fibrin and Lupus-Erythematosus--Systemic

Acquired factor XIII (FXIII) deficiency, arising from an autoantibody against factor XIII, is a rare bleeding disorder. This autoimmune disorder most commonly occurs in the elderly. Patients who develop such acquired FXIII inhibitors may present with catastrophic bleeding events and are hard to be diagnosed with the normal general coagulation tests. Though the disease is relatively rare, it is known to cause significant mortality. In this article we briefly describe a patient who presented with extensive bleeding and a normal activated partial thromboplastin time and prothrombin time (PT), but had an acquired inhibitor to FXIII; her primary disease was systemic lupus erythematosus (SLE). Also, we will focus on the clinical features, treatment modalities, fibrin structure and epitope identification for acquired factor XIII inhibitor with a review of the literature.

Topics: Adult; Blood Coagulation Disorders; Blood Coagulation Factor Inhibitors; Epitopes; Factor VIII; Factor XIII Deficiency; Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Immunosuppressive Agents; Lupus Erythematosus, Systemic

Topics: Abortion, Habitual; Animals; Autoantibodies; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Factor IX; Factor V; Factor VIII; Female; Fibrin; Humans; Immunoglobulins; Isoantibodies; Lupus Coagulation Inhibitor; Lupus Erythematosus, Systemic; Pregnancy; Prothrombin; Thrombosis; von Willebrand Factor

Topics: Acrosin; Angioedema; Animals; Antifibrinolytic Agents; Complement Activation; Contraceptive Agents, Male; Fibrin; Humans; In Vitro Techniques; Lupus Erythematosus, Systemic; Male; Neutrophils; Protease Inhibitors; Rats

Topics: Acute Disease; Adolescent; Adult; Child; Child, Preschool; Chronic Disease; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Immune Complex Diseases; Immunoglobulin A; Immunoglobulin G; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Middle Aged; Nephritis; Nephrosis; Nephrotic Syndrome; Purpura; Streptococcal Infections

The experimental and clinical observations analyzed in this review suggest that the deposition of fibrin within glomeruli is an important pathogenic mechanism in the series of events leading to progressive destruction of glomerular capillaries. Neither the causal factors nor the consequences of this type of reaction are peculiar to the glomerulus. Fibrin deposits can occur in any injured blood vessel and, if not rapidly dealt with by fibrinolysis, will lead to endothelial changes and the development of organizing thrombi. It seems that glomerular capillaries are especially vulnerable; there are several reasons for this. First, some immunologic reactions are triggered within the glomeruli and thus produce a local inflammatory response, leading to fibrin deposition. Secondly, the glomerular filtration function allows a progressive local accumulation of potentially damaging particles, such as circulating fibrinogen derivatives (formed during generalized intravascular clotting), or phlogistic immune complexes (as a result of systemic antigen-antibody interaction); these too cause local injury and fibrin deposition. Finally, the glomerular obliteration resulting from the organization of such fibrin deposits leads to irreversible damage and so has more serious implications for the patient than if the lesions occurred elsewhere, where the formation of functionally useful new capillaries is often possible. It seems reasonable to propose, therefore, that the use of anticoagulant may be natural therapy in cases with the risk of rapid, massive, and continuous fibrin accumulation in glomeruli, where glomerular sclerosis and irreversible renal failure are likely.

Topics: Anticoagulants; Antigen-Antibody Complex; Antigen-Antibody Reactions; Basement Membrane; Blood Coagulation; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Endocarditis, Bacterial; Fibrin; Glomerulonephritis; Humans; Hyalin; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Phagocytosis; Purpura

Topics: Antibodies, Antinuclear; Arthritis, Rheumatoid; Autoantibodies; Autoimmune Diseases; Collagen Diseases; Fibrin; Humans; Kidney; Leukocyte Count; Lupus Erythematosus, Systemic; Myocardium; Rheumatic Fever; Rheumatoid Factor; Skin; Synovial Membrane

Among complications of systemic lupus erythematosus (SLE), thrombotic events are relatively common and contribute significantly to the morbidity and mortality rates. An increased risk of thrombosis in various diseases has been shown to be associated with the lytic stability and mechanical stiffness of the fibrin clot determined by its structure. Here we studied alterations of the fibrin clot properties in relation to disease severity in SLE patients. Plasma clots from 28 SLE patients were characterized by the kinetics of formation and fibrinolytic dissolution (using dynamic turbidimetry), the network and fiber ultrastructure (scanning electron microscopy), viscoelasticity (shear rheometry), and the rate and degree of crosslinking (Western blotting) correlated with the disease activity, blood composition, and compared to clotting of pooled normal human plasma. Clots made from plasma of SLE patients were lysed faster with exogenous t-PA than control clots from normal plasma without a significant difference between those from active (SLEDAI>4) and inactive (SLEDAI<4) SLE patients. Clots from the blood of patients with active SLE were characterized by significantly slower onset, but faster rate of fibrin polymerization and a higher optical density due to thicker fibers compared to those from inactive SLE and control pooled normal plasma. The rheological parameters of the clots (storage and loss moduli) were significantly increased in the active SLE patients along with enhanced fibrin crosslinking and hyperfibrinogenemia. The structural and rheological alterations displayed a strong positive correlation with high fibrinogen levels and other laboratory markers of immune inflammation. In conclusion, changes in the blood composition associated with active systemic inflammation in SLE cause significant alterations in the lytic resistance of fibrin clots associated with changes in polymerization kinetics, viscoelastic properties, and structure. The formation of more rigid prothrombotic fibrin clots in the plasma of SLE patients is likely due to the inflammatory hyperfibrinogenemia and greater extent of crosslinking. However, the higher susceptibility of the SLE clots to fibrinolysis may be a protective and/or compensatory mechanism that reduces the risk of thrombotic complications and improves patient outcomes.

Topics: Adult; Female; Fibrin; Fibrinogen; Fibrinolysis; Humans; Lupus Erythematosus, Systemic; Male; Microscopy, Electron, Scanning; Thrombosis

ESSENTIALS: The lectin pathway's MASP-1/2 activates coagulation factors but the trigger of the activation is unknown. MASP-1/2 activation was assessed by quantifying complexes between MASPs and antithrombin/C1-inhibitor. Activated platelets and fibrin were demonstrated to activate MASP-1 and MASP-2 both in vitro and in vivo. These findings may represent a crossroad between the complement and the coagulation systems.. The activated forms of the complement lectin pathway (LP) proteases MASP-1 and MASP-2 are able to cleave the coagulation factors prothrombin, fibrinogen, factor XIII and thrombin-activatable fibrinolysis inhibitor in vitro. In vivo studies also show that MASP-1 is involved in thrombogenesis.. To clarify the not yet identified mechanisms involved in triggering activation of the LP during thrombotic reactions.. Novel sandwich-ELISAs for detection of complexes between MASP-1 or MASP-2 and the serpins C1 inhibitor (C1-INH) or antithrombin (AT), were used to specifically detect and quantify the activated forms of MASP-1 and MASP-2.. Activated platelets were shown by flow cytometry to bind Ficolin-1, -2 and -3 but not MBL, which was associated with activation of MASP-1 and MASP-2. We also demonstrated that fibrin and the plasmin-generated fibrin fragment DD in plasma, bind and activate MASP-1 and MASP-2. As demonstrated by the ELISA and SDS-PAGE/Western blotting, the fibrin-associated activation was reflected in a specific inactivation by AT during clotting without the assistance of heparin. In all other cases the MASPs were, as previously reported, inactivated by C1-INH. In systemic lupus erythematosus patients with thrombotic disease and in polytrauma patients, the levels of activated MASP-1 and MASP-2 in complex with both AT and C1-INH were associated with markers of thrombotic disease and contact/coagulation system activation.. MASP-1 and MASP-2 are activated during blood clotting. This activation is triggered by activated platelets and by the generation of fibrin during thrombotic reactions in vitro and in vivo, and may represent a novel activation/amplification mechanism in thromboinflammation.

Topics: Adult; Aged; Aged, 80 and over; Antithrombin Proteins; Blood Coagulation; Blood Platelets; Case-Control Studies; Complement C1 Inhibitor Protein; Complement Pathway, Mannose-Binding Lectin; Enzyme Activation; Female; Fibrin; Humans; Inflammation; Lupus Erythematosus, Systemic; Male; Mannose-Binding Protein-Associated Serine Proteases; Middle Aged; Multiple Trauma; Platelet Activation; Protein Binding; Signal Transduction; Thrombosis; Time Factors; Young Adult

The study suggests that patients with systemic lupus erythematosus (SLE) present with distinct inflammatory ultrastructural changes such as platelets blebbing, generation of platelet-derived microparticles, spontaneous formation of massive fibrin network and fusion of the erythrocytes membranes. Lupoid platelets actively interact with other inflammatory cells, particularly with white blood cells (WBCs), and the massive fibrin network facilitates such an interaction. It is possible that the concerted actions of platelets, erythrocytes and WBC, caught in the inflammatory fibrin network, predispose to pro-thrombotic states in patients with SLE.

Topics: Adult; Blood Buffy Coat; Blood Platelets; Cell Communication; Cell-Derived Microparticles; Erythrocytes; Female; Fibrin; Humans; Leukocytes; Lupus Erythematosus, Systemic; Male; Microscopy, Electron, Scanning; Platelet Activation; Platelet-Rich Plasma; Thrombosis; Young Adult

Patients with systemic lupus erythematosus (SLE) have persistent platelet activation and an increased risk of thrombotic events, which cannot be accounted for by traditional cardiovascular risk factors. Factor (F)XII has a potentially important role in thrombus formation and is triggered by activated platelets. We therefore asked whether the contact system is involved in inflammation and vascular disease (VD) in SLE.. Fibrin clots were incubated with purified FXII or whole blood, and the activation and regulation of FXII were studied. Plasma from SLE patients with (n = 31) or without (n = 38) previous VD and from matched healthy controls (n = 68) were analyzed for the presence of complexes formed between contact system enzymes and antithrombin (AT) or C1 inhibitor (C1INH) and evaluated with regard to clinical data and laboratory parameters.. Fibrin clots elicited FXII activation and acted as co-factors for AT. In clotting plasma, the levels of FXIIa-AT increased, and FXIIa-C1INH decreased. A similar reciprocal relationship existed in SLE patients. FXIIa-AT was elevated in the SLE patients with a history of VD, while the corresponding levels of factor FXIIa-C1INH were significantly decreased. FXIIa-AT correlated strongly with platelet parameters. The odds ratio for VD among the SLE patients was 8.9 if they had low levels of FXIIa-C1INH, 6.1 for those with high levels of FXIIa-AT, and increased to 23.4 for those with both decreased levels of FXIIa-C1INH and increased levels of FXIIa-AT.. Activation of FXII is elicited by fibrin during thrombotic reactions in vitro and in vivo, and fibrin acts as a heparin-like co-factor and regulates AT. Patients with SLE had altered levels of FXIIa-serpin complexes, supporting that the contact system is involved in this disease. FXIIa-serpin complexes are strongly associated with previous VD in SLE patients, suggesting that these complexes are potential biomarkers for monitoring and assessing the risk of thrombotic events in SLE.

Topics: Adult; Biomarkers; Blood Coagulation; Blotting, Western; Enzyme-Linked Immunosorbent Assay; Factor XII; Female; Fibrin; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged; Risk Factors; Serpins; Thrombosis

Topics: Adolescent; Cecal Diseases; Diagnosis, Differential; Female; Fibrin; Humans; Ileal Diseases; Lupus Erythematosus, Systemic; Syncope; Thrombosis; United States; Vasculitis; Weight Loss

A high incidence of thromboembolic events has been reported in patients with systemic lupus erythematosus (SLE). Phosphatidylserine (PS) is normally sequestered in the inner leaflet of cell membranes. Externalization of PS during cell activation is mediated by phospholipid scramblase 1 (PLSCR1) and has a central role in promoting blood coagulation. We investigated the underlying pathogenic status of thrombophilia in SLE by analyzing PLSCR1 expression on monocytes from patients with SLE.. Sixty patients with SLE were evaluated. Twenty-three patients had antiphospholipid syndrome (APS/SLE). Plasma D-dimer levels were measured as a marker of fibrin turnover. The cDNA encoding human PLSCR1 was cloned from the total RNA extract from monocytes, and independent clones were sequenced. PLSCR1 mRNA expression in CD14+ cells was determined by real-time polymerase chain reaction. PS exposure on CD14+ cell surface was analyzed by flow cytometry.. Elevated D-dimer levels were found in plasma from SLE patients. Three splice variants of PLSCR1 mRNA were identified in all subjects, and levels of full-length PLSCR1 mRNA were significantly increased in SLE compared to healthy controls (2.9 +/- 1.5 vs 1.3 +/- 0.4, respectively; p < 0.0001). Flow-cytometry analysis showed relative enhancement of PS exposure in the surface of CD14+ cells in SLE patients compared to healthy controls.. Novel PLSCR1 splice variants were identified. Monocytes in SLE patients had enhanced PLSCR1 mRNA expression, as well as increased fibrin turnover and cell-surface PS exposure, indicating that PLSCR1 may, in part, contribute to the prothrombotic tendency in SLE.

Topics: Adult; Aged; Antiphospholipid Syndrome; Cell Membrane; Exocytosis; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Flow Cytometry; Gene Expression; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged; Monocytes; Phosphatidylserines; Phospholipid Transfer Proteins; Protein Isoforms; RNA Splicing; RNA, Messenger; Young Adult

Topics: Cardiac Tamponade; Cardiovascular Diseases; Echocardiography; Fibrin; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged

The main event in blood coagulation is the thrombincatalyzed conversion of fibrinogen into fibrin. This singular transformation of a soluble protein into an insoluble polymeric network occurs with faultless precision. Abnormalities of fibrin polymerization can lead to hemorragic and thrombotic disorders. Increased fibrinogen plasma concentration (Fg) and fibrin polymerization rate (FPR) could be additional risk factors associated with atherothrombosis in antiphospholipid syndrome (APS) and in systemic lupus erythematosus (SLE). Our objective was to investigate Fg and FPR in consecutive patients with APS and SLE. Thirty-nine patients and 31 age- and gender-matched healthy controls were studied. Sixteen patients had primary APS, 13 patients had SLE, and 10 patients had SLE plus APS. The mean of the FPR was significantly increased (0.2799 +/- 0.091) in patients with APS plus SLE as compared with the control group (0.2052 +/- 0.055) (p < 0.05). Fg was higher in APS plus SLE (3.15 g/L +/- 0.43) and in primary APS (3.03 g/L +/- 0.29) than in controls (2.87 g/L +/- 0.49). Our results demonstrated an increased FPR in patients with APS plus SLE. This phenomenon could be an additional risk factor for thrombosis in these autoimmune diseases.

Topics: Adult; Antiphospholipid Syndrome; Blood Coagulation; Female; Fibrin; Fibrinogen; Humans; Kinetics; Lupus Erythematosus, Systemic; Male; Reference Values

Fibrinogen Matsumoto V (M-V) is a dysfibrinogen identified in a 52-year-old woman with systemic lupus erythematous. The triplet AGG encoding the amino acid residue Aalpha19 was replaced by GGG, resulting in the substitution of Arg-->Gly. Residue Aalpha19 has been shown to be one of the most important amino acids in the so-called 'A' site or alpha-chain knob. The thrombin-catalyzed release of fibrinopeptide A from M-V fibrinogen was only slightly delayed yet release of fibrinopeptide B was significantly delayed. Both thrombin-catalyzed fibrin polymerization and fibrin monomer polymerization were markedly impaired compared to normal fibrinogen. In addition, reptilase-catalyzed fibrin polymerization of M-V was much more impaired than thrombin-catalyzed fibrin polymerization. These results indicate 'B' and/or 'b' site of M-V fibrinogen play a more important role in thrombin-catalyzed fibrin polymerization than that of normal control fibrinogen.

Topics: Batroxobin; Blood Coagulation Tests; DNA Mutational Analysis; Female; Fibrin; Fibrinogens, Abnormal; Fibrinopeptide A; Fibrinopeptide B; Genetic Variation; Humans; Kinetics; Lupus Erythematosus, Systemic; Middle Aged; Point Mutation; Thrombin

Anti-beta 2-glycoprotein I antibodies bind to endothelial cells through beta 2-GPI. The antibodies are present in patients with systemic lupus erythematosus and antiphospholipid syndrome and are associated with the pathogenesis of the disease. Anti-endothelial cell antibodies that react with constitutive antigens on ECs are present in patients with vasculiditis and other diseases. Both types of antibodies can activate ECs. Frequent findings in APLS and vasculitis are fibrin deposits and thromboembolic phenomena. These indicate that the coagulation system is activated. However, the mechanism of activation is not clear. ECs generate tissue factor upon stimulation with various substances. In the present study we report that monoclonal anti-beta 2-GPI antibodies and AECAs, derived from a patient with primary APLS and a patient with Takayasu's arteritis, respectively, induce a potent tissue factor in ECs. The production of TF activity, TF antigen and TF mRNA is dose and time dependent. The TF activity was induced also by F(ab)2 but not by Fc fragments and was abolished completely by pre-incubation with ant-TF antibodies. The TF that is induced in ECs by AECAs with and without beta 2-GPI specificity may activate the coagulation and thereby play a major role in the pathogenesis of fibrin deposition and thrombus formation in diseases that are associated with the presence of these antibodies.

Topics: Antibodies; Antigens; Antiphospholipid Syndrome; Apolipoproteins; beta 2-Glycoprotein I; Binding Sites, Antibody; Cells, Cultured; Endothelium, Vascular; Fibrin; Glycoproteins; Humans; Immunoglobulin Fab Fragments; Immunoglobulin Fc Fragments; Lupus Erythematosus, Systemic; Membrane Glycoproteins; RNA, Messenger; Takayasu Arteritis; Thromboembolism; Thromboplastin; Vasculitis

We describe the first case of catastrophic antiphospholipid antibody syndrome (APS) in a patient with progressive systemic sclerosis (SSc). After initial presentation with digital gangrene the patient developed rapidly progressive multiorgan failure and died within 19 hours. Postmortem examination revealed extensive multiorgan arterial microthrombi of days' to months' duration. This suggests that a subclinical state of thrombosis existed before onset of catastrophic APS. Given the poor prognosis of established catastrophic APS there is a need for a means to detect subclinical thrombosis and treat "at risk" patients before clinically apparent thrombosis occurs.

Topics: Adult; Antiphospholipid Syndrome; Brain; Fatal Outcome; Female; Fibrin; Histocytochemistry; Humans; Lupus Erythematosus, Systemic; Mitral Valve

Fibrinolysis triggered by t-PA bound to fibrin is one of the main antithrombotic mechanisms. Defects in the fibrinolytic system-decreased tissue-type plasminogen activator (t-PA) activity and elevated levels of plasminogen activator inhibitor (PAI-1), in patients with SLE have been associated with an increased tendency to thrombosis. In the present study, 43 patients with SLE fulfilling the ACR criteria for the disease, were studied for the presence of autoantibodies to fibrin-bound t-PA, i.e. the physiological active form of this plasminogen activator. A solution of 200 IU/ml of t-PA was incubated with solid-phase fibrin prepared as previously described (Anal Biochem 1986; 153; 201-210). Sera diluted 1:50 were incubated with fibrin-bound t-PA, the plates were then washed, and bound immunoglobulins were detected using a polyvalent peroxidase-labeled goat anti-human Ig. Plates coated with fibrin alone were used as controls. Sera were considered positive when A490/630 obtained with normal human sera in two independent test was greater than the mean plus 2 SD. Eleven of 43 (26%) SLE sera demonstrated antibody reactivity against fibrin-bound t-PA. Within the anti-t-PA positive group there was a higher proportion of SLE patients with severe Raynaud's phenomenon and thrombotic events when compared to the anti-t-PA negative group: 36% vs 6% and 18% vs 6% respectively. These results suggest that autoantibodies to fibrin-bound t-PA could play a role in the pathogenesis of vascular disease in some SLE patients.

Topics: Adult; Antibody Specificity; Autoantibodies; Autoimmune Diseases; Disease Susceptibility; Female; Fibrin; Fibrinolysis; Humans; Lupus Erythematosus, Systemic; Male; Raynaud Disease; Thrombosis; Tissue Plasminogen Activator

We report here, a patient of systemic lupus erythematosus (SLE) with severe fibrinoid necrosis in the afferent arteriole of the glomerulus, in whom antiphospholipid antibody might have contributed to the pathogenesis. A 24-year-old female who was suffering from severe anemia with fragmented red blood cells, acute renal failure and thrombocytopenia, was admitted to our hospital. Further examinations revealed findings compatible with active lupus nephritis. Moreover, she was found to be positive for antiphospholipid antibody, and anticardiolipin antibody, as well as for lupus anticoagulant and syphilis test. Intensive treatment by methylprednisolone pulse therapy, hemodialysis, and double filtration plasmapheresis were performed. However, 13 days after admission she died suddenly because of intracranial hemorrhage. Pathological investigation of renal tissue revealed severe fibrinoid necrosis of the arterioles mainly in the glomerular afferent arteriole associated with diffuse proliferative lupus nephritis. In this case, hemolytic uremic syndrome (HUS) was associated with SLE. Antiphospholipid antibody was considered to be not only an accelerator in the arterial lesions of HUS, but also an initiator of HUS itself.

Topics: Adult; Arterioles; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Kidney Glomerulus; Lupus Erythematosus, Systemic; Necrosis

A 20-year-old black patient with bullous systemic lupus erythematosus developed papular and vesicular lesions on the extensor surfaces of the extremities. Histologically, subepidermal blisters and papillary neutrophilic abscesses with a striking number of lupus erythematosus cells were observed. No circulating anti-basal-membrane-zone antibodies were found. By Western immunoblotting, the patient's serum showed no reactivity against epidermal or dermal extracts.

Topics: Adult; Cell Nucleus; Epidermis; Erythrocytes; Fibrin; Humans; Lupus Erythematosus, Systemic; Male; Mucins; Neutrophils; Skin; Skin Diseases, Vesiculobullous

Circulating lupus anticoagulant (LA) is associated with thrombosis in large and small vessels. To determine how often the presence of LA is associated with thrombosis within the renal microcirculation, 33 patients with systemic lupus erythematosus (SLE), renal dysfunction, and LA were identified over a 25-year period (LA group) and 32 patients with renal SLE but with normal gross coagulation screen were matched for age, sex, and biopsy timing (C group). Prevalences of serositis, neuropsychiatric illness, leukopenia, thrombocytopenia, hemolysis, anti-DS-DNA elevation, and complement reduction were similar. Arthritis was less and biologic false-positive (BFP) syphilis serology more common in LA. More LA patients had thrombotic events (LA 39% v C 13%; P = 0.014); bleeding episodes, including postbiopsy, were similar. At biopsy, hypertension (LA 55%, C 41%), serum creatinine (mean +/- SD: LA 186 +/- 168 mumol/L [2.1 +/- 1.9 mg/dL] v C 150 +/- 168 mumol/L [1.7 +/- 1.9 mg/dL]) and proteinuria (LA 2.6 +/- 3.1 g/24 h v C 3.1 +/- 2.7) were similar. Lesions by World Health Organization (WHO) class, activity, and chronicity indices, as well as immunofluorescence (IF) and electron microscopy (EM) findings, were not significantly different. Occlusive glomerular, arteriolar, and arterial fibrin thrombi, along with varying degrees of renal thrombotic microangiopathy, were seen in five of 33 patients with LA, but zero of 32 C patients (P = 0.053); three of these five patients died soon after biopsy. Overall, mortality was not different between LA and C. We conclude that the majority of patients with SLE, renal dysfunction, and LA exhibit renal morphologic findings indistinguishable from patients without LA. However, a significant minority of LA patients have thrombotic microangiopathy in their biopsy, which is accompanied by a worse prognosis.

Topics: Adolescent; Adult; Blood Coagulation; Capillaries; Female; Fibrin; Hemorrhage; Humans; Kidney; Kidney Glomerulus; Lupus Coagulation Inhibitor; Lupus Erythematosus, Systemic; Lupus Nephritis; Male; Middle Aged; Thrombosis

Topics: alpha-2-Antiplasmin; Amyloidosis; Chemical Phenomena; Chemistry, Physical; Disseminated Intravascular Coagulation; Fibrin; Humans; Lupus Erythematosus, Systemic; Plasminogen; Protein Binding

Topics: Female; Fibrin; Granuloma; Humans; Liver; Liver Neoplasms; Lupus Erythematosus, Systemic; Middle Aged

Plasma fibrinolytic activity was measured in 34 patients with systemic lupus erythematosus (SLE) and 12 normal subjects. Patients with SLE showed a significantly reduced resting level of plasma tissue plasminogen activator (t-PA) compared to normal. The reduction in t-PA was demonstrated both by a functional assay (fibrin-plate lysis, FP) and an immunochemical assay (ELISA). Measurement of the fibrinolytic response following venous occlusion allowed division of the patients into two groups. In the first (24 patients), there was a normal increase in t-PA response, demonstrated both by the functional and immunochemical assays. In the second (10 patients), there was a significantly reduced plasma t-PA response measured by FP. Seven of the patients in this second group, which included four patients with histological evidence of vasculitis, showed a similar failure of t-PA response (ELISA) after venous occlusion. These results suggest that their impaired fibrinolytic response may be related to defective t-PA release secondary to endothelial cell damage. The remaining three patients in the latter group had a normal t-PA (ELISA) response despite a reduced FP response, suggesting the presence of an inhibitor.

Topics: Adult; Aged; Blood Coagulation Disorders; Enzyme-Linked Immunosorbent Assay; Female; Fibrin; Fibrinolysis; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged; Partial Thromboplastin Time; Prothrombin Time; Thrombin Time; Tissue Plasminogen Activator

Using a previously developed in vitro assay of glass adherence of neutrophils following blood clotting, we compared the results of new patients with systemic lupus erythematosus (SLE), juvenile rheumatoid arthritis (JRA) and those of normal controls. In acute phase of the disease, all 33 patients (100%) of SLE, 2 of 35 patients (5.7%) with JRA had a significantly low neutrophil adherence to glass surface (less than 25% of the normal values). During 2 years follow-up in 18 patients with SLE from the onset of the disease, we consistently observed the low cell adherence during the relapses of the disease in all the patients. When remains of glass surfaces were examined under scanning electron microscope (SEM), we found a notable morphologic difference of fibrin configuration between the specimens of active SLE and normal controls. We conclude that the varied results of neutrophil adherence on glass may reflect the forming of different fibrin configuration induced by the in vitro contact system of coagulation. The findings may explain the increased thrombotic complications reported in patients with active SLE.

Topics: Adolescent; Adult; Cell Adhesion; Complement C3; Female; Fibrin; Glass; Humans; Lupus Erythematosus, Systemic; Male; Microscopy, Electron, Scanning; Neutrophils

Topics: Adolescent; Adult; Aged; Biopsy; Child; Complement Activating Enzymes; Complement C1; Complement C1q; Complement C3; Diagnosis, Differential; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulins; Lupus Erythematosus, Discoid; Lupus Erythematosus, Systemic; Male; Middle Aged; Skin; Skin Diseases

Fibrinolytic activities of whole blood and plasma were determined by 125I-fibrin radiometric assay in 16 normal subjects, and in 11 patients with systemic lupus erythematosus (SLE), 14 with progressive systemic sclerosis (PSS), 23 with venous thromboembolic disease, and 20 patients awaiting elective surgery. Mean whole blood and plasma activities for patients with PSS, and for those awaiting elective surgery, were similar to normal values, as was the mean plasma activity in patients with SLE. However, mean whole blood activity in SLE was significantly decreased compared with normals (p less than 0.05), with mean plasma activity accounting for 44% of mean whole blood activity (compared with 17% in normal subjects), representing a 67% decrease in mean calculated cellular phase activity in SLE, when compared with normals. Since the numbers of cells (neutrophils, monocytes) possibly involved in cellular activity were not decreased, the findings suggest a functional defect in fibrinolytic activity of one or more blood cell types in SLE. An additional finding was the participation of the cellular phase as well as the well-known plasma phase of blood in the fibrinolytic response to thromboembolism.

Topics: Female; Fibrin; Fibrinolysis; Humans; Iodine Radioisotopes; Leukocyte Count; Lupus Erythematosus, Systemic; Male; Monocytes; Neutrophils; Plasma; Plasma Cells; Scleroderma, Systemic; Thrombophlebitis

Topics: Adult; Arthritis, Rheumatoid; Collagen Diseases; Factor XIII; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged; Raynaud Disease

The presence of immunoglobulin and complement deposits in cutaneous blood vessels and at the dermal junction was determined in 34 patients with rheumatoid arthritis (RA). Deposits of IgM and C3 were twice as common in the leg than the arm. The deposits were present in 7/14 patients with extraarticular disease and 1/20 patients with articular disease alone. Deposits of IgM were detected at the dermoepidermal junction in 4 patients with RA. All had circulating antinuclear antibodies.

Topics: Adult; Aged; Antibodies, Antinuclear; Arm; Arthritis, Rheumatoid; Blood Vessels; Complement C3; Female; Fibrin; Fluorescent Antibody Technique; Histocytochemistry; Humans; Immunoglobulin M; Leg; Lupus Erythematosus, Systemic; Male; Middle Aged; Osteoarthritis; Rheumatoid Factor; Skin

Analysis of 80 cases of SLE with renal involvement revealed the following. Angiitis involving arterioles and interlobular arteries was observed in 17 out of 42 cases with diffuse proliferative lupus GN. This was not observed in other types of lupus GN. Out of 17 cases of angiitis, 7 were complicated by thrombosis. Irregular deposits of immunoglobulins and complement were demonstrated in the vessel walls and in luminal thrombi and suggested an immune-complex origin. Fibrinogen was also demonstrable frequently. The vascular lesions were associated with severe glomerular and tubulointerstitial injury and a poor prognosis. A relatively favorable outcome was observed in SLE without renal angiitis.

Topics: Arteritis; Complement C3; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immunoglobulins; Kidney; Lupus Erythematosus, Systemic; Microscopy, Electron; Prognosis

Ancrod, which produces in vivo defibrination, has been shown to improve renal function and decrease fibrin deposition and crescents in experimental glomerulonephritis. Ancrod was given for 14 days to 5 patients with glomerulonephritis, moderate to severe renal functional impairment, crescents, and/or fibrin deposition in glomeruli. 4 patients had systemic lupus erythematosus. Ancrod treatment resulted in fibrinogen levels less than 50 mg/dl without bleeding, decrease of previously elevated factor VIII and von Willebrand factor levels, and normalization of in vitro platelet hyperaggregation. Renal function improved in all 5 patients. Serial renal biopsies showed a relatively rapid decrease of glomerular thrombi and necrosis and little increase in glomerular sclerosis. Ancrod administration appears safe, and may have a role in treatment of certain types of glomerulonephritis.

Topics: Adolescent; Adult; Ancrod; Blood Coagulation; Factor VIII; Female; Fibrin; Fibrinogen; Glomerulonephritis; Humans; Kidney; Lupus Erythematosus, Systemic; Middle Aged; Platelet Aggregation; von Willebrand Factor

Neuropathologic examination of an autopsy series of 54 patients of various types of CVD revealed a very high frequency of pathologic changes both in brain parenchyma (in 81%) and vessels (in 78%). A broad but continuous spectrum of primary vascular alterations was observed, ranging from fibrinoid deposits in intact or necrotizing vessel walls to fibrohyalinosis and endothelial proliferations. In acute SLE showing LE cells within brain tissues, immune complex deposits were observed for the first time in brain vessels, in addition to similar deposits in the plexus chorioideus and in hematoxylin bodies. Secondary complications are frequently affecting the brain in CVD; they are mainly sequels of systemic atherosclerosis, hypertension, thromboemboli from SLE endocarditis, cardiac, hepatic or renal dysfunctions, or infections and should be clinically differentiated from primary brain involvement in CVD to ensure the appropriate therapeutic measures.

Topics: Arthritis, Rheumatoid; Brain; Cerebral Arteries; Collagen Diseases; Complement C3; Fibrin; Humans; Immunoglobulin G; Lupus Erythematosus, Systemic; Myositis; Polyarteritis Nodosa; Purpura, Thrombotic Thrombocytopenic; Vascular Diseases; Vasculitis

In 16 patients with systemic lupus erythematosus, blood vessels in the affected region of the skin were examined regarding localization of immune complexes. Deposition of IgG, IgA, IgM, IgE, beta 1C and fibrin in the vessel walls was more frequently observed in intramural and perivascular sites than in intimal sites. IgM and fibrin were usually detected in intramural sites only. In large caliber arteries of the skin the intima was the main site of deposition of immune reactants, whereas, in small-caliber vessels, including capillaries, immune reactants were more often found in intramural and perivascular sites.

Topics: Adolescent; Adult; Complement C1; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulins; Lupus Erythematosus, Systemic; Male; Middle Aged; Skin

Topics: Child; Chromatography, Gel; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Nephrotic Syndrome

Clinical and morphologic signs of intravascular coagulation have been studied in 63 patients with primary glomerulonephritis (GN) and in 19 patients with nephritis associated with systemic lupus erythematosus. A relationship between the frequency of fibrin deposition in the kidneys and severity of clinical signs and marked morphologic changes in GN has been revealed. Signs of local hypercoagulation are of prognostic significance. A more favourable prognosis is characteristic for patients who show nor fibrin deposition in the renal tissue and whose fibrinolytic system provides an adequate reaction.

Topics: Adolescent; Adult; Biopsy, Needle; Child; Child, Preschool; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Glomerulonephritis; Humans; Immune Complex Diseases; Kidney; Lupus Erythematosus, Systemic; Male; Microscopy, Electron; Middle Aged; Nephritis

Topics: Fibrin; Fibrinogen; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immunoglobulin M; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Urine

Cerebral vascular lesions of 26 cases in systemic lupus erythematosus during a period from 1963 to 1978 were examined histologically and the following conclusions were made: 1. The prominent vascular changes of the brain were thrombosis, fibrinoid degeneration, endothelial swelling and proliferation, arteriolosclerosis, and perivascular infiltration of inflammatory cells. 2. From clinico-pathological viewpoints, thrombosis seemed to play an important role in the development of neurological signs. In five cases, characteristic granular or homogeneous thrombi were observed in the small blood vessels including venule. Infarct without proved vascular obstruction but probably due to thrombosis was seen in four cases. The true character of the granular thrombi was not determined, either electronmicroscopically or immunohistochemically. These suggested the presence of a tendency for in situ formation of thrombus. 3. Fibrinoid degeneration seen in four cases mainly affected arterile of less than 50 micrometer in diameter in the cerebral cortex, basal ganglia, and brain stem. This change of arteriole did not play a significant role in neurological signs. 4. Endothelial swelling and proliferation of the small blood vessels were prominent in the cases with thrombosis and fibrinoid degeneration. 5. Perivascular infiltration of the inflammatory cells was observed in about one-half of the cases but its significance was not clear.

Topics: Adolescent; Adult; Blood Vessels; Brain; Brain Diseases; Cerebral Hemorrhage; Cerebral Infarction; Cerebrovascular Disorders; Child; Encephalitis; Endothelium; Female; Fibrin; Humans; Intracranial Arteriosclerosis; Intracranial Embolism and Thrombosis; Lupus Erythematosus, Systemic; Male; Middle Aged

Cytoid bodies represent roundish or polygonal, approximately cell-sized structures in histological sections. Such bodies have been reported to be of pathologic significance in several cutaneous disorders. Histological, immunological and electron microscopic investigations were performed in order to (1) characterize the different types of cytoid bodies in human skin, (2) elucidate their origin and nature and (3) determine their significance in cutaneous histopathology. A distinct identification of elastic globes, Russell bodies, Civatte bodies, amyloid bodies and cytoid fibrin bodies could be made. In addition, other substances such as nuclear or cytoplasmic debris, cytolytic fragments or basement membrane proliferations were found in form of cytoid aggregates in several dermatoses. However, none of the different groups of cytoid bodies was evaluated to be of pathognomonic significance for a specific disease. All of them are rather symptomatic for a number of anatomical or pathological principles and events in the dermo-epidermal junction area. Thus, the presence of cytoid bodies is not a major diagnostic aid in histopathology but may give valuable hints for a better interpretation of the morphogenesis of etiologically unrelated skin disorders.

Topics: Amyloid; Elastin; Fibrin; Humans; Lupus Erythematosus, Systemic; Skin; Skin Diseases; Skin Manifestations; Staining and Labeling

Detailed immunopathologic studies of early or silent renal alterations in systemic lupus erythematosus have been sparse. The renal biopsies of 16 lupus patients with normal renal function, including 8 with hematuria and/or proteinuria of recent onset, and 8 without clinically detectable renal disease were investigated by light, immunofluorescence, and electron microscopy. Immunoglobulins, complement components, and electron-dense deposits were detected in glomeruli of all patients, regardless of morphologic appearance or lack of clinical evidence of renal involvement. Features of membranous glomerulonepritis were observed in 4 patients with substantial proteinuria. In the remaining 12 patients, including 3 with hematuria and 4 with slight proteinuria, either minimal glomerular alterations or features of mesangial proliferative glomerulonephritis were seen. Transformation of the original disease was demonstrated in 3 of 3 patients rebiopsied within 2 years. The significance of these findings is discussed in relation to a) the spectrum of clinical and immunopathologic alterations in lupus nephritis and b) transformation of the original disease.

Topics: Adolescent; Adult; Basement Membrane; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immunoglobulins; Kidney; Kidney Glomerulus; Lupus Erythematosus, Systemic; Male; Middle Aged

Rheumatoid arthritis (RA) was differentiated from systemic lupus erythematosus (SLE) by direct immunofluorescent techniques on skin specimens, using monospecific antisera for IgG, IgM, C3, C1q, properdin, and fibrin. Of 30 patients with RA studied, 20 had dermal vessel deposits of immunoglobulins and complement components in unaffected skin without the characteristic dermal-epidermal junctional fluorescence of SLE. Of 24 SLE patients studied, 24 had granular deposits of immunoglobulins and complement components in unaffected skin at the dermal-epidermal junction.

Topics: Arthritis, Rheumatoid; Complement C1; Complement C3; Complement System Proteins; Fibrin; Humans; Immunoglobulin G; Immunoglobulin M; Immunoglobulins; Lupus Erythematosus, Systemic; Middle Aged; Properdin; Skin

Plasma proteins which interfere with blood coagulation have often been described in patients with systemic lupus erythematosus (SLE). The most frequent type interferes with the conversion of prothrombin to thrombin and thus prolongs the prothrombin time. Infrequently, SLE patients exhibit anticoagulants which appear to block the earlier stages of coagulation such as those involving factor VIII or the formation of activated factor XI (factor XIa). The anticoagulant reported here was studied by means of a sequential clotting system utilizing crude coagulation factors and was noted to interfere with the action of activated plasma thromboplastin antecedent (PTA) during the activation of factor IX. This anticoagulant was found in gamma-globulin-rich ethanol fractions of plasma. After gel filtration, it was found principally in fractions containing IgM globulins but also, to a lesser extent, in IgG-rich fractions. In this respect, it is similar to anticoagulants reported in certain other cases of SLE. Attempts to confirm the immunoglobulin nature of the anticoagulant by immunoabsorption were, however, inconclusive

Topics: Absorption; Antibodies, Antinuclear; Anticoagulants; Blood Coagulation Tests; Chromatography, Gel; DNA, Single-Stranded; Factor IX; Factor XI; Female; Fibrin; Fibrinogen; Humans; Lupus Erythematosus, Systemic; Middle Aged; Prothrombin; Prothrombin Time; Radioimmunoassay; Thrombin

The urinary concentration of fibrin-fibrinogen degradation products (F.D.P.) was measured in 90 patients with proteinuria above 2 g/1 and correlated with proteinuria, differential protein clearances, serum urea and creatinine, and renal biopsy findings. There was a linear correlation (r equals 0-7; P less than 0-001) between the urinary F.D.P. excretion and the selectivity of the proteinuria such that patients with highly selective proteinuria excreted only small amounts of F.D.P. whereas those with non-selective proteinuria excreted much higher levels. There was a significant correlation between the urinary F.D.P. excretion and the urine:serum (U:S) ratio of IgG excretion but not with the U:S ratio or urinary excretion of albumin or transferrin. Sephadex G200 column chromatography of the concentrated urine in 26 cases showed that patients with highly selective proteinuria excreted predominantly F.D.P. of low molecular weight in the urine whereas those with non-selective proteinuria excreted mainly fibrinogen and products of high molecular weight. Hence the type and quantity of F.D.P. in the urine are determined primarily by the differential filtration of fibrinogen and the various degradation products from the plasma through the glomerular basement membrane, which in turn is determined by the "pore size" of the basement membrane. In clinical nephrology measurement of the urinary F.D.P. level provides a rapid and convenient means of estimating the differential protein clearance.

Topics: Albuminuria; Amyloidosis; Chromatography; Fibrin; Fibrinogen; Filtration; Glomerular Filtration Rate; Glomerulonephritis; Humans; Hypersensitivity; Hypertension, Malignant; Immunodiffusion; Immunoglobulin G; Lupus Erythematosus, Systemic; Molecular Weight; Nephrotic Syndrome; Proteinuria; Purpura; Thrombosis; Transferrin

Skin lesions and clinically normal skin of thirteen patients with systemic lupus erythematosus (SLE) were examined, by the use of immunofluorescent techniques, to determine the presence of CIq, C3, C3 proactivator (C3PA), properdin, immunoglobulins (IgG, IgA, and IgM), and fibrin. IgM deposition was present in all thirteen skin lesions and in eleven normal areas tested, whereas IgG deposition occurred in eleven of the lesions but in only six normal areas. IgA was the least frequently encountered immunoglobulin. CIq deposition occurred in all thirteen skin lesions, and C3 deposition was present in twelve. Seven of nine and eight of eleven clinically normal areas demonstrated CIq and C3 deposition, respectively. Although less intense that CIq and C3 deposition, properdin deposition occurred in eight of the thirteen skin lesions tested but in only two of nine normal areas. C3PA deposition was of greater intensity than was properdin, but was seen in only five lesions and three clinically normal areas. Seven skin lesions and two normal areas also demonstrated fibrin deposition. Although alternate pathway activation is apparent, our findings suggest that the classical pathway (CI to C9) is the primary complement pathway involved in SLE skin.

Topics: Adult; Animals; Complement C3; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immune Sera; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Lupus Erythematosus, Systemic; Male; Middle Aged; Properdin; Rabbits; Skin

Direct immunofluorescent (IF) staining was performed on biopsy specimens from fifty-three patients with active lichen planus. In fifteen of these cases uninvolved skin sites were also examined. Globular or cytoid body-like deposits of immunoglobulins, mainly IgM, were detected in forty-six of the active lesions, and in half the uninvolved skin biopsies. The deposition of fibrin in the papillary dermis and around follicular structures was seen only in the active lichen planus papules. The significance of these findings was assessed by comparison with the IF results obtained in 252 biopsies from various cutaneous disorders, stained by the same technique during the period of this study. Although the presence of immunoglobulin cytoid bodies and fibrin was found to be highly characteristic of lichen planus, these findings were not specifically diagnostic. Morphologically identical deposits were seen not infrequently in lupus erythematosus and in eczema. Active lesions of dermatitis herpetiformis, erythema multiforme and other rare dermatoses also showed these cytoid body-like immunoglobulin deposits.

Topics: Fibrin; Humans; Immunoglobulin M; Immunoglobulins; Lichen Planus; Lupus Erythematosus, Systemic; Skin

Topics: Collagen; Connective Tissue; Epithelial Cells; Fibrin; Humans; Lupus Erythematosus, Systemic; Macrophages; Microscopy, Electron; Neutrophils; Skin

Topics: Adult; Autopsy; Biopsy; Complement System Proteins; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immunoglobulin A; Immunoglobulin E; Immunoglobulin G; Immunoglobulin M; Kidney; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Microscopy, Electron; Nephritis; Prognosis; Time Factors

Topics: Adult; Albuminuria; Basement Membrane; Blood Pressure; Capillaries; Complement System Proteins; Creatinine; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immune Sera; Immunoglobulin G; Kidney; Kidney Glomerulus; Lupus Erythematosus, Systemic; Male; Middle Aged; Renal Artery; Scleroderma, Systemic; Urea

Topics: Adult; Anti-Bacterial Agents; Bacterial Infections; Blood Vessels; Disseminated Intravascular Coagulation; Drug Hypersensitivity; Female; Fibrin; Humans; Lupus Erythematosus, Systemic; Prednisone; Purpura, Thrombotic Thrombocytopenic; Splenectomy

Topics: Female; Fibrin; Fibrinogen; Humans; Hyalin; Inclusion Bodies; Lupus Erythematosus, Systemic; Purpura, Thrombotic Thrombocytopenic

Topics: Adult; Anti-Glomerular Basement Membrane Disease; Antibodies, Viral; Antibody Formation; Antibody Specificity; Complement Fixation Tests; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Hemagglutination Inhibition Tests; Herpesvirus 4, Human; Humans; Immunodiffusion; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Lupus Erythematosus, Systemic; Male; Measles virus; Nephrosis, Lipoid; Orthomyxoviridae; Respirovirus; Rubella virus; Serum Albumin

Topics: Adolescent; Adult; Aged; Blood Cell Count; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Complement System Proteins; Creatinine; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Humans; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Male; Middle Aged; Proteinuria; Prothrombin Time

Topics: Abortion, Induced; Adolescent; Biopsy; Female; Fibrin; Glomerulonephritis; Humans; Kidney; Kidney Function Tests; Lupus Erythematosus, Systemic; Pregnancy; Pregnancy Complications; Prognosis; Proteinuria

Topics: Adolescent; Adult; Aged; Animals; Antifibrinolytic Agents; Biopsy; Child; Female; Fibrin; Fibrinolysis; Fluorescent Antibody Technique; Humans; Immunoglobulins; Lichen Planus; Lupus Erythematosus, Discoid; Lupus Erythematosus, Systemic; Male; Microscopy, Fluorescence; Middle Aged; Rabbits; Skin

Topics: Arthritis, Rheumatoid; Autopsy; Collagen Diseases; Dermatomyositis; Diagnosis, Differential; Fibrin; Granuloma; Histocytochemistry; Humans; Lung; Lupus Erythematosus, Systemic; Polyarteritis Nodosa; Pulmonary Alveoli; Pulmonary Fibrosis; Rheumatic Fever; Scleroderma, Systemic

Topics: Adrenal Cortex Hormones; Arthritis, Rheumatoid; Cartilage; Collagen Diseases; Connective Tissue; Dermatomyositis; Fibrin; Giant Cell Arteritis; Humans; Lupus Erythematosus, Systemic; Rheumatic Fever; Scleroderma, Systemic

Topics: Adult; Blood Coagulation Tests; Blood Urea Nitrogen; Child; Disseminated Intravascular Coagulation; Female; Fibrin; Glomerulonephritis; Hematologic Diseases; Humans; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Nephritis; Nephrotic Syndrome; Urinary Tract Infections; Vascular Diseases

Topics: Blood Vessels; Diphtheria; Fibrin; Granulomatosis with Polyangiitis; Humans; Hypertension, Malignant; Lupus Erythematosus, Systemic; Necrosis; Polyarteritis Nodosa; Pyelonephritis; Rheumatic Fever; Sepsis; Splenic Artery; Tuberculosis, Meningeal; Vascular Diseases

Topics: Animals; Electrophoresis; Fibrin; Humans; Immune Sera; Immunodiffusion; Kidney; Kidney Diseases; Lupus Erythematosus, Systemic; Rabbits; Urine

Topics: Adult; Autopsy; Biopsy; Connective Tissue; Elastic Tissue; Eosinophils; Female; Fibrin; Histocytochemistry; Humans; Inflammation; Lupus Erythematosus, Discoid; Lupus Erythematosus, Systemic; Microscopy; Microscopy, Electron; Middle Aged; Necrosis

Topics: Adolescent; Adult; Anemia, Hemolytic; Beta-Globulins; Blood Coagulation Disorders; Blood Coagulation Tests; Child; Child, Preschool; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Heparin; Humans; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Nephritis; Nephrotic Syndrome; Purpura; Uremia; Urinary Tract Infections

Topics: Adrenal Cortex Hormones; Adult; Antimalarials; Blood Vessels; Female; Fibrin; Humans; Lupus Erythematosus, Discoid; Lupus Erythematosus, Systemic; Male; Middle Aged; Skin

Topics: Child; Female; Fibrin; Humans; Lupus Erythematosus, Systemic

Topics: Arteries; Arterioles; Fibrin; Humans; Lupus Erythematosus, Systemic; Necrosis; Polyarteritis Nodosa