fibrin and Nephrotic-Syndrome

Topics: Antithrombin III; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Fibrin; Fibrinogen; Fibrinolysis; Humans; Nephrotic Syndrome; Renal Veins; Thromboembolism; Thrombophlebitis; Thrombosis

Topics: Arachidonic Acids; Arteriosclerosis; Aspirin; Blood Platelets; Calcium; Coronary Disease; Cyclic AMP; Diabetes Mellitus; Dietary Fats; Female; Fibrin; Humans; Myeloproliferative Disorders; Nephrotic Syndrome; Oxygenases; Platelet Adhesiveness; Platelet Aggregation; Pre-Eclampsia; Pregnancy; Prostaglandins; Thrombosis

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: Autoantibodies; Autoimmune Diseases; Basement Membrane; Blood Coagulation; Complement System Proteins; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immune Complex Diseases; Immunoglobulin E; Kidney Glomerulus; Nephrotic Syndrome

Soluble fibrin (SF) is produced by activated blood coagulation reaction and is useful to diagnose thrombotic diseases. We measured plasma and urine SF levels in nephritic patients to assess the hypercoagulability state associated with the disease. Before they received anti-coagulation or anti-platelet therapies, 60 patients underwent measurement of plasma SF and D-dimer levels by Latex agglutination turbidimetric immnoassay (LA). Urinary SF levels were also measured by LA. Plasma and urinary thrombin antithrombin III complex (TAT) levels were measured by enzyme immunoassay (EIA). Plasma SF levels showed a good correlation with plasma TAT levels but only weak positive correlations were observed between plasma D-dimer and SF or TAT levels. Plasma SF and D-dimer levels were significantly higher in the Iatients with nephrotic-range hypoalbuminemia (< or =3 g/dL) than those without it. Contrarily there was no significant difference in plasma TAT levels between these two groups of patients. In almost all patients, urinary SF levels were under the detection limit. However, TAT was excreted into urine more frequently in patients showing the nephrotic range of hypoalbuminemia at 38.2% than in non-nephrotic patients at 8.0%. Thus, plasma SF levels more precisely indicate activated blood coagulation reaction than plasma TAT levels in nephrotic patients, probably because the plasma SF is not excreted into urine, while plasma TAT is.

Topics: Antithrombin III; Biomarkers; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Latex Fixation Tests; Nephelometry and Turbidimetry; Nephrotic Syndrome; Peptide Hydrolases; Thrombophilia

Simultaneous natural changes in lipoprotein(a) [Lp(a)] and plasminogen occur in the nephrotic syndrome and offer a unique opportunity to investigate their effects on plasminogen activation under conditions fashioned in vivo. Plasminogen, Lp(a), and apolipoprotein(a) in plasma were characterized, and their competitive binding to carboxy-terminal lysine residues of fibrin and cell membrane proteins was determined in nephrotic children during a flare-up of the disease (61 cases) and after 6 weeks (33 cases) and 6 months (42 cases) of remission. Low plasminogen concentrations (median 1.34 micromol/L, range 0.39 to 1.96 micromol/L) and high Lp(a) levels (median 0.27 g/L, range 0.07 to 2. 57 g/L) were detected at flare-up. These changes were associated with an increased Lp(a) binding ratio onto fibrin (3.13+/-0.48) and cells (1.53+/-0.24) compared with binding ratios of control children (1.31+/-0.19 and 1.05+/-0.07, respectively) with normal plasminogen and low Lp(a) (median 0.071 g/L). After 6 weeks and 6 months of remission, the values for net decrease in Lp(a) binding to fibrin were 1.7+/-0.22 (after 6 weeks) and 1.88+/-0.38 (after 6 months) and were correlated with low Lp(a) concentrations (median 0.2 g/L, range 0.07 to 0.8 g/L; and median 0.12 g/L, range 0.07 to 1.34 g/L) and inversely associated with increased plasminogen levels (median 1.82 micromol/L, range 1.4 to 2.1 micromol/L; and median 1.58 micromol/L, range 1.1 to 2.1 micromol/L). These studies provide the first quantitative evidence that binding of Lp(a) to lysine residues of fibrin and cell surfaces is directly related to circulating levels of both plasminogen and Lp(a) and that these glycoproteins may interact as competitive ligands for these biological surfaces in vivo. This mechanism may be of relevance to the atherothrombotic role of Lp(a), particularly in nephrotic patients.

Topics: Adolescent; Apolipoproteins A; Binding, Competitive; Cell Line; Child; Child, Preschool; Female; Fibrin; Fibrinolysis; Genetic Variation; Humans; Infant; Lipids; Lipoprotein(a); Male; Membrane Proteins; Nephrotic Syndrome; Phenotype; Plasminogen; Serum Albumin

In the present study we have investigated the effect of individual variations in the concentration of Lp(a) on plasmin formation at the surface of fibrin. The plasma Lp(a) concentrations from 20 nephrotic children were high at flare-up of the disease (0.43+/-0.45 g/l) and decreased progressively with remission at both 6 weeks (0.28+/-0.24 g/l) and 6 months (0.24+/-0.288 g/l). In contrast, the concentration of plasminogen showed an inverse variation, with low values at flare-up (1.27+/-0.34 microM) and normal values at remission (1.66+/-0.17 microM at 6 weeks and 1.99+/-0.21 microM at 6 months). An increase in plasmin formation (from 0.62+/-0.49 to 0.73+/-0.61, and 0.84+/-0.75 pmol/well) and a decrease in apo(a) binding (from 5.45+/-2.42 to 4.54+/-2.12, and 3.93+/-1.51 fmol/well) on the surface of fibrin, were concomitantly observed from flare-up to remission at 6 weeks and at 6 months, respectively. Values for plasmin formation parallel the amount of plasminogen bound. The low concentration of plasminogen found at flare-up may also have contributed to the increased binding of Lp(a) as indicated by a decrease in the maximal amount of Lp(a) bound (Bmax) to fibrin as a function of plasma plasminogen concentrations. Bmax was 1.51 fmol in the absence of plasminogen and decreased to 1.1 fmol and 0.93 fmol at respectively 1 and 2 microM of plasminogen. Altogether, these data constitute the first quantitative evidence indicating that plasmin formed at the surface of fibrin may vary with modifications of the concentration of Lp(a) in vivo.

Topics: Adolescent; Child; Child, Preschool; Female; Fibrin; Fibrinolysin; Genetic Variation; Humans; Infant; Lipoprotein(a); Male; Nephrotic Syndrome

Porosity, viscoelasticity and morphological properties of plasma fibrin from 16 nephrotic patients and 16 healthy volunteers were compared. Nephrotic patients were characterized by formation of tight and rigid plasma fibrin gels which resulted in a slower rate of fibrin lysis studied either under pressure-driven permeation or diffusional transport of fibrinolytic agents. These latter findings indicated that both abnormal fibrin network conformation and abnormal fibrin fiber structure were involved in hypofibrinolysis. Albumin supplementation up to 40 mg/ml partially restored normal fibrin architecture and increased the rate of fibrinolysis in these patients. Multiparametric analysis showed that nephrotic patients were mainly characterized by a low plasma albumin level (R = -0.85), a low albumin to fibrinogen ratio (R = -0.89) and a high resistance to lysis (R = -0.82). High triglycerides level was the only plasma modification related to the slower fibrin lysis rate (R = -0.54). High fibrin rigidity (G') was the only fibrin parameter simultaneously related to the nephrotic state (R = 0.75) and the lysis resistance (R = -0.71). After eliminating the effects of age, albumin and fibrinogen levels, low fibrin porosity (Ks) and low fiber mass-length ratio (mu) were the main features of the nephrotic state. These findings are discussed in relation to both the pathophysiology of thrombotic complications in nephrotic syndrome and their pharmacological prevention.

Topics: Adolescent; Adult; Aged; Elasticity; Female; Fibrin; Fibrinolysis; Fibrinolytic Agents; Gels; Humans; Lipids; Male; Microscopy, Confocal; Middle Aged; Nephrotic Syndrome; Porosity; Serum Albumin; Thrombophilia; Thrombosis; Viscosity

Little information is available that documents the incidence and possible etiology of a prolonged thrombin time (TT) found in children with nephrotic syndrome. We speculated that this prolonged TT might best be explained by an altered fibrinogen similar to that found in the newborn.. We describe 20 children with nephrosis, an unexplained prolonged TT and reptilase time (RT), and an elevated fibrinogen level. Thrombin and/or plasmin effect on plasma fibrinogen was studied by analyzing for soluble monomer, D-dimer, fibrin degradation products, B beta 1-42 peptide, and by polyacrylamide gel electrophoresis (PAGE) and agarose electrophoresis. Structural changes in the fibrinogen molecule were investigated using two-dimensional gel (2D gel) electrophoresis. Fibrinogen was purified via glycine precipitation, and the sialic acid (SA) content was determined.. No evidence for in vivo thrombin and/or plasmin effect on fibrinogen could be detected in 13 of 20 children tested. Additionally, no fibrin/fibrinogen degradation products or soluble fibrin complexes were detected using PAGE or agarose electrophoresis in this group of patients. The B beta isoforms of nephrosis fibrinogen were similar in isoelectric point on 2D gel electrophoresis to those of fetal fibrinogen and demonstrated a greater electronegative shift when compared with normal adult fibrinogen. Also, the SA content of nephrosis and fetal fibrinogen were greater than that measured in adult fibrinogen. Both nephrosis and fetal fibrinogen were more resistant to neuraminidase treatment than was normal adult fibrinogen.. These data support the notion that an altered fibrinogen exists in some children with nephrotic syndrome characterized by an increased TT and RT, elevated fibrinogen, and both an increased negative charge and SA content.

Topics: Adult; Blood Coagulation Tests; Child; Electrophoresis, Gel, Two-Dimensional; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Humans; Infant, Newborn; N-Acetylneuraminic Acid; Nephrotic Syndrome; Prospective Studies; Sialic Acids; Thrombin; Thrombin Time

Increased in vitro platelet aggregability and hypercoagulability are generally held to be main determinants in the prethrombotic state in nephrosis. In vivo, however, thrombotic events depend on the dynamic interaction of flowing blood with the vessel wall. The present study confirms that aggregability of platelets of nephrotic patients is significantly increased by mere stirring or by exogenous stimuli as adenosine diphosphate and arachidonic acid. Moreover, the nephrotic patients have high von Willebrand factor and decreased red blood cell deformability, which normally increase platelet-vessel wall interaction. However, perfusion studies under well-defined flow conditions, in which anticoagulated nephrotic blood was exposed to deendothelialized human umbilical artery segments and sprayed collagen, showed normal platelet adhesion and only a modest increase in the deposition of platelet aggregates. This suggests that some factor counteracts platelet-vessel wall interaction under flow conditions in the nephrotic syndrome. When tissue factor associated with endothelial extracellular matrix (ECM) was allowed to generate thrombin, perfusions with nephrotic blood over this ECM resulted in a strong increase in fibrin generation. The capacity of patient blood to form increased amounts of fibrin appeared strongly correlated with the level of hyperfibrinogenemia. Platelet adhesion as well as aggregation in these experiments was even decreased below control values. This suggests that fibrin coverage may block the direct contact between blood platelets and matrix. We therefore also studied the isolated effect of high fibrinogen on platelet-vessel wall interaction by increasing fibrinogen concentrations in normal blood. Modulation of fibrinogen concentrations in normal blood could mimic all the observations in nephrotic blood: platelet aggregation in suspension increased with increasing concentrations of fibrinogen, while platelet adhesion and aggregate formation under flow conditions decreased. In perfusions over tissue factor-rich matrix, fibrin deposition increased. Therefore, our observations indicate that nephrotic hyperaggregability in suspension is not associated with increased platelet vessel wall-interaction under flow conditions. The latter is probably counteracted by high levels of fibrinogen. Our observations further suggest that hyperfibrinogenemia may be a major thrombotic risk factor in nephrosis by inducing more fibrin depositions.

Topics: Adenosine Diphosphate; Adolescent; Adult; Angiotensin III; Arachidonic Acid; Biopsy; Blood Coagulation Factors; Blood Platelets; Collagen; Endothelium, Vascular; Erythrocyte Deformability; Extracellular Matrix; Female; Fibrin; Fibrinogen; Humans; In Vitro Techniques; Kidney; Male; Microscopy, Electron, Scanning; Middle Aged; Muscle, Smooth, Vascular; Nephrotic Syndrome; Platelet Adhesiveness; Platelet Aggregation; Thrombosis; Umbilical Arteries

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

Clotting studies have been performed on 64 consecutive patients with nephrotic syndrome. The thrombin time was prolonged in 59. Fibrin polymerization was studied in 42 of the 59 patients with a prolonged thrombin time and an abnormality was present in 22. There was a significant correlation between the prolongation of the thrombin time and impairment of polymerization (p = 0.018). No correlation was found between these two parameters and the patient's sex, age and drug therapy. Furthermore there was no correlation with the prothrombin time, APTT, fibrinogen, FDP, antithrombin III and platelet counts. There was however a significant negative correlation between the thrombin time and the serum albumin level (p less than 0.05). No abnormal bleeding was observed during or after renal biopsy in these patients. Renal biopsy may be performed safely despite the grossly prolonged thrombin time and abnormal fibrin polymerization in patients with the nephrotic syndrome.

Topics: Adult; Blood Coagulation; Female; Fibrin; Humans; Male; Middle Aged; Nephrotic Syndrome; Thrombin Time

Blood coagulation function was serially studied in 84 children with nephrotic syndrome. Fifty-eight had minimal change disease, six had focal glomerulosclerosis and 20 had other forms of renal disease associated with the nephrotic syndrome. Qualitatively similar abnormalities in fibrinogen metabolism were present in all groups with clinically overt nephrotic syndrome; plasma fibrinogen concentration and high molecular weight fibrin(ogen) complexes (HMWFC) were grossly elevated (P less than 0.001 in most groups). With disease remission fibrinogen and HMWFC concentrations decreased to the normal range, usually with concomitant transient increase in plasma fibrinolytic activity (P less than 0.02). Alterations in concentrations of other proteins involved in coagulation and fibrinolysis differed depending on the underlying cause for the nephrotic syndrome. Antithrombin III concentration was normal except in the focal glomerulosclerosis group. The results demonstrate that a coagulopathy characterized by pathological degree of thrombin action on fibrinogen complicates the nephrotic state and may be initiated by different mechanisms. It is suggested that this coagulopathy, which remits with clinical improvement, is consequent upon local intrarenal activation of the blood coagulation system.

Topics: Adolescent; alpha 1-Antitrypsin; alpha-Macroglobulins; Antithrombin III; Blood Coagulation Disorders; Child; Child, Preschool; Factor XIII; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Glomerulosclerosis, Focal Segmental; Humans; Molecular Weight; Nephrosis, Lipoid; Nephrotic Syndrome

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

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.

Topics: Animals; Autoimmune Diseases; Blood Coagulation; Disseminated Intravascular Coagulation; Female; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Hemostasis; Male; Mercuric Chloride; Mercury; Nephrotic Syndrome; Rats; Time Factors

The localization of intrarenal cross-linked fibrin was examined by the effect of monochloroacetic acid treatment on the kidney sections. In acute glomerulonephritis or in mild diffuse or focal proliferative type of nephritis, cross-linked fibrin was observed mainly within glomerular capillary walls. Extension of cross-linked fibrin deposit over the mesangium or sclerotic area was seen in moderate to severe proliferative type of nephritis or in membranoproliferative glomerulonephritis. In hemolytic uremic syndrome or disseminated intravascular coagulation syndrome, cross-linked fibrin was detected within glomeruli and vessels.

Topics: Acetates; Child; Disseminated Intravascular Coagulation; Factor XIII; Fibrin; Glomerulonephritis; Hemolytic-Uremic Syndrome; Histocytochemistry; Humans; IgA Vasculitis; Immunoglobulin G; Kidney; Kidney Diseases; Nephrotic Syndrome; Tissue Distribution

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

In order to determine the role of intrarenal vascular coagulation (IVC) in chronic glomerulonephritis, coagulant parameters in renal blood (RVB), urine FDP's and renal histology were examined in 70 patients with chronic glomerulonephritis (CGN). RVB was obtained by Seldinger's technique. A correlation was obtained between an increase of fibrinogen, FDP and soluble fibrin monomer complexes (SFMC) in RVB and the degree of intraglomerular fibrin deposition shown on immunofluorescence. An increase of FDP's, SFMC and a slight decrease of fibrinolytic activity in RVB were observed in patients with CGN with decreased renal function or with the nephrotic syndrome. Daily excretion of FDP in the urine and the extent of intraglomerular fibrin deposition were greater in nephrotics than in non-nephrotics. We conclude that measurement of coagulation parameters in RVB is a reliable and sensitive method of assessing IVC, and that IVC plays an important role in aggravation of chronic glomerulonephritis, particularly when the nephrotic syndrome is present.

Topics: Chronic Disease; Fibrin; Fibrin Fibrinogen Degradation Products; Glomerulonephritis; Histocytochemistry; Humans; Kidney Failure, Chronic; Kidney Glomerulus; Nephrotic Syndrome; Renal Veins

The morphologic features observed in the renal biopsy specimens from three patients with massive obesity complicated by the nephrotic syndrome are described. In the two patients with active disease, the majority of the glomeruli showed focal to extensive fibrin deposition both within and adjacent to capillary loops, associated with adhesions to Bowman's capsule, with a variable endocapillary proliferative response. In the patient with inactive disease, the majority of the glomeruli appeared normal. However, fibrin-like material, similar to that seen in the active phase, was infrequently found ultrastructurally in the subendothelial portion of the capillary loops. Subendothelial vacuolated material was also observed. Although intravascular coagulation was suggested in this disorder, only minor coagulation abnormalities were discovered. In two of the patients, the massive proteinuria has resolved with weight reduction.

Topics: Adult; Diagnosis, Differential; Female; Fibrin; Humans; Kidney; Kidney Glomerulus; Male; Middle Aged; Nephrotic Syndrome; Obesity

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

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

During experimental Masugi nephritis in the rabbit, were demonstrated various disturbances in hemostasis: a) during the initial stage: immediate, severe and transient fall in the platelet count without any change in Factor V;b)during the secondary stage, from the 7th to the 8th day onwards, increase in platelets and fibrinogen, in relation with the intensity of the nephrotic syndrome; c) in parallel, appearance of urinary fibrinogen split products in relation to the intensity of the glomerular lesions, evidence for the presence of intraglomerular fibrin. These facts confirm the role played by platelets in coagulation phenomena secondary to the immune reaction. They indicate, furthermore, the existence of hemostasis disorders during the nephrotic syndrome.

Topics: Animals; Antigens; Blood Cell Count; Blood Coagulation; Blood Platelets; Complement System Proteins; Ducks; Factor V; Fibrin; Fibrinogen; Glomerulonephritis; Hematocrit; Immune Sera; Kidney Glomerulus; Nephrotic Syndrome; Platelet Aggregation; Proteinuria; Rabbits

Topics: Acute Disease; Adolescent; Adult; Aged; Chronic Disease; Female; Fibrin; Humans; Kidney Diseases; Male; Middle Aged; Nephrotic Syndrome

Topics: Adolescent; Adult; Aged; Child; Female; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Humans; Male; Middle Aged; Nephrotic Syndrome

Several coagulation factors were studied in twenty children less than 16 years old, bearing nephrotic syndrome. Four of them were in remission. In nephrotic syndrome there is hypercoagulability. Coagulations factors such as fibrinogen, platelet factor III, prothrombin time, and factor V are markedly altered, and to a lesser degree, total number of platelets. Fibrin degradation products factors II, VII, X and VIII are also altered. During remission, all of them improve or become normal. In no case fibrin breakdown products were found in the blood. However, if found in urine, they would be considered as a pronostic index in nephropaties. Although etiologic factors remain unknown for most of the above-mentioned alterations, increased fibrinogen synthesis, decreased fibrinolytic plasms activity and renal damage have been demonstrated.

Topics: Adolescent; Age Factors; Biopsy; Blood Coagulation Disorders; Blood Coagulation Tests; Child; Child, Preschool; Fibrin; Fibrinolysis; Humans; Kidney; Microscopy, Electron; Nephrotic Syndrome

Topics: Complement C6; Fibrin; Humans; Immunoglobulin A; Kidney Glomerulus; Nephrotic Syndrome; Obesity; Proteinuria

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

Topics: Chlorambucil; Complement Fixation Tests; Complement System Proteins; Eosinophils; Female; Fibrin; Humans; Hyalin; Immunoglobulin G; Immunoglobulin M; Infant; Infant, Newborn; Kidney Glomerulus; Kidney Tubules; Male; Nephrotic Syndrome; Prednisone; Prognosis; Renal Dialysis; Sclerosis

Topics: Animals; Fibrin; Fluorescent Antibody Technique; Haplorhini; Immunoglobulin M; Kidney; Kidney Glomerulus; Malaria; Microscopy, Electron; Nephrotic Syndrome; Plasmodium; Plasmodium malariae; Splenectomy

Topics: Animals; Biopsy; Disease Models, Animal; Fibrin; Immunoglobulin G; Injections, Intravenous; Kidney; Kidney Glomerulus; Kidney Transplantation; Kidney Tubules; Nephrotic Syndrome; Proteinuria; Puromycin; Rats; Time Factors; Transplantation, Homologous

Topics: Adolescent; Azathioprine; Biopsy; Child; Child, Preschool; Female; Fibrin; Glomerulonephritis; Humans; Immunoglobulin G; Infant; Kidney Glomerulus; Male; Microscopy, Fluorescence; Nephrotic Syndrome; Prednisone; Proteinuria; Purpura; Skin; Syndrome

Topics: Fibrin; Fibrinogen; Glomerulonephritis; Humans; Nephrotic Syndrome

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

We have investigated the formation of fibrin, platelet aggregates, and subendothelial deposits in lipoid nephrosis. Fibrin formation was found in 10 cases of active lipoid nephrosis. Platelet aggregates were found in eight cases and subendothelial deposits in nine. Fibrin and platelets were also found in cases of nephrotic syndrome due to other causes, and in glomerulonephritis. Fibrin was generally absent in lipoid nephrosis in remission and in benign recurrent hematuria. It is suggested that what seems to be a lower incidence in females is more apparent than real and that fibrin or related material may be present in a less easily identifiable form. Steroid therapy apparently had no effect on the presence or absence of fibrin. Most instances were associated with elevated serum cholesterol and alpha(2)-globulin. It is suggested that elevated serum lipids as well as the disease process in the kidney play a role in this phenomenon. It is further suggested that intraglomerular fibrin formation could lead to irreversible renal damage in lipoid nephrosis.

Topics: Adolescent; Adult; Aged; Alpha-Globulins; Biopsy; Blood Platelets; Child; Child, Preschool; Cholesterol; Chronic Disease; Female; Fibrin; Glomerulonephritis; Hematuria; Histocytochemistry; Humans; Kidney Glomerulus; Male; Microscopy, Electron; Middle Aged; Nephrosis, Lipoid; Nephrotic Syndrome; Sex Factors; Steroids

Topics: Adolescent; Adult; Aged; Antigens; Antithrombins; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Child; Child, Preschool; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Hemiplegia; Humans; Immune Sera; Immunodiffusion; Male; Middle Aged; Nephrotic Syndrome; Phlebitis; Pulmonary Artery; Renal Veins; Thrombophlebitis; Thrombosis

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: 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: Animals; Antifibrinolytic Agents; Blood Proteins; Fibrin; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Lipoproteins; Nephrotic Syndrome; Nucleosides; Plasminogen; Proteins; Puromycin; Rats

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