fibrin and Uremia

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

To examine whole blood coagulation in uremic patients presenting for surgery with the thromboelastogram and the Sonoclot analyzer.. Prospective, observational study.. Operating rooms of a university-affiliated hospital.. 30 ASA physical status II and III patients with chronic renal failure, and 30 age-matched and gender-matched patients with normal renal function, presenting for elective surgery.. Blood sampling for thromboelastograph and Sonoclot analysis immediately after anesthetic induction, prior to surgical incision.. Thromboelastographic indices of coagulation, reflecting coagulation factor function (R time), fibrinogen-platelet interaction (K time and alpha angle), and qualitative platelet function (maximum amplitude) were hypercoagulable in the uremic group compared with the control group (p < 0.05). Fibrinolysis (%) was decreased in the uremic group (p < 0.05). Fibrin formation (initial slope) and platelet function (time to peak) of the Sonoclot trace also were hypercoagulable in the uremic group (p < 0.05).. The high incidence of arteriovenous graft and fistulae thromboses in uremic patients belies in vitro laboratory evidence of platelet dysfunction. We have demonstrated perioperative hypercoagulability in uremic patients with viscoelastic measures of whole blood coagulation. These data suggest that traditional concern for coagulopathy and platelet dysfunction in uremic patients may require re-assessment in light of this "pro-thrombotic" state.

Topics: Adult; Blood Coagulation Disorders; Blood Viscosity; Elective Surgical Procedures; Female; Fibrin; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Thrombelastography; Uremia

A two-step dose-ranging study was undertaken with CY216 (Fraxiparin) in 8 patients on 7 sessions each. The different doses were administered each time as a single bolus injection at the start of hemodialysis without heparinized priming nor further administration during the 4-hour session. In the first step, the clinical efficacy of 4 different doses of Fraxiparin was compared with that of standard heparin on the percentage of sessions free of clot formation in the extracorporeal circulation (ECC). Safety was evaluated by the compression time for hemostasis at the puncture sites. The second step was a randomized comparison of 3 Fraxiparin dosages. In addition to the clinical assessment of efficacy, the following biological parameters were measured: fibrinopeptide A (FPA), anti-Xa (AXa) activity calibrated against Fraxiparin, thrombin time (TT), activated partial thromboplastin time, blood counts, hemoglobin, hematocrit, plasma creatinine and urea, and residual blood volume in the dialyzer. A 'standard' dosage of 10,000 AXa Institut Choay units of Fraxiparin was shown to prevent clot formation in the ECC. It resulted in a marked increase in TT, without any lengthening of the puncture site compression time. After 4 h, AXa and FPA levels in the venous line were related to the doses used (p less than 0.05). After 48 h AXa activity was very low. Dialysance and tolerance were excellent. Thus, a single dose of Fraxiparin unrelated to body weight and not determined by the measurement of the whole-blood activated clotting time appeared to be a safe and effective means for preventing fibrin formation in 4-hour dialysis sessions.

Topics: Adult; Aged; Blood Coagulation; Dose-Response Relationship, Drug; Female; Fibrin; Heparin, Low-Molecular-Weight; Humans; Male; Middle Aged; Renal Dialysis; Uremia

The mechanisms contributing to an increased risk of thrombosis in uremia are complex and require clarification. There is scant morphological evidence of membrane-dependent binding of factor Xa (FXa) and factor Va (FVa) on endothelial cells (EC) in vitro. Our objectives were to confirm that exposed phosphatidylserine (PS) on microparticle (MP), EC, and peripheral blood cell (PBC) has a prothrombotic role in uremic patients and to provide visible and morphological evidence of PS-dependent prothrombinase assembly in vitro. We found that uremic patients had more circulating MP (derived from PBC and EC) than controls. Additionally, patients had more exposed PS on their MPs and PBCs, especially in the hemodialysis group. In vitro, EC exposed more PS in uremic toxins or serum. Moreover, reconstitution experiments showed that at the early stages, PS exposure was partially reversible. Using confocal microscopy, we observed that PS-rich membranes of EC and MP provided binding sites for FVa and FXa. Further, exposure of PS in uremia resulted in increased generation of FXa, thrombin, and fibrin and significantly shortened coagulation time. Lactadherin, a protein that blocks PS, reduced 80% of procoagulant activity on PBC, EC, and MP. Our results suggest that PBC and EC in uremic milieu are easily injured or activated, which exposes PS and causes a release of MP, providing abundant procoagulant membrane surfaces and thus facilitating thrombus formation. Blocking PS binding sites could become a new therapeutic target for preventing thrombosis.

Topics: Adult; Aged; Animals; Blood Coagulation; Cattle; Cell-Derived Microparticles; Coagulants; Endothelial Cells; Factor Xa; Female; Fibrin; Flow Cytometry; Human Umbilical Vein Endothelial Cells; Humans; Male; Membrane Glycoproteins; Microscopy, Confocal; Middle Aged; Milk Proteins; Phosphatidylserines; Thrombin; Thromboplastin; Thrombosis; Uremia

Several recent studies have demonstrated the central role of Fc receptors (FcR) rather than the complement system in triggering hypersensitivity reactions. We investigated the role of FcR for IgG (FcgammaR) using a murine model of accelerated anti-glomerular basement membrane (GBM) antibody-mediated glomerulonephritis as a representative of type II hypersensitivity diseases. Intravenous injection of rabbit anti-GBM antibody after preimmunization with normal rabbit IgG induced proteinuria and azotemia in wild-type C57BL/6 and CD40(+/-) mice but not in FcR gamma chain (FcRgamma)(-/-) mice or CD40(-/-) mice. Light microscopic findings revealed marked tissue damage in the glomeruli of wild-type C57BL/6 and CD40(+/-) mice. However, no tissue damage except polymorphonuclear cell infiltration was observed in the glomeruli of FcRgamma(-/-) mice. The glomeruli of CD40(-/-) mice were almost normal. Immunohistochemistry revealed the binding of rabbit IgG to the GBM in all mice injected with anti-GBM antibody. However, depositions of mouse IgG and complement to the glomeruli were not observed in CD40(-/-) mice, and deposition of fibrin was not observed in FcRgamma(-/-) or CD40(-/-) mice. These findings suggest that FcgammaR may initiate anti-GBM antibody-mediated renal disease. We conclude that FcgammaR rather than the complement system is critically involved in the development of type II hypersensitivity diseases.

Topics: Animals; Anti-Glomerular Basement Membrane Disease; Antigen-Antibody Complex; Autoantibodies; Basement Membrane; CD40 Antigens; Complement System Proteins; Female; Fibrin; Gene Deletion; Immunization; Immunoglobulin G; Kidney Glomerulus; Leukocyte Count; Mice; Mice, Inbred C57BL; Mice, Knockout; Neutrophil Infiltration; Neutrophils; Proteinuria; Rabbits; Receptors, IgG; Uremia

The autopsy data at the University of Southern California Liver Unit was studied during a 6-year period to investigate the relationship of fibrinous pericarditis with liver diseases. We found 18 cases of fibrinous pericarditis in 220 patients with alcoholic liver disease but none in 32 patients with fulminant and subacute hepatitis without alcoholism or in 39 patients with nonalcoholic cirrhosis. Although all the 18 patients with pericarditis had azotemia, 3 patients had pericarditis develop only in mild renal function impairment. These findings suggest that chronic alcoholism may precipitate pericarditis during the hepatorenal syndrome.

Topics: Adult; Aged; Aged, 80 and over; Fibrin; Hepatitis, Alcoholic; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Pericarditis; Retrospective Studies; Uremia

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

Fibrosing uremic pleuritis is a newly recognized late complication of uremia. Extreme incarceration of the lining and chest wall can occur with disabling restriction of pulmonary function. Decortication of the chest wall and the lung can be carried out safely with minimal bleeding and restoration of pulmonary function.

Topics: Adult; Female; Fibrin; Hemorrhage; Humans; Lung; Lung Diseases; Pleurisy; Radiography; Time Factors; Uremia; Wound Healing

Topics: Adult; Animals; Blood Urea Nitrogen; Creatinine; Disseminated Intravascular Coagulation; Female; Fibrin; Glomerulonephritis; Humans; Hyalin; Kidney; Kidney Glomerulus; Lung; Male; Middle Aged; Pneumococcal Infections; Pneumonia, Pneumococcal; Proteinuria; Rats; Sepsis; Streptococcus pneumoniae; Thrombosis; Uremia

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: Aspirin; Blood Coagulation; Complement System Proteins; Diabetic Nephropathies; Dipyridamole; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Heparin; Humans; Iodine Radioisotopes; Kidney; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Plasminogen; Proteinuria; Thrombosis; Transplantation, Homologous; Uremia; Warfarin

Topics: Albuminuria; Animals; Chromatography, Gel; Chromatography, Ion Exchange; Fibrin; Fibrinogen; Glomerular Filtration Rate; Glomerulonephritis; Humans; Immunoelectrophoresis; Kidney Transplantation; Molecular Weight; Muramidase; Nephrosis; Plasminogen; Rabbits; Streptokinase; Transplantation, Homologous; Uremia

Topics: Anemia, Hemolytic; Child, Preschool; Fibrin; Hemolytic-Uremic Syndrome; Heparin; Humans; Male; Plasminogen; Streptokinase; Uremia

Topics: Anemia, Hemolytic; Child, Preschool; Complement System Proteins; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infant; Kidney; Kidney Function Tests; Male; Prognosis; Uremia

Topics: Anemia, Hemolytic; Blood Coagulation; Blood Coagulation Factors; Blood Platelets; Fibrin; Fibrinogen; Hemolytic-Uremic Syndrome; Heparin; Humans; Uremia

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 Disease; Blood Coagulation Factors; Blood Urea Nitrogen; Child; Creatinine; Female; Fibrin; Fibrinolysis; Glomerulonephritis; Heparin; Humans; Penicillin V; Prednisolone; Streptococcal Infections; Uremia

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: Anemia, Hemolytic; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Blood Transfusion; Child; Diagnosis, Differential; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Fibrin; Fibrinolysis; Hemorrhagic Disorders; Heparin; Hepatitis; Humans; Infections; Pediatrics; Uremia

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: Adolescent; Adult; Age Factors; Aged; Animals; Anticoagulants; Arthritis, Rheumatoid; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Cardiovascular Diseases; Cattle; Child; Child, Preschool; Dogs; Electrophoresis; Female; Fibrin; Fibrinolysin; Fibrinolysis; Fibrinolytic Agents; Hemorrhage; Hemorrhagic Disorders; Humans; Infant; Male; Menstruation; Methods; Middle Aged; Neoplasms; Plasminogen; Pregnancy; Rabbits; Sex Factors; Thromboembolism; Thrombosis; Uremia

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

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: 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