fibrin and Nephritis

Topics: Animals; Fibrin; Humans; Kidney Glomerulus; Macrophages; Nephritis

This article reviews the mediation systems participating or potentially participating in inflammatory disease, especially in immunologic injury of the glomerulus. Mediator systems are separated into 3 mechanisms: the first involves complement and neutrophils; the second involves systems unrelated to neutrophils and complement components from C3 to C9; and the third involves blood monocytes. Major emphasis is given to an analysis of factors that potentially participate in the second mechanism. These include humoral factors such as the coagulation system and Hageman factor systems and cellular factor such as platelets or cells resident in the glomerulus. Studies on a role of vasoactive amines are presented. The importance of separating neutrophil-dependent and -independent mechanisms in these studies is emphasized. A review of current knowledge of the biochemical mechanisms involved in the Hageman factor system is presented because of the potential role of these components in the development of inflammation.

Topics: Animals; Basement Membrane; Complement System Proteins; Factor XII; Fibrin; Fibrinogen; Glomerulonephritis; Immune Complex Diseases; Inflammation; Intrinsic Factor; Kidney Glomerulus; Nephritis; Rabbits; 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

Topics: Arthritis; Blood Coagulation Factors; Blood Platelets; Chronic Disease; Complement System Proteins; Connective Tissue; Disseminated Intravascular Coagulation; Endotoxins; Factor XII; Fibrin; Fibrinogen; Fibrinolysin; Glomerulonephritis; Humans; Inflammation; Kinins; Leukocytes; Nephritis; Shwartzman Phenomenon

Topics: Animals; Anti-Inflammatory Agents; Antibodies; Antigens; Antineoplastic Agents; Autoimmune Diseases; Complement System Proteins; Corticosterone; Fibrin; Glomerulonephritis; Humans; Mice; Mice, Inbred NZB; Mice, Inbred Strains; Nephritis; Plasmodium malariae; Rodent Diseases

Topics: Animals; Anticoagulants; Autoimmune Diseases; Blood Coagulation Disorders; Disease Models, Animal; Fibrin; Heparin; Humans; Kidney; Kidney Cortex Necrosis; Kidney Diseases; Kidney Glomerulus; Mice; Nephritis; Rabbits; Shwartzman Phenomenon; Thrombosis

Goodpasture's, or anti-glomerular basement membrane (GBM), disease presents with rapidly progressive glomerulonephritis and lung haemorrhage, and is caused by autoimmunity to the NC1 domain of the alpha3 chain of type IV collagen (alpha3(IV)NC1). This study examines the development of crescentic nephritis and alveolar haemorrhage in a model of Goodpasture's disease, experimental autoimmune glomerulonephritis (EAG), induced in WKY rats by immunization with rat GBM in adjuvant. An increase in circulating anti-GBM antibodies and albuminuria was observed by week 2, which increased further by weeks 3 and 4, while a decrease in creatinine clearance was observed by week 2, which decreased further by weeks 3 and 4. The kidneys of animals with EAG showed linear deposits of IgG on the GBM and a transient glomerular infiltration by CD4+ T cells at week 2. By week 3 there were large deposits of fibrin in Bowman's space, and glomerular infiltration by CD8+ T cells and macrophages, accompanied by focal necrotizing glomerulonephritis with crescent formation. Ultrastructural studies showed glomerular endothelial cell swelling and epithelial cell foot process effacement at week 2. As the lesion progressed, capillary loops became occluded and the mesangium became expanded by mononuclear cells. By week 3 there was detachment of the endothelium from the GBM, and accumulation of fibrin beneath the disrupted endothelial cells and in Bowman's space. Occasional breaks were observed in the continuity of the basement membrane, and cytoplasmic projections from infiltrating mononuclear cells could be seen crossing the capillary wall between the lumen and the crescent. The lungs of animals with EAG showed patchy binding of IgG to the alveolar basement membrane (ABM) at week 2, and infiltration of the interstitium by CD8+ T cells and macrophages by weeks 3 and 4, accompanied by both interstitial and alveolar haemorrhage. Ultrastructural studies showed focal mononuclear cell infiltrates in alveolar walls at week 2. Occasional breaks were observed in the basement membrane and adjacent endothelium by weeks 3 and 4, together with accumulation of surfactant and erythrocytes within the alveolar spaces. This study defines for the first time the relationship between the immunological and pathological events during the evolution of EAG, and provides the basis for further work on the pathogenesis of Goodpasture's disease.

Topics: Animals; Anti-Glomerular Basement Membrane Disease; Antibodies; Autoantibodies; Autoimmune Diseases; Autoimmunity; Basement Membrane; Creatinine; Disease Models, Animal; Fibrin; Glomerulonephritis; Hemorrhage; Kidney Glomerulus; Lung Diseases; Male; Microscopy, Electron; Nephritis; Pulmonary Alveoli; Rats; Rats, Inbred WKY

A particular Lewis rat substrain (LEW/Maa) develops chronic glomerulonephritis in the anti-Thy 1 model (aThy 1-GN) characterized by increased microaneurysm formation, chronic glomerular sclerosis and persistent albuminuria. This phenotype is accompanied by increased and prolonged glomerular induction of inducible nitric oxide synthase (iNOS) when compared to the LEW/Moe substrain, in which aThy 1-GN resolves quickly. We investigated the effect of selective iNOS inhibition by l-N6-(1-iminoethyl)-lysine (L-NIL) administration on aThy 1-GN in LEW/Maa rats.. Nephritic rats were studied over a period of 7 days. L-NIL-treated animals received 20 mg/day L-NIL in the drinking water starting two days prior to disease induction. iNOS activity was determined in cultured glomeruli and in urine samples, respectively. Severity of aThy 1-GN was determined by scoring glomerular matrix expansion and microaneurysm formation, and by albuminuria measurements (ELISA). Immunohistochemical evaluation was performed including staining for macrophages (ED-1), platelets (PL-1) and fibrin deposition.. L-NIL treated rats (+NIL) showed a significant decrease in peak nitrate production by ex vivo cultured glomeruli, and in urinary nitrate excretion versus untreated nephritic rats (-NIL). Mean arterial pressure remained unchanged in both +NIL and -NIL rats. +NIL rats developed significantly increased albuminuria (+44%) associated with a significant increase in glomerular platelet (+45%) and fibrin deposition (+48%).. Selective inhibition of iNOS aggravated albuminuria in chronic aThy 1-GN in LEW/Maa rats. Induction of iNOS during the inflammatory phase of this model may be a partially protective mechanism by interfering with intraglomerular coagulation processes.

Topics: Albuminuria; Animals; Blood Platelets; Blood Pressure; Chronic Disease; Enzyme Inhibitors; Fibrin; Isoantibodies; Kidney Glomerulus; Lysine; Nephritis; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Rats; Rats, Inbred Lew; Thrombosis

A 26-year-old male presented with oedema, massive albuminuria and microscopic haematuria. Kidney biopsy revealed enlarged cellular glomeruli infiltrated by polymorphs and eosinophils with focal fibrin deposits along the basement membrane. Microfilariae were seen in the lumen of few glomerular capillaries. Antistreptolysin titre was negative. The absence of other aetiological factors and presence of microfilariae within glomeruli suggests that nephrotic syndrome may be due to a filarial nephritis.

Topics: Adult; Biopsy; Eosinophils; Fibrin; Filariasis; Hematuria; Humans; Kidney Glomerulus; Male; Nephritis; Nephrotic Syndrome

We have compared the effects of ancrod and recombinant tissue plasminogen activator (rtPA) on nephrotoxic nephritis induced in pre-immunized rabbits by the administration of nephrotoxic globulin (NTG; sheep anti-rabbit glomerular basement membrane). We used three different doses of NTG: in each experiment three groups of six rabbits were preimmunized with normal sheep globulin and given NTG: group A received no further treatment; group B received rtPA, 2 mg/kg 12 hourly; group C received ancrod 2 U/kg 12 hourly. Animals were bled daily for estimation of plasma fibrinogen and serum creatinine, then killed on day 5 and kidneys removed for histology. 1 ml/kg of NTG caused massive glomerular necrosis, all three groups having severe renal failure. With 0.5 ml/kg of NTG, ancrod and rtPA both effectively prevented fibrin deposition in Bowman's space, but all animals had severe proliferative glomerulonephritis and marked renal failure. With 0.25 ml/kg of NTG, control animals developed severe proliferative nephritis and advanced renal failure, ancrod provided almost complete protection, and the rtPA group had renal injury and functional impairment intermediate between the other two groups. We conclude that renal failure in severe nephrotoxic nephritis is fibrin-independent, but in less fulminant nephritis renal function can be protected by defibrination with ancrod. rtPA is capable of reducing glomerular fibrin accumulation as effectively as ancrod, but provides inferior protection of renal function.

Topics: Ancrod; Animals; Fibrin; Kidney; Kidney Glomerulus; Male; Nephritis; Rabbits; Tissue Plasminogen Activator

To clarify the role of immune cell infiltration and fibrin deposition in glomerular injury, renal biopsy specimens taken from patients with primary IgA nephritis and Henoch-Schönlein purpura nephritis (HSPN) were evaluated using monoclonal antibodies specific to mononuclear cell surfaces and cross-linked fibrin (XFb). Monocytes/macrophages were the predominant cell type infiltrating glomeruli in IgA nephritis and HSPN. The intraglomerular monocyte population in both diseases was significantly higher than that in normals, mesangial proliferative (non-IgA) glomerulonephritis or minimal change nephrotic syndrome. In IgA nephritis, there was a clear correlation between glomerular monocyte accumulation and the degree of proteinuria. Although the monocyte influx tended to decline with time in HSPN, it remained unchanged in IgA nephritis. XFb deposition was found in the glomeruli of 27 out of 48 patients with IgA nephritis, and in 15 out of 20 with HSPN. The degree of XFb deposition in IgA nephritis correlated significantly with the degree of mesangial proliferation. These findings indicate a close relationship of monocyte/macrophage infiltration and XFb deposition with glomerular injury in IgA nephritis.

Topics: Adolescent; Blood Coagulation; Cell Count; Child; Child, Preschool; Fibrin; Glomerulonephritis, IGA; Humans; IgA Vasculitis; Macrophages; Monocytes; Nephritis

The plasminogen activator 960 IU/mg protein activity isolated from cultured fluid of the calf kidney cells was introduced to albino rats (180-200 g) with experimental Heynmann nephritis every day during 4 days. Nephritis caused activation of haemostasis and inhibition of fibrinolysis in the blood. There was increased excretion of the fibrin, fibrinogen degradation products in urine as a results of the local fibrin deposition in diseased kidneys. The fibrinolytic activity of the cortical zone of kidney was markedly decreased. The plasminogen activator, infused to experimental animals, resulted in normalization of the altered indexes.

Topics: Animals; Cattle; Cells, Cultured; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Hemostasis; Kidney; Male; Nephritis; Rats; Tissue Plasminogen Activator

The effect of hypofibrinogenemia with batroxobin on proliferative glomerular lesions of Masugi nephritis was examined in the rat. Batroxobin-treated rats had a relatively low level of plasma fibrinogen and a reduction in glomerular fibrin deposition. Mean nuclear counts in the outer cortical glomeruli were less in the batroxobin-treated group than in the untreated group on the 7th day. However, the difference in the overall severity of the glomerular histologic lesions between the two groups was not significant. Continual injections of the same dosage of batroxobin failed to maintain hypofibrinogenemia, possibly due to the antibody formation. These results suggest that relatively low plasma levels of fibrinogen are obviously not effective enough to prevent the development of the proliferative lesions in rat Masugi nephritis.

Topics: Afibrinogenemia; Animals; Batroxobin; Fibrin; Fibrinogen; Kidney Glomerulus; Male; Nephritis; Peptide Hydrolases; Rats; Rats, Inbred Strains

Topics: Animals; Endopeptidases; Fibrin; Glomerulonephritis; Nephritis; Rabbits; Urokinase-Type Plasminogen Activator

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

The glomerular fibrinolytic activity (GFA) was measured during the development of glomerulonephritis induced by the intravenous injection of horse or rabbit antiglomerular basement membrane antibodies in rats either untreated or preimmunized with horse or rabbit Ig. A variety of nephritides was produced ranging from proteinuria with no or mild changes in glomerular architecture to severe diffuse proliferative glomerulonephritis with close to 100% crescent formation. GFA was measured on preparations of isolated glomeruli using a radioassay based on lysis of 125I fibrin adsorbed on a solid phase. In some experiments a fibrin plaque technique was also used. Both methods clearly demonstrated a marked increase in GFA with a good correlation between the two sets of results when the glomerular architecture is preserved. The increase in GFA is related both to the severity of the nephritis estimated by the percentage of glomeruli showing crescent formation and to the extent of the fibrin deposits. The results therefore indicate that the persistence of fibrin in the glomeruli and particularly in crescents is not due to a loss of GFA.

Topics: Animals; Basement Membrane; Complement C3; Fibrin; Immune Sera; Immunoglobulins; Kidney Glomerulus; Male; Nephritis; Rats

The sympathetic nervous system and catecholamines play a major role in fibrin deposition in organs in rabbits after endotoxin administration. Glomerular fibrin deposition is also a key factor in the pathogenesis of nephrotoxic nephritis in rabbits, but the role of the sympathetic nervous system in this type of fibrin deposition has not been defined. We investigated sympathetic nervous system involvement in nephrotoxic nephritis using a model of isolated chemical sympathectomy with 6-hydroxydopamine. Different quantities of pooled nephrotoxic serum were injected intravenously into control and sympathectomized rabbits to produce a known spectrum of pathology in normal rabbits. Animals were killed and their organs were analyzed to ascertain that sympathectomy had been accomplished. Biochemical, immunohistologic, and histopathologic evaluation of the animals, comparing controls and sympathectomized rabbits, revealed no differences in the degree of renal damage for a given quantity of nephrotoxic serum. We conclude that, in the rabbit model, the sympathetic nervous system plays no significant role in the pathogenesis of fibrin deposition and glomerular damage in nephrotoxic nephritis.

Topics: Animals; Catecholamines; Fibrin; Kidney; Nephritis; Rabbits; Sympathetic Nervous System

Topics: Animals; Blood Coagulation; Fibrin; Fibrinogen; Fibrinolysis; In Vitro Techniques; Kidney Glomerulus; Male; Nephritis; Rats

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.

Topics: Ancrod; Animals; Basement Membrane; Complement C3; Creatinine; Disease Models, Animal; Endopeptidases; Fibrin; Fibrinolysis; Fluorescent Antibody Technique; Immune Sera; Immunoglobulin G; Kidney Glomerulus; Male; Nephritis; Rabbits

The role of complement has been studied in the autologous phase of nephrotoxic nephritis (NTN) in rabbits. No reduction in glomerular fibrin deposition, crescent formation or protection from renal failure was observed in either the standard model of NTN when decomplementing doses of cobra venom factor (CVF) were given before the autologous phase or in a telescoped model when CVF was administered before the nephrotoxic antibody. In the latter situation glomerular fibrin deposition and crescent formation were found in the absence of detectable deposition of C3. However, substantial protection was observed when circulating polymorphonuclear leucocytes (PMN) were depleted by antipolymorph serum. These observations establish the existence of a system of allergic glomerular injury mediated by PMN but independent of C3. It is postulated that this system may account for the glomerular injury seen in patients with Goodpasture's syndrome in whom glomerular C3 deposition is not found.

Topics: Animals; Antibodies; Basement Membrane; Blood Coagulation Tests; Cell Division; Complement C3; Complement System Proteins; Creatinine; Fibrin; Immunoglobulin G; Kidney Glomerulus; Leukocyte Count; Leukocytes; Male; Nephritis; Proteinuria; Rabbits; Snake Venoms; Time Factors; Urea

The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.

Topics: Animals; Antibodies; Antilymphocyte Serum; Complement C3; Fibrin; Fluorescent Antibody Technique; Kidney; Kidney Glomerulus; Leukocytes; Male; Mechlorethamine; Nephritis; Neutrophils; Proteinuria; Rabbits

The protective effects of anticoagulants in nephrotoxic nephritis in rabbits have been studied, using various doses of heparin and defibrination with ancrod. Massive doses of heparin (2000 units/kg/day) were required before significant reduction in glomerular fibrin deposition, extracepillary cell proliferation and urea retention occurred. Doses of 300 and 1000 units/kg/day were insufficient to modify fibrin deposition and cell proliferation. Defibrination with ancrod provided protection, judged by histological and functional criteria, comparable to 2000 units of heparin/kg/day; but fibrin could still be demonstrated in the glomeruli of animals treated with 2000 units of heparin/kg/day, contrasting with the virtual absence of fibrin in animals given ancrod.

Topics: Ancrod; Animals; Basement Membrane; Blood Coagulation Tests; Complement C3; Dose-Response Relationship, Drug; Endopeptidases; Fibrin; Heparin; Immunoglobulin G; Kidney Glomerulus; Male; Nephritis; Rabbits

Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events.

Topics: Ancrod; Animals; Antibodies; Antigen-Antibody Complex; Basement Membrane; Disease Models, Animal; Endopeptidases; Fibrin; Immunoglobulin G; Kidney Glomerulus; Male; Nephritis; Proteinuria; Rabbits; Serum Albumin, Bovine; Serum Sickness; Urea

Topics: Blood Coagulation; Child; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Humans; Kidney; Nephritis

Topics: Animals; Basement Membrane; Complement System Proteins; Factor XIII; Fibrin; Immune Sera; Kidney Glomerulus; Leukocytes; Nephritis; Rabbits

Topics: Adult; Biopsy; Blood Platelets; Blood Pressure; Complement System Proteins; Female; Fibrin; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Kidney; Liver; Male; Nephritis; Pedigree; Proteinuria; Renin; Reticulocytes; Uremia

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: Fibrin; Fibrinogen; Graft Rejection; Half-Life; Heparin; Humans; Iodides; Iodine Radioisotopes; Kidney Transplantation; Nephritis; Thyroid Gland; Transplantation, Homologous; Warfarin

Topics: Animals; Fibrin; Immune Sera; Kidney Glomerulus; Mechlorethamine; Nephritis; Rabbits; Snakes; Venoms

Topics: Child; Child, Preschool; Female; Fibrin; Fibrinogen; Hematuria; Humans; Infant; Kidney Diseases; Male; Nephritis; Nephrosis; Nephrotic Syndrome; Proteinuria; Purpura; Urinary Tract Infections

Topics: Fibrin; Fibrinogen; Fibrinolysis; Humans; Nephritis

Biopsy of renal tissue from four patients with idiopathic focal nephritis and three patients with Henoch-Schönlein syndrome showed that C3 and properdin were deposited with IgA in the glomerular mesangium, C1q could not be detected. These observations suggest that glomerular injury in disorders characterized by mesangial deposits of IgA and C3 is mediated via the properdin system.

Topics: Biopsy; Complement System Proteins; Fibrin; Fluorescent Antibody Technique; Glycine; Glycoproteins; Humans; Immunoglobulin A; Immunoglobulin G; Kidney Glomerulus; Nephritis; Properdin; Purpura

Topics: Adenosine Diphosphate; Adult; Animals; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Erythrocytes; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemagglutination Inhibition Tests; Humans; Immunoglobulin A; Immunoglobulin G; Kidney Glomerulus; Male; Middle Aged; Nephritis; Platelet Aggregation; Polymers; Renal Veins; Sheep; Thrombin

Topics: Animals; Anticoagulants; Fibrin; Fluorescent Antibody Technique; Kidney; Kidney Glomerulus; Nephritis; Rabbits; Serum Albumin; Sheep; Venoms

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

The defibrinating agent ancrod (Arvin) was used instead of heparin for intermittent haemodialysis. It was an effective, and apparently safe, anticoagulant and reduced the deposition of fibrin and leucocytes on the Cellophane membrane. Administration was more complicated and urea dialysance was less with ancrod than with heparin.

Topics: Adult; Anticoagulants; Cellophane; Chronic Disease; Fibrin; Fibrinogen; Heparin; Humans; Leukocytes; Male; Membranes, Artificial; Middle Aged; Nephritis; Polycystic Kidney Diseases; Renal Dialysis; Urea; Venoms

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: Animals; Dicumarol; Female; Fibrin; Fibrinogen; Fibrinolytic Agents; Heparin; Mice; Nephritis; Proteinuria

Topics: Animals; Basement Membrane; Complement System Proteins; Fibrin; Fibrinogen; Fibrinolytic Agents; Fluorescent Antibody Technique; gamma-Globulins; Glomerulonephritis; Heparin; Immune Sera; Kidney; Kidney Glomerulus; Mice; Nephritis; Proteinuria; Rabbits

In chronic renal failure and after acute renal failure, fibrinogen levels are raised and there is diminished fibrinolysis as the result of renal damage. A similar situation is found in nephrosis, possibly due to fibrinolytic inhibitors. Increased levels of cryofibrinogen were found in one quarter of cases of acute nephritis, nephrosis, and acute and chronic renal failure. In addition, after acute renal failure low platelet counts, prolonged thrombin times, and high levels of fibrin degradation products, yet with diminished fibrinolysis, indicate that intravascular coagulation has occurred. A positive result for fibrin degradation products was found in 17 of 20 cases of acute renal failure but in none of 10 cases of chronic uraemia. Intravascular coagulation is a process in which fibrin is deposited in the glomerular filters and may account for anuria, and, in the renal vasculature, where it may cause ischaemic tubular necrosis.

Topics: Acute Kidney Injury; Blood Coagulation Disorders; Blood Coagulation Tests; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Inhibition Tests; Humans; Immunoelectrophoresis; Kidney Diseases; Kidney Failure, Chronic; Nephritis; Nephrotic Syndrome; Plasminogen; Uremia

Topics: Animals; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Tests; Female; Fibrin; Fluorescent Antibody Technique; Male; Mice; Microscopy, Electron; Nephritis; Serum Albumin; Serum Globulins; Staining and Labeling; Warfarin

Topics: Animals; Blood Coagulation; Electrons; Fibrin; Fluorescent Antibody Technique; gamma-Globulins; Glomerulonephritis; Immune Sera; Kidney Glomerulus; Microscopy; Microscopy, Electron; Nephritis; Pathology; Phagocytosis; Rabbits; Research; Sheep; Toxicology; Warfarin

Topics: Anemia; Anemia, Hypochromic; Biomedical Research; Blood Chemical Analysis; Collagen Diseases; Enzyme Inhibitors; Fibrin; Hemophilia A; Hepatitis; Hepatitis A; Jaundice; Jaundice, Obstructive; Leukemia; Liver Cirrhosis; Multiple Myeloma; Nephritis; Nephrotic Syndrome; Physiology; Purpura; Thrombin; Uremia