥10 net mean fluorescence intensity units; (b) a level of complement C3 protein in a biological sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody in a biological sample from the subject. [0169] Embodiment P20. The method of Embodiment P19, wherein the level of PC4d protein is in a whole blood biological sample. [0170] Embodiment P21. The method of Embodiments P19 or P20, wherein the level of complement C3 protein is in a serum sample or plasma sample. [0171] Embodiment P22. The method of any one of Embodiments P19 to P21, wherein the level of anti-PS/PT antibody is in a serum, plasma, or whole blood sample. [0172] Embodiment P23. The method of any one of Embodiments P19 to P22, wherein the level of PC4d is determined using an antibody specific for C4d, and the level of C3 is determined using an antibody specific for C3. [0173] Embodiment P24. The method of any one of Embodiments P19 to P23, wherein the level of anti-PS/PT IgG antibody is determined using an enzyme-linked immunosorbent assay (ELISA) in which ELISA plates are coated with PS/PT. [0174] Embodiment P25. The method of any one of Embodiments P19 to P24, wherein the threshold C3 marker level is <81.1 mg protein per deciliter (mg/dl) serum or plasma measured using a C3-specific antibody. [0175] Embodiment P26. The method of any one of Embodiments P19 to P25, wherein the threshold anti-PS/PT IgG level is >30 units measured using ELISA. [0176] Embodiment P27. The method of any one of Embodiments P19 to P26, wherein the subject is being treated with hydroxychloroquine (HCQ), and wherein the method further comprises determining a level of HCQ in a whole blood sample from the subject, wherein an HCQ level below a threshold HCQ whole blood level indicates that the subject is at risk of arterial thrombosis, and/or indicates reduced efficacy of HCQ. [0177] Embodiment P28. The method of Embodiment P27, wherein the threshold HCQ whole blood level is 500 ng/ml. [0178] Embodiment P29. The method of any one of Embodiments P19 to P28, wherein the subject is identified as having thrombosis, at risk of thrombosis, or in need of modified therapy for thrombosis, wherein the method further comprises treating the subject with an anti- thrombotic agent, or increasing the dosage of an anti-thrombotic agent selected from hydroxychloroquine, heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban and edoxaban. [0179] Embodiment P30. The method of Embodiment P29, further comprising treating the subject with an anti-platelet agent or increasing the dosage of an anti-platelet agent, wherein the anti-platelet agent is selected from abciximab, eptifibatide, tirofiban, aspirin, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, and vorapaxar. [0180] Embodiment P31. The method of any one of Embodiments P1 to P30, wherein the subject is a human subject. [0181] Embodiment P32. The method of any one of Embodiments P1 to P31, wherein the PC4d level, C3 level, and anti-PS/PT IgG antibody level are determined 2, 3, 4, or more times. [0182] Embodiment P33. A method of treating arterial thrombosis in a systemic lupus erythematosus, subject comprising determining: (a) a level of PC4d ≥10 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein < 81.1 mg/dl in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody > 30 units in a third blood sample from the subject measured using ELISA; and (d) treating the subject with an effective amount of one or more therapeutic. [0183] Embodiment P34. The method of Embodiment P33, step (c) further comprising: (i) calculating a thrombosis risk score by adjusting the level of the markers by one or more transformation analyses, wherein the one or more transformation analyses comprises logistic regression analysis; and (ii) comparing the thrombosis risk score to one or more of a standard thrombosis risk score. [0184] Embodiment P35. The method of Embodiments P33 or P34, wherein the therapeutic is selected from hydroxychloroquine, heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban, edoxaban, abciximab, eptifibatide, tirofiban, aspirin, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, and vorapaxar. [0185] Embodiment P36. A method of treating myocardial infarction (MI) in a systemic lupus erythematosus, subject comprising determining: (a) a level of PC4d ≥10 net mean fluorescence intensity units measured using flow cytometry in a first blood sample from the subject; (b) a level of complement C3 protein < 81.1 mg/dl in a second blood sample from the subject; and (c) a level of anti-phosphatidyl serine/prothrombin (PS/PT) IgG antibody > 30 units in a third blood sample from the subject measured using ELISA; and (d) treating the subject with an effective amount of one or more therapeutic. [0186] Embodiment P37. The method of Embodiment P33, step (c) further comprising: (i) calculating a risk score by adjusting the level of the markers by one or more transformation analyses, wherein the one or more transformation analyses comprises logistic regression analysis; and (ii) comparing the risk score to one or more of a standard thrombosis risk score. [0187] Embodiment P38. The method of Embodiments P36 or P37, wherein the therapeutic is selected from hydroxychloroquine, heparin, dalteparin, fondaparinux, enoxaparin, warfarin, dabigatran, rivaroxaban, apixaban, betrixaban, edoxaban, abciximab, eptifibatide, tirofiban, aspirin, cangrelor, cilostazol, clopidogrel, dipyridamole, prasugrel, ticlopidine, ticagrelor, and vorapaxar. [0188] Embodiment P39. A method for preparing a sample from a systemic lupus erythematosus, subject useful for analyzing a plurality of markers involved in arterial thrombosis and/or myocardial infarction, comprising: (a) collecting whole blood from said subject; (b) producing a platelet fraction derived from whole blood from said subject comprising lysing red blood cells, and measuring a level of PC4d in said platelet fraction using a methodology configured to identify whether the PC4d level is >10 mean fluorescence intensity units; and (c) producing a first serum fraction or a first plasma fraction from the whole blood from said subject and measuring a level of C3 in said fractions; and (d) producing a second serum fraction or a second plasma fraction from the whole blood from said subject and measuring a level of PS/PT complex antibody in said fraction. [0189] Embodiment P40. The method of Embodiment P39, wherein said measuring the level of PC4d further comprises binding platelets using a platelet specific antibody. [0190] Embodiment P41. The method of Embodiments P39 or P40, wherein said measuring the level of PC4d further comprises fluorescence-activated cell sorting. [0191] Embodiment P42. The method of one of Embodiments P39 to P41, wherein said measuring the level of C3 comprises an immunoturbidity assay. [0192] Embodiment P43. The method of one of Embodiments P39 to P42, wherein said measuring the level of PS/PT complex antibodies comprises an immunoassay. EXAMPLES [0193] Example 1 [0194] The study herein investigated the association of PC4d and the thrombotic risk score with thrombosis in a separate patient cohort. For this analysis, the inventors used a lower cutoff to define PC4d positivity (10 net MFI instead of 20 net MFI), which resulted in unexpectedly superior results in identifying cardiovascular events or risk factors (e.g., arterial thrombosis, myocardial infarction) in subjects with SLE. [0195] Methods [0196] Patients (n=150) with a clinical diagnosis of SLE and fulfilling the ACR and/or SLICC classification of SLE (n=2 patients only fulfilled SLICC criteria) were enrolled at the lupus clinic of Columbia University. (Petri et al, Arthritis Rheum.2012;64(8):2677-2686) [0197] Venous blood samples were shipped to Exagen, Inc. (Vista, CA) and tested for PC4d, complement C3, and anti-PS/PT. PC4d was measured by flow cytometry according to Exagen’s standard operating procedures; serum C3 was determined by turbidimetry (The Binding Site, San Diego, CA); serum anti-PS/PT was measured by immunoassay (INOVA Diagnostics, San Diego, CA). Manufacturer cut-offs were used for C3 and anti-PS/PT. In particular, C3 was considered low if < 81.1 mg/dL and anti-PS/PT was considered positive if > 30 chemiluminescence units (CU). Two cutoffs were used for PC4d: it was considered positive if ≥ 10 net MFI or ≥ 20 net MFI. [0198] The thrombotic risk score was calculated as described using anti-PS/PT IgG only. In addition, a cutoff of either 10 or 20 net MFI was used for PC4d. In particular, 1 point each was assigned to abnormal C3, anti-PS/PT, and PC4d with cutoff of either 10 or 20 net MFI). (Petri et al, Lupus Sci Med. 2019; 6(1):e000318). [0199] Of the 150 patients, 28 suffered a total of 31 thrombotic events in the 5 years before enrollment in the study. There were 13 arterial events: 8 cerebrovascular accidents (CVA) (defined as acute ischemic central vascular events with characteristic radiographic imaging at time of diagnosis) and 5 myocardial infarctions (defined as acute coronary syndromes with elevated troponin levels supporting myocardial injury). Transient ischemic attacks (TIA) and myocarditis and were excluded. Venous events (n=18) included 12 deep vein thrombosis, 4 pulmonary embolisms, 1 portal vein thrombosis, 1 mesenteric vein thrombosis. [0200] To evaluate the association between history of thrombotic events and PC4d or the thrombotic score, chi-square test for independence (association) were performed. Diagnostic performances were evaluated with the Diagnostic Odds Ratio (DOR). All statistical analysis was performed using R (Version 3.6.2, R Foundation for Statistical Computing) with the epiR package (Version 1.0-14, Telmo Nunes et al.). [0201] Results [0202] Chi-square test for independence analysis showed that PC4d ≥ 10 net MFI was associated with history of thrombotic events (venous or arterial), arterial events, and venous events. Interestingly, all 5 individuals with MI had PC4d ≥ 10 net MFI, resulting in a strong association of PC4d with MI (p=0.002) (Table 1). Similar results were obtained with PC4d ≥ 20 net MFI. It was unexpectedly discovered that the diagnostic odds ratio (DOR) was higher when a cutoff of 10 was used to assess PC4d positivity compared to a cutoff of 20 net MFI (Table 1). [0203] Number of subjects negative (PC4d(-)) or positive (PC4d(+)) for PC4d who experienced or did not experience any of the events (arterial thrombosis, venous thrombosis, cardiovascular accidents (CVA), deep vein thrombosis (DVT) or myocardial infarction) is reported. Data was analyzed with PC4d at cutoffs 10 and 20 net MFI, as indicated. P value of the chi square analysis ( ² ) and diagnostic odds ratio (DOR) with 95% confidence intervals (95%CI) are reported. [0204] Table 1 [0205] The DOR of the thrombotic score are reported in Table 2. DOR of thrombotic score calculated using PC4d ≥ 10 net MFI was greater than when using a cutoff of 20. For example, a thrombotic score ≥ 2 had DOR=3.15 (95% CI 1.21, 8.19) when PC4d was ≥ 10 and DOR=2.32 (95% CI 0.73, 7.36) when PC4d was ≥ 20 for any thrombosis. Similar results were obtained for arterial thrombosis (DOR=4.44 (95% CI 1.24, 15.91) vs DOR=3.46 (95% CI 0.82, 14.68)). [0206] Interestingly, DOR was higher for arterial than venous thrombosis. DOR of thrombotic score ≥ 2 was 4.44 (95% CI 1.24, 15.91) for arterial thrombosis vs 2.65 (95% CI 0.89, 7.88) for venous with PC4d ≥ 10 net MFI; DOR of thrombotic score ≥ 2 was 3.46 (95% CI 0.82, 14.68) for arterial thrombosis vs 2.71 (95% CI 0.77, 9.57) for venous thrombosis with PC4d ≥ 20 net MFI. Surprisingly, these data demonstrate that the thrombotic score has a stronger association with arterial thrombosis than with venous thrombosis. [0207] In addition, the thrombotic score was strongly associated with myocardial infarction; DOR for thrombotic score with PC4d ≥ 10 net MFI was infinite because all patients with myocardial infarction had PC4d above this threshold. [0208] In Table 2, sensitivity, specificity, and diagnostic odds ratio (DOR) with 95% confidence intervals (95% CI) are reported for thrombotic scores ≥ 1, ≥ 2, ≥ 3. The thrombotic scores were calculated using cutoffs for PC4d of 10 or 20 net MFI, as indicated. Data was analyzed for any thrombosis (arterial or venous), arterial thrombosis, venous thrombosis, cardiovascular accidents (CVA), deep vein thrombosis (DVT) or myocardial infarction (MI). [0209] Table 2

[0210] Conclusions [0211] The data presented herein shows that PC4d positivity is associated with a history of either venous or arterial vascular events. The association, as determined by chi-square analysis and logistic regression, is greater if a cutoff of 10 net MFI (≥ 10 net MFI) is used compared to 20 net MFI (≥ 20 net MFI) (Table 1). These data demonstrate that PC4d ≥ 10 net MFI is a better marker for risk of thrombosis than PC4d ≥ 20 net MFI. The association of PC4d with arterial thrombosis and, in particular, MI is especially interesting, as contrasting data has been reported in the literature. (Petri et al, Lupus Sci Med.2019; 6(1):e000318; Lood et al, Lupus. 2012; 21(13):1423-1432; Lood et al, PLoS One.2014; 9(6):e99386; Mehta et al, Stroke.2008; 39(12):3236-3241). [0212] In addition to PC4d, the thrombotic score associated with a history of either venous or arterial vascular events. DOR of thrombotic score calculated using PC4d ≥ 10 net MFI was greater than when using a cutoff of ≥ 20 net MFI, surprisingly demonstrating that the lower cutoff is superior for the calculation of the thrombotic score as a biomarker for risk of cardiovascular event. In addition, the thrombotic score was more strongly associated with arterial than venous thrombosis in this study. [0213] Example 2 [0214] Using a cross-sectional design, we examined the association of PC4d, measured by flow cytometry, with thrombosis. PC4d was dichotomized and we evaluated the ability of different cutoff values, ranging from 5 to 20 net MFI, to discriminate for the history of vascular events. The thrombotic risk was calculated. [0215] 150 SLE patients (40 ± 13 years old, 91% female, 33% Hispanic, 26% African American) were included; 38% had antiphospholipid antibodies (aPL). Thirty-one vascular events (18 venous, 13 arterial) occurred within five years of study enrollment. Arterial and venous events, as compared to no events, were associated with higher PC4d levels (median (IQR) 13.6 (4.4-24.0) and 13.2 (3.2-22.3) vs.4.0 (2.5-8.3) net MFI, respectively, p< 0.05). In a multivariable model adjusting for all significant co-variates identified in the univariable analysis (aPL, smoking, antimalarial use and prednisone >7.5mg/day), the association between all vascular events and PC4d (natural log transformed) remained significant (OR 1.795%CI 1.2-2.5, p=0.005). [0216] The optimal PC4d cut-off point for vascular thromboses was identified to be 10 net MFI, with a sensitivity and specificity for venous events of 56% and 78%, and for arterial 62% and 78% (Tables 3A-3B); PC4d≥10 net MFI, as compared to PC4d≥20 net MFI, resulted in a greater detection of individuals with vascular events (16/28 vs 11/28 respectively). Stratifying by aPL status, PC4d10 was associated with a history of any vascular event, with a stronger association seen in patients positive for both aPL and PC4d - OR 4.695% CI 1.3-16.9 for PC4d+/aPL- and OR 13.095% CI 3.7-46.0 for PC4d+/aPL+ as compared with PC4d-/aPL- patients (Figure). A thrombotic score ≥ 2 (calculated using PC4d≥10) was associated with all events (arterial and venous) – OR 3.15 (95% CI 1.21, 8.19) and with arterial thrombosis - OR 4.44 (95% CI 1.24, 15.91) (Table 4). [0217] Table 3A. Sensitivity and specificity of different PC4d cutoff levels for history of venous vascular events. [0218] Table 3B. Sensitivity and specificity of different PC4d cutoff levels for history of arterial vascular events. [0219] Table 4. Sensitivity, specificity, and odds ratio (OR) with 95% confidence intervals (95% CI) are reported for thrombotic score ≥ 2. The thrombotic score was calculated using cutoff for PC4d of 10 MFI. NaN: not a number. [0220] PC4d and the thrombotic score associate with thrombotic events in SLE. The 10 net MFI PC4d cutoff was optimal for identifying patients with thromboses, and more specifically arterial events. PC4d10 could function more effectively as a biomarker of cardiovascular events, providing a novel risk indicator independent of aPL antibodies. [0221] The section headings used herein are for organizational purposes only and are not to be construed as limiting the subject matter described. All documents, or portions of documents, cited in the application including, without limitation, patents, patent applications, articles, books, manuals, and treatises are incorporated by reference in their entirety for any purpose. [0222] While various embodiments and aspects of the disclosure are shown and described herein, it will be obvious to those skilled in the art that such embodiments and aspects are provided by way of example only. Variations, changes, and substitutions will now occur to those skilled in the art without departing from the disclosure. It should be understood that various alternatives to the embodiments of the disclosure described herein might be employed in practicing the disclosure.