fibrin and Acute-Kidney-Injury

Urinary proteomics has become one of the most attractive topics in disease biomarker discovery. MS-based proteomic analysis has advanced continuously and emerged as a prominent tool in the field of clinical bioanalysis. However, only few protein biomarkers have made their way to validation and clinical practice. Biomarker discovery is challenged by many clinical and analytical factors including, but not limited to, the complexity of urine and the wide dynamic range of endogenous proteins in the sample. This article highlights promising technologies and strategies in the MS-based biomarker discovery process, including study design, sample preparation, protein quantification, instrumental platforms, and bioinformatics. Different proteomics approaches are discussed, and progresses in maximizing urinary proteome coverage and standardization are emphasized in this review. MS-based urinary proteomics has great potential in the development of noninvasive diagnostic assays in the future, which will require collaborative efforts between analytical scientists, systems biologists, and clinicians.

Topics: Acute Kidney Injury; Antigens, Neoplasm; Antigens, Nuclear; Biomarkers; Biomarkers, Tumor; Cell Cycle Proteins; Fibrin; Humans; Insulin-Like Growth Factor Binding Proteins; Mass Spectrometry; Nuclear Matrix-Associated Proteins; Proteome; Proteomics; Tissue Inhibitor of Metalloproteinase-2; Urinalysis; Urinary Bladder Neoplasms

Topics: Acute Kidney Injury; Animals; Blood Coagulation; Child; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Glomerulonephritis; Graft Rejection; Hemolytic-Uremic Syndrome; Heparin; Humans; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Mice; Phagocytosis; Pre-Eclampsia; Pregnancy; Rabbits; Transplantation, Homologous

Topics: Acute Kidney Injury; Angiotensin II; Animals; Anticoagulants; Blood Coagulation; Blood Coagulation Disorders; Catecholamines; Disseminated Intravascular Coagulation; Female; Fibrin; Heparin; Humans; Hypertension, Renal; Kidney Diseases; Kidney Glomerulus; Pre-Eclampsia; Pregnancy; Renin; Thrombosis; Uremia

Topics: Acute Kidney Injury; Adolescent; Adult; Child; Child, Preschool; Diarrhea; Female; Fibrin; Humans; Hypocalcemia; Infant; Infant, Newborn; Kidney; Kidney Tubules; Male; Microscopy, Electron; Muscles; Muscular Diseases; Myofibrils; Myoglobinuria; Necrosis; Phosphorus; Respiratory Distress Syndrome, Newborn; Respiratory Tract Infections; Staining and Labeling; Tetany; Thrombosis

Ischemic acute kidney injury is common, deadly, and accelerates the progression of chronic kidney disease, yet has no specific therapy. After ischemia, reperfusion is patchy with early and persistent impairment in regional renal blood flow and cellular injury. We tested the hypothesis that intrarenal coagulation results in sustained renal ischemia following reperfusion, using a well-characterized model. Markedly decreased, but heterogeneous, microvascular plasma flow with microthrombi was found postischemia by intravital microscopy. Widespread tissue factor expression and fibrin deposition were also apparent. Clotting was accompanied by complement activation and inflammation. Treatment with exosomes derived from renal tubular cells or with the fibrinolytic urokinase, given 24 h postischemia when renal failure was established, significantly improved microvascular flow, coagulation, serum creatinine, and histological evidence of injury. These data support the hypothesis that intrarenal clotting occurs early and the resultant sustained ischemia is a critical determinant of renal failure following ischemia; they demonstrate that the coagulation abnormalities are amenable to therapy and that therapy results in improvement in both function and postischemic inflammation.

Topics: Acute Kidney Injury; Animals; Creatinine; Disease Models, Animal; Fibrin; Inflammation; Ischemia; Kidney; Reperfusion; Reperfusion Injury; Thromboplastin; Urokinase-Type Plasminogen Activator

To describe an intravascular fibrin sheath associated with a hemodialysis catheter in a dog.. A 4-year-old dog presented for hemodialysis to treat acute kidney injury. Hemodialysis catheter dysfunction during the course of treatment was temporarily alleviated using a tissue plasminogen activator. A thrombus composed of fibrin and granulation tissue creating a sheath around the catheter and focally adherent to the vessel wall was identified on postmortem evaluation.. Fibrin sheath formation is a commonly recognized problem of central venous catheters used for hemodialysis in people and is likely a common problem in veterinary patients undergoing dialysis as well. This report provides a description of the clinical features of the catheter dysfunction, response to treatment, postmortem radiographic and direct imaging, and histology of the fibrin sheath, and also provides a brief review of potential management techniques that have been described in people.

Topics: Acute Kidney Injury; Animals; Catheterization, Central Venous; Catheters, Indwelling; Diagnosis, Differential; Dog Diseases; Dogs; Equipment Design; Fibrin; Male; Osteotomy; Postoperative Complications; Recombinant Proteins; Renal Dialysis; Thrombosis; Tissue Plasminogen Activator

Disseminated intravascular coagulation (DIC)-positive kidneys have historically been turned down for fear of poor outcomes. Higher severity injuries, which are prone to DIC, are typically seen in younger, otherwise healthy potential donors. The continued kidney allograft shortage has generated interest in the use of these DIC-positive grafts. There have been some reports of acceptable outcomes of renal transplantation using kidneys from donors with DIC. There are multiple clinical series demonstrating good outcomes from DIC-positive kidneys when the extent of glomeruli containing fibrin thrombi is less than 50% and donor renal function is preserved. These grafts are frequently associated with a period of delayed graft function.. We report 2 transplants with kidneys from brain dead donors with known DIC.. Both donors had renal failure and pretransplant renal biopsies showing 100% of the glomeruli containing fibrin thrombi. The recipients experienced delayed graft function requiring hemodialysis which was discontinued on postoperative days 18 and 39 for cases 1 and 2, respectively. Both patients are now over 14 months posttransplant with stable allograft function.. Until clearer organ selection criteria are established, caution should be exercised when considering the use of kidneys with a similar phenotype and allocation decisions made by a multidisciplinary transplant team on a case-by-case basis.

Topics: Acute Kidney Injury; Aged; Allografts; Biomarkers; Biopsy; Delayed Graft Function; Disseminated Intravascular Coagulation; Donor Selection; Female; Fibrin; Humans; Kidney Glomerulus; Kidney Transplantation; Male; Middle Aged; Predictive Value of Tests; Renal Dialysis; Risk Assessment; Risk Factors; Time Factors; Tissue Donors; Treatment Outcome; Young Adult

Acute renal failure, a serious condition characterised by a drastic decline in renal function, often follows ischaemia/reperfusion (I/R) episodes. I/R is characterised by necrosis, inflammation and activation of coagulation, in concert causing renal tissue damage. In this context, activated protein C (APC) might be of importance in the pathogenesis of renal I/R. APC is a serine protease which has anticoagulant but also several anti-inflammatory and cytoprotective effects such as protection of endothelial barrier function. It was our objective to study the role of cytoprotective and anticoagulant functions of APC during renal I/R. C57BL/6j mice subjected to renal I/R were treated with intraperitoneally injected exogenous human APC, or two mutant forms of APC (200 µg/kg) which specifically lack anticoagulant or signalling properties. In a different experiment mice received specific monoclonal antibodies (20 mg/kg) that block the cytoprotective and/or anticoagulant properties of endogenous APC. Treatment with APC reduced tubular injury and enhanced renal function without altering the inflammatory response and did reduce renal fibrin deposition. Administration of APC mutant lacking anticoagulant properties reduced renal damage and enhanced renal function. Blocking the anticoagulant and cytoprotective functions of endogenous APC resulted in elevated tubular damage and reduced tubular cell proliferation, however, without influencing renal function or the inflammatory response. Furthermore, blocking both the anticoagulant and cytoprotective effects of APC resulted in dramatic renal interstitial haemorrhage, indicative of impaired vascular integrity. Blocking only the anticoagulant function of APC did not result in interstitial bleeding. In conclusion, the renoprotective effect of APC during I/R is independent of its anticoagulant properties.

Topics: Acute Kidney Injury; Animals; Anticoagulants; Cell Proliferation; Disease Models, Animal; Fibrin; Humans; Kidney; Male; Mice; Mice, Inbred C57BL; Mutant Proteins; Protein C; Recombinant Proteins; Reperfusion Injury; Signal Transduction

Sepsis-induced acute kidney injury (AKI) contributes to the high mortality and morbidity in patients. Although the pathogenesis of AKI during sepsis is poorly understood, it is well accepted that plasminogen activator inhibitor-1 (PAI-1) and vitronectin (Vn) are involved in AKI. However, the functional cooperation between PAI-1 and Vn in septic AKI has not been completely elucidated. To address this issue, mice were utilized lacking either PAI-1 (PAI-1-/-) or expressing a PAI-1-mutant (PAI-1R101A/Q123K) in which the interaction between PAI-1 and Vn is abrogated, while other functions of PAI-1 are retained. It was found that both PAI-1-/- and PAI-1R101A/Q123K mice are associated with decreased renal dysfunction, apoptosis, inflammation, and ERK activation as compared to wild-type (WT) mice after LPS challenge. Also, PAI-1-/- mice showed attenuated fibrin deposition in the kidneys. Furthermore, a lack of PAI-1 or PAI-1-Vn interaction was found to be associated with an increase in activated Protein C (aPC) in plasma. These results demonstrate that PAI-1, through its interaction with Vn, exerts multiple deleterious mechanisms to induce AKI. Therefore, targeting of the PAI-1-Vn interaction in kidney represents an appealing therapeutic strategy for the treatment of septic AKI by not only altering the fibrinolytic capacity but also regulating PC activity.

Topics: Acute Kidney Injury; Animals; Apoptosis; Cytokines; Disease Models, Animal; Endotoxemia; Fibrin; Inflammation Mediators; Intercellular Adhesion Molecule-1; Lipopolysaccharides; Male; MAP Kinase Signaling System; Mice; Mice, Knockout; Neutrophil Infiltration; Plasminogen Activator Inhibitor 1; Protein Binding; Vitronectin

Tissue factor (TF) is involved in monocrotaline (MCT)/lipopolysaccharide (LPS) hepatotoxicity. It is not known whether MCT/LPS can cause renal toxicity and whether TF is involved in this toxicity. Thus, the present study was undertaken to investigate the potential renal toxicity after MCT/LPS co-treatment and the involvement of TF in this toxicity. MCT was delivered to ND4 male mice (200 mg/kg) per os followed 4 h later by treatment with LPS ip (6 mg/kg) to investigate its effect on kidney. We injected TF antisense oligonucleotide (TF-AS) intravenously (i.v) in mice prior to LPS treatment, to block TF, and measured their blood urea nitrogen (BUN), creatinine (CRE), alkaline phosphatase (ALP), and potassium. In MCT/LPS co-treated group, fibrin was detected on the glomerular capillary lumina, distal tubules of renal cortex, and the necrotic tubules of renal medulla. An elevation of BUN, creatinine, and the BUN/creatinine ratio was seen in mice with MCT/LPS co-treatment, compared to animals receiving LPS or MCT alone. Simultaneously, an aggressive tubular necrosis was seen in the medullary tubules in the same group which may account for the oliguria observed in these animals. Fourfold inductions in the plasma TF level was detected at 10 h after MCT/LPS co-treatment which increased to 18-fold at 24 h. Increased blood level of leptin, interleukin-6 (IL-6) and downregulation of tubular chemokine (C-X-C motif) ligand 16 (CXCL16) are characteristic features in MCT/LPS co-treated animal. On the other hand, mice injected with TF-AS in the presence of MCT/LPS co-treatment showed no elevation of the blood BUN, creatinine, potassium, and normal levels of the proinflammatory molecules. TF-AS injection significantly prevented glomerular and tubular fibrin deposition, tubular necrosis, and improvement of the animal survivability. Renal toxicity involving TF can be prevented successfully by the use of TF-AS.

Topics: Acute Kidney Injury; Alkaline Phosphatase; Animals; Blood Urea Nitrogen; Chemokine CXCL16; Chemokine CXCL6; Creatinine; Fibrin; Interleukin-6; Kidney; Leptin; Lipopolysaccharides; Male; Mice; Monocrotaline; Oligonucleotides, Antisense; Potassium; Thromboplastin

T helper (Th)17 cells might contribute to immune-mediated renal injury. Thus, we sought to define the time course of IL-17A-induced kidney damage and examined the relation between Th17 and Th1 cells in a model of crescentic anti-glomerular basement membrane glomerulonephritis. Renal injury and immune responses were assessed in wild-type and in IL-17A-deficient mice on days 6, 14, and 21 of disease development. On day 6, when mild glomerulonephritis developed, IL-17A-deficient mice were protected from renal injury. On day 14, when more severe disease developed, protection from renal injury due to IL-17A deficiency was less evident. On day 21, when crescentic glomerulonephritis was fully established, disease was enhanced in IL-17A(-/-) mice, with increased glomerular T-cell accumulation and fibrin deposition, and augmented Th1 responses. Mice lacking the Th17-promoting cytokine, IL-23 (p19), also developed more severe disease than wild-type animals on day 21. In contrast, mice deficient in the key Th1-promoting cytokine, IL-12 (p35), had decreased Th1 and increased Th17 responses and developed less severe crescentic glomerulonephritis than wild-type animals. These studies show that IL-17A contributes to early glomerular injury, but it attenuates established crescentic glomerulonephritis by suppressing Th1 responses. They provide further evidence that Th1 cells mediate crescentic injury in this model and that Th1 and Th17 cells counterregulate each other during disease development.

Topics: Acute Kidney Injury; Animals; Anti-Glomerular Basement Membrane Disease; Cell Adhesion Molecules; Cell Survival; Fibrin; Immunity, Cellular; Immunoglobulins; Interferon-gamma; Interleukin-12; Interleukin-17; Interleukin-23; Male; Mice; Mice, Inbred C57BL; Th1 Cells

Glomerular and microvascular thrombosis due to the activation of inflammation and coagulation pathway contribute to the occurrence of acute renal failure in sepsis. The protease-activated receptors (PARs) have been shown to play an important role in the interplay between inflammation and coagulation. We hypothesized that PAR-2 blocking would improve glomerular and vascular thrombosis by attenuating inflammation and coagulation, leading to the prevention of acute renal failure, and assessed the effects of the PAR-2 blocking peptide (PAR-2 BP) in a rat model of LPS-induced acute renal failure. Levels of TNF-alpha were significantly expressed 1 h after LPS administration, followed by 1) an increase in levels of tissue factor, factor VIIa, factor Xa, thrombin and plasminogen activator inhibitor 1; 2) unchanged levels of tissue factor pathway inhibitor; and 3) subsequent deposition of fibrin in kidney tissues, which led to the elevation of creatinine and blood urea nitrogen. Time-dependent PAR-2 expression was observed at both the gene and protein levels. Immunoreactivities of PAR-2 and fibrin were observed in the glomerulus and small arteries. Protease-activated receptor blocking peptide suppressed TNF-alpha elevation and attenuated activation of the coagulation, thus leading to a decrease in fibrin formation and its deposition in the glomerulus. However, the levels of creatinine and blood urea nitrogen remained unchanged. These results show that PAR-2 plays a key role in the inflammatory and coagulation process of LPS-induced renal failure; however, PAR-2 inhibition alone does not affect improvement in the renal function.

Topics: Acute Kidney Injury; Animals; Blood Coagulation; Blood Urea Nitrogen; Disease Models, Animal; Endotoxins; Fibrin; Inflammation; Lipopolysaccharides; Male; Rats; Rats, Wistar; Receptor, PAR-2; Time Factors

Inflammation and thrombosis coexist in several disorders. Although it is recognized that leukocytes may induce a procoagulant state at sites of inflammation, the critical molecular determinants of this process remain largely unknown.. To examine mechanisms of inflammation-induced thrombosis, we developed a murine model of thrombotic glomerulonephritis (TGN), a known cause of acute renal failure in patients. This model, induced by lipopolysaccharide and antibody to the glomerular basement membrane, led to rapid glomerular neutrophil recruitment, thrombotic glomerular lesions with endothelial cell injury, and renal dysfunction. In mice immunodepleted of neutrophils or lacking the leukocyte-specific integrin Mac-1, neutrophil recruitment, endothelial injury, glomerular thrombosis, and acute renal failure were markedly attenuated despite the robust generation of renal cytokines. Neutrophil elastase is a likely effector of Mac-1 because its activity was reduced in Mac-1-deficient mice and the phenotype in mice deficient in Mac-1 or neutrophil elastase was similar. Platelets accumulated in glomerular capillaries within 4 hours of TGN before evidence of thrombosis. Platelet immunodepletion before TGN markedly exacerbated hematuria (hemorrhage), inflammation, and injury, whereas thrombocytopenic Mac-1-deficient mice remained resistant to disease, indicating that initial glomerular platelet deposition protects the vessel wall from neutrophil-mediated sequelae. The subsequent thrombosis relied on the interaction of Mac-1 on recruited neutrophils with glycoprotein Ibalpha on platelets as antibody-mediated disruption of this interaction attenuated TGN without affecting renal neutrophil accumulation.. These observations establish Mac-1 on neutrophils as a critical molecular link between inflammation and thrombosis and suggest it as an attractive target for antithrombotic therapy.

Topics: Acute Kidney Injury; Animals; Antibodies; Blood Platelets; Cytokines; Disease Models, Animal; Female; Fibrin; Glomerulonephritis; Leukocyte Elastase; Macrophage-1 Antigen; Male; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Neutrophils; Platelet Glycoprotein GPIb-IX Complex; Thrombocytopenia; Thrombosis

Disseminated intravascular coagulation (DIC) is a lethal situation in severe infections, characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. Current clinical trials are not promising. In this study, we investigated the protective effect of curcumin in a lipopolysaccharide (LPS)-induced DIC model in rats. Experimental DIC was induced by sustained infusion of LPS (10 mg/kg body weight) for 4 h through the tail vein. Curcumin (60 mg/kg body weight) was given intraperitoneally 3 h before LPS infusion. Results showed that, in vivo, curcumin reduced the mortality rate of LPS-infused rats by decreasing the circulating TNF-alpha levels and the consumption of peripheral platelets and plasma fibrinogen. Furthermore, in vivo curcumin also has the effect of preventing the formation of fibrin deposition in the glomeruli of kidney. These results reveal the therapeutic potential of curcumin in infection-related coagulopathy of DIC.

Topics: Acute Kidney Injury; Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Platelets; Curcumin; Disease Models, Animal; Disseminated Intravascular Coagulation; Endotoxemia; Escherichia coli; Fibrin; Fibrinogen; Injections, Intraperitoneal; Kidney Glomerulus; Lipopolysaccharides; Male; Rats; Rats, Sprague-Dawley; Survival Rate; Tumor Necrosis Factor-alpha

Ischaemic-reperfusion injury as a model of acute renal failure (ARF) results in increased macromolecular permeability, tubular obstruction, and renal oedema. To investigate the role for coagulation in this model, anticoagulated and saline-pretreated rats were subjected to 60 min unilateral renal artery occlusion (RAO). After 15 min of reflow, specimens were collected for electron and light microscopic examination. Morphometry was employed to study podocyte changes and Bowman's space dilatation as measures of increased permeability and tubular obstruction, respectively. After 15 min of reflow, Bowman's space increased significantly and the podocytes were markedly widened and flattened. Rats pretreated with heparin or warfarin showed less widening of Bowman's space than saline-treated rats, whereas no significant difference was seen regarding the podocyte changes. In saline-treated rats, fibrin-positive material was seen in the tubules but not in the urine sediments collected after 90 min of reflow, either due to fibrinolysis or poor urinary elimination. The results suggest that anticoagulation does not preclude the glomerular sieving of macromolecules, but seems to reduce tubular obstruction, probably by preventing conversion of filtered fibrinogen into fibrin.

Topics: Acute Kidney Injury; Animals; Anticoagulants; Female; Fibrin; Fluorescent Antibody Technique, Direct; Kidney Glomerulus; Kidney Tubules; Microscopy, Electron; Rats; Rats, Sprague-Dawley; Renal Artery Obstruction; Reperfusion Injury

Although the importance of injury with consequent activation of endothelium is well-recognized in diseases affecting the glomerular endothelial cell (GEN), research on GEN injury in vivo has been hampered by the lack of adequate animal models. Here we report the establishment and characterization of a new GEN injury model in rats. This model was induced by selective renal artery perfusion with anti-GEN IgG and resulted in the severe acute renal failure with marked platelet deposition and development of a thrombotic microangiopathy involving glomeruli. Peritubular capillary endothelial cells were also damaged that was associated with severe tubular necrosis. Although the glomerular changes were severe, half of the glomeruli recovered by day 10, while interstitial changes remained throughout our observation time course. Proliferation of GEN was observed during the recovery phase. An increased expression of endothelial nitric oxide synthase in GEN was also observed, and may be an adaptive mechanism to counteract the thrombosis and ischemia. This model should be useful to investigate the pathophysiology of renal microvascular diseases and the mechanisms of GEN injury, activation and recovery in vivo.

Topics: Acute Kidney Injury; Anemia; Animals; Blood Urea Nitrogen; Collagen; Complement System Proteins; Disease Models, Animal; Endothelial Growth Factors; Endothelium, Vascular; Fibrin; Kidney; Kidney Glomerulus; Laminin; Lymphokines; Macrophages; Male; Nitric Oxide Synthase; Proteinuria; Rats; Rats, Wistar; Thrombocytopenia; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

We have recently developed a model of thrombotic microangiopathy with injury to the glomerular endothelial cell (GEN) induced by heterologous antibody to rat GEN. In addition to GEN injury rats developed glomerular platelet aggregation and fibrin deposition, acute renal failure, and acute tubular necrosis with interstitial inflammation. To study the role of complement in mediating this lesion, we induced the disease in normal complement PVG rats and measured the effects of generalized complement depletion with cobra venom factor (CVF) and of selective C6 deficiency using genetically C6 deficient PVG animals. Complement sufficient rats developed severe endothelial injury accompanied by platelet aggregation, fibrin deposition, decrease in endothelial cells assessed by antibody staining in the glomerulus, and macrophage infiltration. These changes were associated with marked reduction in renal function. These features were either absent or markedly diminished in complement depleted or C6 deficient rats. This demonstrates that C5b-9, the terminal product of activation of the complement cascade, plays an important role in the pathogenesis of this immune renal microvascular endothelial injury model. Thus, the complement system may play a pathogenic role in renal microvascular diseases such as thrombotic microangiopathy.

Topics: Acute Kidney Injury; Animals; Blood Platelets; Complement C3; Complement C6; Complement Hemolytic Activity Assay; Complement Membrane Attack Complex; Disease Models, Animal; Endothelium; Fibrin; Glomerulonephritis; Immunoglobulin G; Kidney Glomerulus; Macrophages; Male; Microcirculation; Microscopy, Electron; Rats; Rats, Inbred Strains

To investigate whether fibrin deposition in the kidney occurs in ischaemic acute renal failure, rats were subjected to a left renal artery occlusion (RAO) for 1 h and contralateral nephrectomy. The animals were killed 0, 5, 15 and 60 min after re-establishment of the circulation. Kidney tissue was snap-frozen for immunofluorescence microscopy and scanning electron microscopy, and immersion-fixed for light microscopy and transmission electron microscopy. Immunofluorescence studies showed small amounts of immune reactive fibrinogen/fibrin deposits in the peritubular capillaries. Substantial amounts of fibrinogen/fibrin positive material was observed in Bowman's space and in the tubular lumina. Scanning electron microscopy of freeze-dried tissue disclosed granular and fibrillar material in Bowman's space. A temporary enlargement of Bowman's space was noted; it may have been caused by tubular obstruction. No deposits were found in the control (right) kidneys and in kidneys of heparinized rats subjected to RAO. The results indicate that fibrin deposition occurs in the ischaemic model of acute renal failure in rat, both intravascularly and in the urinary space. Its importance for the development of renal functional impairment remains to be studied.

Topics: Acute Kidney Injury; Animals; Female; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Kidney; Kidney Glomerulus; Microscopy, Electron, Scanning; Rats; Rats, Inbred Strains; Renal Artery Obstruction

This article deals with the clinical importance of antithrombin III (AT III) in renal disease. Patients with nephrotic syndrome demonstrates a high risk of thromboembolism. A renal AT III loss is an important pathogenetic factor in these events. Patients with serumalbumin below 2.0 g/dl are mostly endangered. In patients with acute oligoanuric renal failure low AT III-levels due to consumption were often found that lead to diminished protection against intravascular coagulation processes and can therefore contribute to progression of illness. An AT III-substitution may be of some benefit in these patients. Additionally AT III was given in patients with dialysis-dependent renal failure and low levels of AT III leading to a reduced incidence of thrombosis of the extracorporeal system. Unnecessary high doses were also avoided and a minimal heparinization could be performed more efficiently in bleeding risk patients. Furthermore, AT III-levels during renal transplantation and during organ rejection are reported.

Topics: Acute Kidney Injury; Antithrombin III; Antithrombin III Deficiency; Female; Fibrin; Humans; Kidney Diseases; Nephrotic Syndrome; Pregnancy; Puerperal Disorders; Risk; Sepsis; Thromboembolism; Thrombosis

In 50 patients without renal insufficiency, fibrinolytic activity, as reflected by euglobulin lysis time, was determined in blood obtained from the renal veins, the renal artery and a peripheral vein. Fibrinolytic activity was found to be significantly higher in the renal veins than in the renal artery and the peripheral vein. Other coagulation and fibrinolysis parameters did not show such differences. In addition, a patient with acute oligoanuric renal failure was investigated. This patient demonstrated reduced overall fibrinolytic activity, but there were no differences between the activity in the blood of the renal veins and that of the renal artery or peripheral vein. It seems, therefore, that the kidneys release plasminogen activators into the systemic circulation. This may be decreased in renal failure, probably contributing to the well-known diminished fibrinolysis in some kidney diseases.

Topics: Acute Kidney Injury; Fibrin; Fibrinolysis; Humans; Kidney Glomerulus; Plasminogen Activators; Renal Artery; Renal Veins; Urokinase-Type Plasminogen Activator

Topics: Acute Kidney Injury; Blood Platelets; Disseminated Intravascular Coagulation; Factor VIII; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Glomerulonephritis; Humans; Kidney Glomerulus; Platelet Aggregation; Prognosis

The term "Endotheliotropic Hemolytic Nephroangiopathy" (EHN) comprises various clinically or pathomorphologically defined disease states with severe renal lesions (e.g. hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency) which, to date, have been considered as different entities. We attempted to assign accompanying glomerular changes based upon light and electron microscopy to the above mentioned clinical pictures and their various stages. The accordingly classified glomerular lesions (G1--G3 and Ga) are of critical importance in pathohistological differential diagnosis. Since it is assumed that fibrin is a causing event in the pathogenesis of the vascular lesions, quantitative evaluation of glomerular fibrin deposits was done. The results, when viewed with respect to time, lead to the conclusion that the microthrombotic component represents a secondary phenomenon. Thus, the primary and hence pathogenetically most important finding is a severe damage to the endothelium of the terminal renal vasculature. This endothelial damage although being expressed with variable intensity has to be regarded as the common denominator inherent to all types of glomerular lesions in EHN.

Topics: Acute Kidney Injury; Adult; Aged; Biopsy; Child; Child, Preschool; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infant; Kidney Glomerulus; Male; Microscopy, Electron; Middle Aged; Nephrosclerosis; Pregnancy; Puerperal Disorders

Infusion of thrombin and the fibrinolysis inhibitor tranexamic acid during ether anaesthesia in the rat gives rise to fibrin deposition in the renal glomeruli. This resulted in renal insufficiency as indicated by an increase in the serum urea nitrogen, reduction in the renal blood flow and patchy cortical necrosis in the kidneys. The plasma renin activity was elevated initially probably due to the ether anaesthesia. Infusion of the angiotensin II antagonist saralasin prevented the renal insufficiency if it was given during the thrombin infusion but not if it was given afterwards. The deposition of fibrin in the kidneys was also reduced. The results indicate that angiotensin II is involved in the pathogenesis of the renal injury.

Topics: Acute Kidney Injury; Angiotensin II; Animals; Female; Fibrin; Rats; Rats, Inbred Strains; Renal Artery Obstruction; Renal Circulation; Renin; Renin-Angiotensin System; Saralasin; Thrombin

Topics: Acute Kidney Injury; Animals; Blood Coagulation Tests; Blood Pressure; Disseminated Intravascular Coagulation; Dogs; Fibrin; Fibrinogen; Fibrinolysis; Inulin; Kidney; Osmolar Concentration; p-Aminohippuric Acid; Platelet Count; Shock, Hemorrhagic; Sodium; Urine

Topics: Acute Kidney Injury; Animals; Blood Vessels; Brain; Coronary Vessels; Edema; Fibrin; Folic Acid; Kidney; Kidney Tubules; Liver; Male; Mesentery; Muscle, Smooth; Necrosis; Pancreas; Rats; Time Factors

Topics: Acute Kidney Injury; Anemia; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Fibrin; Hemostasis; Humans; Kidney Diseases; Kidney Failure, Chronic; Peritoneal Dialysis; Polycythemia; Renal Dialysis

The clinical and renal biopsy findings from two patients in whom renal functional abnormalities developed in the late postpartum period are described. Both biopsies showed fibrin deposition in the renal vasculature, in one case marked and in the other mild. The patient with the more severely damaged kidney subsequently died, and the other is alive but with evidence of slowly progressing renal damage. The clinicopathological spectrum and pathogenesis of late postpartum renal failure are discussed.

Topics: Acute Kidney Injury; Animals; Biopsy; Blood Coagulation; Disseminated Intravascular Coagulation; Ergot Alkaloids; Female; Fibrin; Fluorescent Antibody Technique; Hemolytic-Uremic Syndrome; Humans; Hypertension; Ischemia; Kidney; Kidney Glomerulus; Pregnancy; Puerperal Disorders

Two patients who developed reversible renal failure during intermittent rifampicin therapy are described. Both had febrile reactions to rifampicin. The first was also found to have uraemia associated with swelling of the glomerular endothelial cells. The second developed tubular necrosis unassociated with haemolysis or shock. The pathogenesis of the renal lesion in these two patients, as revealed by light microscopy, immunofluorescence studies and electron microscopy, is discussed.

Topics: Acute Kidney Injury; Adult; Antibodies; Endothelium; Ethambutol; Fever; Fibrin; Humans; Immune Complex Diseases; Ischemia; Kidney Glomerulus; Kidney Tubules; Male; Necrosis; Rifampin; Tuberculosis, Pulmonary; Uremia

Acute renal failure developed in a 55-year-old man 6 days after he had received a cadaver renal allograft. This was associated with thrombocytopenia. Extensive intraglomerular fibrin deposition was seen in a renal biopsy specimen. He was treated with corticosteroids, azathioprine, cyclophosphamide and hemodialysis with regional heparinization but not with systemic anticoagulation. This was followed by complete recovery of both renal function and histologic damage despite the fact that he did not receive anticoagulant therapy. This suggests that treatment with anticoagulants may not be necessary for all patients with intraglomerular deposits of fibrin.

Topics: Acute Kidney Injury; Azathioprine; Biopsy, Needle; Cadaver; Cyclophosphamide; Fibrin; Graft Rejection; Humans; Kidney Glomerulus; Kidney Transplantation; Male; Methylprednisolone; Middle Aged; Renal Dialysis; Thrombocytopenia; Transplantation, Homologous

Rats were kept for 4 weeks on a dietary regimen with a low or high sodium intake to increase or reduce, respectively, the renin activity of the kidneys and plasma. Fibrinolysis was inhibited by intravenous injection of AMCA and thrombin was infused into the jugular vein, giving rise to heavy intravascular fibrin deposition in the kidneys. Shortly after the thrombin infusion the glomerular filtration rate (GFR) decreased equally in saline-loaded and normal rats. 48 h after the thrombin infusion the GFR was still markedly reduced in saline-deprived and normal rats but had returned to preinfusion values in the saline-loaded rats. The results might indicate that the renin-angiotensin system is involved in the presistence of the renal functional impairment after intravascular coagulation in the rat kidney.

Topics: Acute Kidney Injury; Animals; Diet; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Glomerular Filtration Rate; Rats; Renin; Sodium; Sodium Chloride; Thrombin; Tranexamic Acid

Topics: Acute Kidney Injury; Biopsy; Cell Migration Inhibition; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immune Complex Diseases; Male; Necrosis; Peritoneal Dialysis; Proteinuria; Remission, Spontaneous; Streptococcal Infections

Topics: Acute Kidney Injury; Anemia; Basement Membrane; Blood Coagulation Disorders; Capillaries; Epithelial Cells; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Hematuria; Histocytochemistry; Humans; Immunoglobulins; Kidney; Kidney Glomerulus; Kidney Tubules; Microscopy, Electron; Prognosis; Proteinuria; Statistics as Topic

Topics: Acute Kidney Injury; Adrenal Cortex Hormones; Angiotensin II; Animals; Anticoagulants; Blood Platelets; Disease Models, Animal; Disseminated Intravascular Coagulation; Endotoxins; Fibrin; Fibrinolysis; Kidney; Kidney Glomerulus; Mechlorethamine; Microscopy, Electron; Polymyxins; Pressure; Rabbits; Receptors, Adrenergic; Shwartzman Phenomenon; Thrombin; Thrombosis; Ureter

Topics: Acute Kidney Injury; Aged; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Heparin; Humans; Kidney; Male; Middle Aged; Myocardial Infarction; Shock, Cardiogenic

Topics: Acute Kidney Injury; Enzyme Activation; Fibrin; Fluorescent Antibody Technique; Graft Rejection; Immune Sera; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Kidney Cortex; Kidney Glomerulus; Kidney Transplantation; Plasminogen; Properdin; Renal Artery; Renal Veins; Serum Albumin; Thrombosis; Transplantation, Homologous

In 15 out of 35 patients with myelomatosis histological examination showed intravascular fibrin within the glomeruli, and this was associated with proliferation of the mesangial complex in 12. The presence of intravascular fibrin and mesangial proliferation was not associated with any specific immunoglobulin abnormality or with the presence or absence of Bence Jones proteinuria. In addition to fibrin being present within glomerular capillaries it was also shown in intertubular capillaries in three cases of myelomatosis with acute tubular necrosis. It is suggested that intraglomerular coagulation and fibrin deposition may contribute to the genesis of renal failure in myelomatosis.

Topics: Acute Kidney Injury; Autopsy; Bence Jones Protein; Biopsy, Needle; Capillaries; Disseminated Intravascular Coagulation; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulin A; Immunoglobulin D; Immunoglobulin G; Kidney; Kidney Glomerulus; Kidney Tubules; Male; Microscopy; Multiple Myeloma; Proteinuria; Retrospective Studies; Thromboembolism; Urea

Topics: Acute Kidney Injury; Awards and Prizes; Fibrin; Germany, West; History of Medicine; Humans; Internal Medicine; Solubility

Discrimination between the physiological cleavage fragments of fibrinogen and fibrin offers an approach to differentiation between fibrinogenolytic processes and fibrinolysis after coagulation. By use of the cleavage-associated neoantigen of fibrinogen (fg-D(neo)) as a molecular marker, characteristic differences between the D regions of fibrinogen derivatives and fibrin derivatives can be demonstrated. The expression of fg-D(neo) by X, Y, D:E complex, and D-fragments of fibrinogen or fibrin is shown to be quantitative and unitary. Characteristic differences between fg-D(neo) sites present on fibrinogen cleavage fragments, as contrasted to fibrin cleavage fragments, are indicated by different competitive inhibition slopes, and appear to reflect differential binding affinity of selected anti-fg-D(neo) antibodies for the specific molecular site. There is a linear relationship between the slope of quantitative competitive inhibition and the relative molar ratio of fibrinogen and fibrin derivatives. Identical immunochemical expressions are observed in vitro and in vivo, and support the thesis that cleavage in vivo is produced by plasmin. The differential immunochemical features of fg-D(neo) expression may be the result of stable conformational and/or subtle structural differences between the D region of fibrinogen and fibrin cleavage fragments and suggest that precise changes in the D region are associated with the fibrin transition. These molecular features not only provide additional insight into the molecular immunology and structure of fibrinogen, but also appear to offer a new molecular approach to discrimination between fibrinogenolytic mechanisms as contrasted to fibrinolysis secondary to coagulation.

Topics: Abruptio Placentae; Acute Kidney Injury; Adenocarcinoma; Binding Sites, Antibody; Binding, Competitive; Blood Coagulation Disorders; Epitopes; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Immune Sera; Iodine Isotopes; Male; Melanoma; Meningococcal Infections; Peritonitis; Pregnancy; Prostatic Neoplasms; Radioimmunoassay; Structure-Activity Relationship

Topics: Acute Kidney Injury; Adult; Arteries; Capillaries; Cell Division; Epithelial Cells; Epithelium; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infarction; Kidney Glomerulus; Postpartum Hemorrhage; Pregnancy; Puerperal Disorders

Topics: Acute Kidney Injury; Aminocaproates; Animals; Autoradiography; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Fibrinolysis; Fluorescent Antibody Technique; Glycerol; Half-Life; Hemoglobins; Hemoglobinuria; Iodine Isotopes; Ischemia; Kidney; Kidney Cortex Necrosis; Kidney Glomerulus; Kidney Tubules; Rabbits; Rats; Serum Albumin, Radio-Iodinated; Sympathectomy

Topics: Acute Kidney Injury; Animals; Blood Urea Nitrogen; Diagnosis, Differential; Disease Models, Animal; Fibrin; Fibrinogen; Graft Rejection; Hydronephrosis; Iodine Radioisotopes; Kidney Transplantation; Ligation; Protein Binding; Rabbits; Renal Artery Obstruction; Renal Veins; Thrombophlebitis; Thrombosis; Transplantation, Homologous

Topics: Acute Kidney Injury; Adult; Anticoagulants; Azathioprine; Biopsy; Cyclophosphamide; Dipyridamole; Female; Fibrin; Fluorescent Antibody Technique; Glomerular Filtration Rate; Glomerulonephritis; Heparin; Humans; Kidney Glomerulus; Male; Middle Aged; Prednisolone; Snake Venoms; Time Factors; Warfarin

Topics: Abruptio Placentae; Acute Kidney Injury; Animals; Anuria; Disseminated Intravascular Coagulation; Female; Fibrin; Iodine Radioisotopes; Kidney; Kidney Glomerulus; Mercury Poisoning; Methemoglobin; Pregnancy; Rabbits; Shock; Shwartzman Phenomenon; Tourniquets

Topics: Acute Disease; Acute Kidney Injury; Adult; Biopsy; Blood Vessels; Capillaries; Female; Fibrin; Follow-Up Studies; Humans; Kidney; Kidney Glomerulus; Microscopy, Electron; Microscopy, Fluorescence; Pre-Eclampsia; Pregnancy; Prognosis; Proteinuria; Puerperal Disorders

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Azathioprine; Child; Child, Preschool; Epithelial Cells; Epithelium; Female; Fibrin; Glomerulonephritis; Glucocorticoids; Heparin; Humans; Hyperplasia; Infant; Infant, Newborn; Kidney Glomerulus; Male; Middle Aged; Renal Dialysis

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Anticoagulants; Australia; Azathioprine; Biopsy; Creatinine; Cyclophosphamide; Dipyridamole; Female; Fibrin; Glomerulonephritis; Heparin; Humans; Kidney; Kidney Glomerulus; Male; Middle Aged; Prednisolone; Prognosis; Renal Dialysis; Seasons; Steroids; Warfarin

Topics: Acute Kidney Injury; Basement Membrane; Blood Coagulation Disorders; Diabetic Nephropathies; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Hemagglutination Tests; Hemolytic-Uremic Syndrome; Humans; Ischemia; Kidney; Kidney Diseases; Male; Middle Aged; Pre-Eclampsia; Pregnancy; Thrombosis; Urokinase-Type Plasminogen Activator

Topics: Acute Kidney Injury; Erythrocytes; Fibrin; Glomerulonephritis; Graft Rejection; Hemagglutination Inhibition Tests; Humans; Kidney Diseases; Kidney Transplantation; Pyelonephritis; Transplantation, Homologous; Ureteral Obstruction

Topics: Acute Kidney Injury; Animals; Antigens; Fibrin; Fibrinogen; Glomerulonephritis; Humans; Kidney Diseases

Topics: Acute Kidney Injury; Disseminated Intravascular Coagulation; Female; Fibrin; Glomerulonephritis; Heparin; Kidney Diseases; Nephritis, Interstitial; Pregnancy; Pregnancy Complications, Infectious; Sepsis

Topics: Acute Kidney Injury; Biopsy; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Epithelium; Fibrin; Fibrinolysis; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Male; Middle Aged; Multiple Myeloma; Plasminogen

The concentration of serum fibrinogen-fibrin-related antigen (F.R.-antigen) was measured in a group of 142 patients with various renal disorders, in 38 of whom urine F.R.-antigen was also estimated. Raised serum F.R.-antigen levels were present in 48% of the patients, with no particular preponderance in any diagnostic category apart from acute reversible intrinsic renal failure in which high levels were invariably present. Significantly-raised serum levels were also present in the patients with microangiopathic haemolytic anaemia and in those with the more severe degrees of renal impairment. Urine F.R.-antigen was increased in 34 of the 38 patients. The amount of F.R.-antigen in the urine correlated with the degree of proteinuria but not with the serum F.R.-antigen levels. The evidence relating to intravascular coagulation in renal disease is reviewed, and it is suggested that there is a high incidence of localized fibrinogen or fibrin degradation in the kidney, which is related more to factors such as the presence of uraemia and microangiopathic haemolytic anaemia rather than to the diagnostic category.

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Anemia, Hemolytic; Antigens; Child; Child, Preschool; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemagglutination Inhibition Tests; Humans; Hypertension, Malignant; Kidney Diseases; Male; Middle Aged; Proteinuria; Uremia

Topics: Acute Kidney Injury; Angiography; Animals; Antibodies; Antigen-Antibody Reactions; Blood Coagulation; Complement System Proteins; Dextrans; Dogs; Fibrin; Glomerular Filtration Rate; Histamine H1 Antagonists; Immunosuppression Therapy; Ischemia; Kidney; Kidney Transplantation; Oxygen Consumption; Sodium; Transplantation Immunology; Transplantation, Homologous; Vasoconstrictor Agents

Topics: Acute Kidney Injury; Adolescent; Adult; Antigens; Blood; Blood Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Graft Rejection; Humans; Kidney Transplantation; Male; Middle Aged; Postoperative Complications; Transplantation, Homologous; Urine

Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Agglutination Tests; Arteries; Arteriosclerosis Obliterans; Blood Coagulation Tests; Contraceptives, Oral; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Humans; Liver Cirrhosis; Male; Methods; Middle Aged; Neoplasm Metastasis; Protamines; Pulmonary Embolism; Staphylococcus; Sulfates; Thrombosis; Veins

Topics: Acute Disease; Acute Kidney Injury; Antifibrinolytic Agents; Blood Cell Count; Blood Coagulation Factors; Blood Platelets; Blood Urea Nitrogen; Chronic Disease; Creatinine; Fibrin; Fibrinolysis; Humans; Immunoelectrophoresis; Plasminogen; Renal Dialysis; Uremia

Topics: Acute Kidney Injury; Adult; Anemia, Hemolytic; Azathioprine; Beta-Globulins; Biopsy; Female; Fibrin; Haptoglobins; Heparin; Humans; Obstetric Labor Complications; Oxytocics; Prednisone; Pregnancy; Puerperal Disorders

A single dose of endotoxin given to rats with obstructive jaundice produced death with intravascular coagulation. This action was apparently due to delayed clearance of endotoxin from the circulation. The finding is relevant to "hepatorenal failure," which can be caused by bacteraemia after biliary tract operations.

Topics: Acute Kidney Injury; Animals; Blood Coagulation Tests; Blood Platelets; Cholestasis; Endotoxins; Escherichia coli; Fibrin; Fibrinogen; Kidney Diseases; Liver Diseases; Prothrombin Time; Rats; Thrombelastography; Thrombin

Topics: Acute Kidney Injury; Animals; Aprotinin; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Fibrinolytic Agents; Kidney; Kidney Function Tests; Kidney Glomerulus; Liver; Lung; Rabbits; Sodium Chloride; Spleen; Thrombelastography; Thrombin

Topics: Acute Kidney Injury; Aged; Autopsy; Fibrin; Humans; Kidney Cortex Necrosis; Leg; Male; Middle Aged; Thrombosis

Topics: Acute Kidney Injury; Anemia, Hemolytic; Blood Coagulation; Blood Platelets; Blood Transfusion; Blood Urea Nitrogen; Creatinine; Fibrin; Fibrinogen; Heparin; Humans; Infant; Male; Reticulocytes; Thrombocytopenia

Topics: Acute Kidney Injury; Anemia, Hemolytic; Anuria; Blood Cell Count; Blood Coagulation Factors; Blood Transfusion; Central Nervous System Diseases; Disseminated Intravascular Coagulation; Erythrocytes, Abnormal; Fibrin; Hematuria; Hemoglobins; Hemolysis; Heparin; Humans; Hyperkalemia; Infant; Kidney; Kidney Glomerulus; Peritoneal Dialysis; Thrombocytopenia

Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Amylases; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Female; Fibrin; Humans; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Male; Middle Aged; Pancreas; Pancreatitis

Topics: Acute Kidney Injury; Adult; Arthus Reaction; Eosinophils; Female; Fibrin; Heparin; Histocompatibility; Humans; Kidney; Kidney Cortex Necrosis; Kidney Glomerulus; Kidney Transplantation; Male; Shwartzman Phenomenon; Thrombosis; Transplantation Immunology; Transplantation, Homologous

Topics: Acute Kidney Injury; Esophagus; Extracorporeal Circulation; Fibrin; Fibrinolysis; Hemorrhage; Hemorrhagic Disorders; Humans; Kidney; Lung; Pleura; Pneumonectomy; Postoperative Complications; Splenectomy; Thrombosis

Topics: Acute Kidney Injury; Cholelithiasis; Cholestasis; Diabetic Nephropathies; Factor XIII; Fibrin; Fibrinogen; Glomerulonephritis; Humans; Kidney Failure, Chronic; Nephrotic Syndrome; Pyelonephritis; Renal Dialysis; Tuberculosis, Renal; Uremia; Wound Healing

Topics: Acute Kidney Injury; Aged; Bronchopneumonia; Diagnosis, Differential; Fibrin; Humans; Hypertension, Portal; Kidney Cortex Necrosis; Kidney Glomerulus; Liver Cirrhosis; Male; Mesenteric Veins; Portal Vein; Sclerosis; Shwartzman Phenomenon; Splenic Vein; Thrombosis

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