Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is described in which a patient developed TT prolongation and bleeding during CMV hepatitis following successful renal transplantation. Bence-Jones proteinuria was noted, but there was no other evidence of myeloma. Bence-Jones proteinuria, TT prolongation, and bleeding abated as hepatitis resolved. In vitro, a protein isolated from the patient's urine was capable of prolonging the TT markedly, but it did not impair thrombin esterase activity. The effect of the protein seemed to be inhibition of fibrin polymerization. Sephadex gel filtration revealed a single TT-prolonging peak at 11,000 daltons, containing kappa, lambda, and delta antigens. By radioimmunoassay, virtually all the protein present reacted as beta2-microglobulin. Incubation with anti-beta2-microglobulin antiserum markedly attenuated anticoagulant activity. The paraprotein observed transiently in this patient's urine during hepatitis had potent anticoagulant activity and may well have accounted for his abnormal TT and bleeding diathesis; this paraprotein was not distinguishable from beta2-microglobulin.
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PMID:Impaired fibrin polymerization in viral hepatitis. Report of a case: probable identity of the inhibitor with beta2-microglobulin. 21 57

32 patients with different histologically proven forms of glomerulonephritis were treated with heparin for an average of 31 days. A dosage of heparin was chosen, which allowed an increase in thrombin time to 20-40 seconds. Histological findings alone do not allow any prediction concerning the therapeutic success of heparin treatment in glomerulonephritis. According to our results and comparable information given in the literature, the following therapeutic scheme can be recommended: Best results are seen in patients with a slow decrease of GFR (i.e. less than 30 ml/min) during the year preceding the beginning of the treatment. In rapid progredient glomerulonephritis, however, as in patients without any changes of GFR during this time, predictions as to the course of illness cannot be made. A high level of fibrin split products in serum may be expected to be the most valuable sign of therapeutic effect, as could be documented in 7 out of 8 successfully treated patients. Hypertension and proteinuria were not influenced by the treatment. Because of severe side effects the heparin treatment of glomerulonephritis should not be initiated in patients with severe hypertension.
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PMID:[Treatment of glomerulonephritis with heparin (author's transl)]. 87 75

The association of thrombocytopenia, macrothrombocytopathia, nephritis and deafness is rare. Reported here is a new case of this triple association. The clinical course, the nephropathologic findings and the bilateral neurologic hearing loss were similar to those already reported, with a slowly progressive impairment of renal function accompanied by a persistent proteinuria. The platelet diameters were increased. These macroplatelets contained granules of normal structure but with an irregular distribution in the cytoplasm. In other areas the cytoplasm was rich in surface connected system. The survival of these platelets and their contraction were normal. Their aggregation and excretion in response to collagen, adenosine diphosphate and thrombin, and the values of platelet factor 3 activity were all decreased. The degranulation defect, also present, was observed in the absence of a decrease in intracellular cyclic adenosine 5'-monophosphate (AMP) suggesting a relationship between these two findings.
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PMID:Thrombocytopenia, macrothrombocytopathia, nephritis and deafness. 94 91

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

Thromboses and disorders of hemostasis in nephrotic syndrome. Thromboembolic complications are common in nephrotic syndrome (NS). This article reviews the factors of thrombogenesis in NS, including: 1) a hypercoagulable state with platelet hyperaggregability, hyperfibrinogenemia and elevated factor VIII, decrease in plasma levels of coagulation inhibitors antithrombin III and free protein S, reduced fibrinolytic activity; 2) excessive intravascular thrombin formation marked by increased plasma levels of fibrinopeptide A. The intensity of hemostasis disorders coincides with that of NS. Most disorders are related to hypoalbuminemia and proteinuria. In agreement with experimental data, the role of intraglomerular activation of coagulation during active phases of glomerulopathies has to be considered. This could explain the predominance of renal vein thrombosis in several glomerulopathies with NS. Several coagulation disorders in SN have implications for therapy.
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PMID:[Thrombosis and disorders of hemostasis in nephrotic syndrome]. 140 55

We studied the relationship between vascular complications and coagulation and fibrinolysis parameters in 75 subjects with collagen diseases. Thirty normal healthy persons served as controls. We found that patients with collagen diseases were in a state of a hypercoagulation and hyperfibrinolysis. In SLE (systemic lupus erythematosus) in particular, coagulation and fibrinolysis parameters appeared to be indices of vascular complications. Increases in the levels of thrombin-antithrombin III complex (TAT) and alpha 2-plasmin inhibitor-plasmin (PIP) were particularly associated with proteinuria, while increases in fibrinopeptide A (FPA) levels were associated with Raynaud's phenomenon. Administration of glucocorticoid seemed to improve the hypercoagulation and hyperfibrinolytic states of patients with collagen diseases. Analysis of the multimeric structure of von Willebrand factor (vWF) revealed a tendency for large and intermediate multimers (LIM) of plasma vWF to increase in SLE patients with accompanying vascular complications, whereas such increases were not observed in SLE patients without any vascular complications. Therefore, analysis of the multimeric structure of vWF appeared to be a useful indicator of vascular complications in collagen diseases.
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PMID:Plasma coagulation and fibrinolysis parameters in patients with collagen diseases, and analysis of the multimeric structure of von Willebrand factor (vWF). 175 53

A 13-year-old boy was admitted to this hospital for evaluation of pitting edema of both legs. Three years ago, he had been diagnosed to have nephrotic syndrome. Two and half years ago, because of persistent heavy proteinuria, poor response to steroids and frequent relapse of disease, a renal biopsy was done; characteristics of IgM nephropathy was shown. About a year previously, the patient felt dizziness and weakness of the left side of his body upon awakening one morning. Neurologic examination showed loss of muscle tone, muscle power and deep tendon reflexes. Sensory and cranial nerve function were intact. Blood pressure was normal. The CT scan of brain showed a patch of low attenuation area in the right temporal region, obliteration of the right cortical sulci and mild compression of right lateral ventricle. A diagnosis of nephrotic syndrome with right cerebral infarction was made. The patient's condition became stable two days later after mannitol infusion, correction of electrolytes, and supportive therapy. According to literature, most cases of nephrotic syndrome complicate with renal thrombosis, pulmonary emboli, and deep vein thrombosis. Few cases complicate with cerebral thrombosis and infarction. If patient have low plasma albumin and anti-thrombin III level, hyperfunction of platelet aggregability and use long-term diuretic therapy, they may be at higher risk of thromboembolic complications. If thromboembolic complications exist, anticoagulation treatment should be instituted. Prophylactic therapy with aspirin or dicumarol is not currently recommended.
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PMID:[Nephrotic syndrome complicated with cerebral infarction: report of one case]. 182 17

Plasma concentration of fibrinogen (Fbg), plasminogen (PLG), antithrombin III (AT III), alpha 2-plasmin inhibitor (alpha 2-PI), thrombin antithrombin III complex (TAT) and plasmin alpha 2-plasmin inhibitor complex (PIC) were evaluated in 23 nephrotic patients with proteinuria more than 3.5 g/day, including 4 cases with clinical evidence of thromboembolism. Among patients without thromboembolism, concentration of PLG and AT III was in the normal range but that of Fbg and alpha 2-PI was significantly elevated (p less than 0.01 for Fbg and p less than 0.001 for alpha 2-PI respectively). Also there was a positive relationship between AT III and serum albumin (p less than 0.05). Two fifth of these patients had an had an increased level of TAT, and also had a higher level of PIC compared with normal control (p less than 0.01). There was a positive relationship between TAT and PIC, TAT and Fbg (p less than 0.05), PIC and Fbg (p less than 0.01). TAT and PIC levels were markedly elevated in the patients with thromboembolism. From aforementioned data, it was suggested that patients with nephrotic syndrome would be in the prethrombotic state and the increased level of Fbg is one of the major risk factors of thromboembolic complications in these patients. Furthermore measurement of TAT and PIC are the useful means for the diagnosis of these complications.
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PMID:[Concentration of thrombin antithrombin III complex and plasmin alpha 2-plasmin inhibitor complex in nephrotic syndrome]. 183 41

We made serial measurements of the platelet intracellular free calcium concentration in 167 patients with non-insulin-dependent diabetes mellitus (77 males and 90 females) over a two-year period, and investigated the relationship between this parameter and diabetic angiopathy. We measured both the basal and thrombin-stimulated platelet free calcium concentrations using fura-2/AM as a fluorescent indicator. The patients were grouped according to the severity of nephropathy, retinopathy, and hypertension and their hemoglobin A1c levels. The basal platelet calcium level of the diabetic patients was higher than that of a healthy control group. There were high levels in the patients with mild nephropathy and retinopathy, but low levels in those with severe disease, and the platelet calcium level reflected the degree of progression of diabetic angiopathy. Stimulated platelet calcium varied with the progression of nephropathy, being highest in early nephropathy and lowest after proteinuria developed. Our findings suggested that abnormalities of calcium handling may be related to the onset of diabetic vascular complications, especially diabetic nephropathy.
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PMID:Platelet free Ca2+ concentration in non-insulin-dependent diabetes mellitus. 184 17

Nephrotic syndrome (NS) is associated with several disorders of hemostasis: thrombocytosis and platelet hyperaggregability; increased plasma levels of factors V and VIII, and of fibrinogen with blood hyperviscosity; decreased plasma levels of natural anticoagulants: free protein S, and antithrombin III compensated by increased levels of alpha 2-macroglobulin; lowered fibrinolytic activity. Intensity of hypercoagulability is related to the degree of hypoalbuminemia; however, the role of hypercoagulability in the increased incidence of thromboembolic events, including renal vein thrombosis, is not proved. Clotting disorders are due to urinary losses of anticoagulants or to increased liver synthesis of procoagulants stimulated by hypoalbuminemia. Moreover, changes in clotting factors levels may be due to intravascular thrombin formation (marked by increased plasma levels of fibrinopeptide A). During active phases of glomerulonephritides (GN) with NS, thrombin formation might in fact arise in glomeruli, following activation of the glomerular hemostasis system. Isolated glomeruli from human crescentic GN, rabbit nephrotoxic GN and rat HgCl2 autoimmune GN produce excessive amounts of procoagulant (tissue factor) activity (PCA). Sequential studies of the self-limited HgCl2 GN showed that glomerular PCA, proteinuria and glomerular fibrin deposits peaked concomitantly at the acme of the disease, suggesting that immunologically mediated glomerular damage had triggered the extrinsic coagulation pathway.
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PMID:Coagulation factors in nephrotic syndrome. 225 77


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