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)

Since platelet factor 4 (PF4), a cationic (pI 7.6) platelet secretory protein, binds avidly to glomerular polyanions both in vitro and in vivo, and is implicated in neutrophil chemotaxis, we studied by indirect immunofluorescence microscopy the presence of PF4 deposits in glomeruli of patients with poststreptococcal nephritis (APSGN). Goat antihuman PF4 serum was used as primary antibody and fluorescein-conjugated IgG fraction of rabbit antigoat IgG as second antibody. Controls consisted of nonimmune goat serum or anti-PF4 serum preabsorbed with human PF4, as primary antibodies. Glomerular deposits of PF4 were demonstrated in renal tissues obtained by biopsy in 14 of 20 patients studied; the deposits were particularly intense in 9 patients. PF4 was bound to the mesangium and to the capillary walls. There was a significant positive correlation between intraglomerular deposits of PF4 and the levels of proteinuria (p = 0.024). These findings provide further evidence for a role of platelets in the pathogenesis of APSGN and suggest that PF4 may contribute to alter the glomerular permeability in this disease.
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PMID:Glomerular localization of platelet factor 4 in streptococcal nephritis. 152 42

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

Forty-seven patients with IgA nephropathy were classified as having mesangial pattern (M: 29 cases) or mesangiocapillary pattern (C: 18 cases) according to an intraglomerular distribution of fibronectin (FN) observed by the immunofluorescence (IF) technique. The relationships between these IF patterns and the clinical pictures, and that between these IF patterns and prognosis of the disease were investigated. Significantly higher diastolic blood pressure, proteinuria, serum creatinine (Cr), total cholesterol and IgA, and lower total protein were noted in C pattern as compared with M pattern. beta-thromboglobulin, fibrinogen (Fib) and platelet factor 4 were found to be significantly higher in C pattern. Platelet aggregation (ADP 1 microM/ml) and FN tended to increase (p less than 0.1) as well. The distribution of FN in the glomeruli was similar to those of IgA and Fib, although perfect agreement was not observed. The picture in which FN might be infiltrated into the endothelial side of the glomerular basement membrane from the mesangium was observed in C pattern by the immunoelectron microscopic study. In the follow-up study, proteinuria showed a tendency to decrease in M pattern. On the other hand no marked change was observed in C pattern. C pattern showed high serum Cr levels throughout the course of the study as compared with M pattern. A significantly greater number of C pattern cases had serum Cr of 2 mg/dl or higher, C pattern showed a significant decrease of 1/Cr over time as compared with M pattern. Higher serum Fib and FN, platelet aggregation (ADP 1 microM/ml), antithrombin III and plasminogen were observed in C pattern as compared with M pattern. These results suggest that an involvement of tissue FN, especially the existence of FN in the capillary loop, may be an aggravating factor of IgA nephropathy, in addition to an augmented platelets-blood coagulation mechanisms. Therefore, it may be possible to evaluate the prognosis of IgA nephropathy by FN deposit patterns.
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PMID:[Studies on the intraglomerular distribution of fibronectin in IgA nephropathy--in relation to clinical pictures and prognosis]. 219 63

Abnormalities of platelet aggregation and coagulation have been reported in insulin dependent diabetes mellitus (IDDM), although there is controversy concerning their relationship to microangiopathy. We have studied platelet function and haemostasis in 55 patients with IDDM, 23 without, 14 with mild (background retinopathy) and 18 with severe (proliferative retinopathy, or background retinopathy plus proteinuria) complications. Studies were done on 2 occasions 8 weeks apart and the results compared with 28 control subjects. There was evidence of increased in vivo platelet aggregation in the diabetic group v controls shown by raised values of beta-thromboglobulin (61 +/- 42, mean +/- SD, v 18 +/- 14 micrograms/ml, p less than 0.001), platelet factor 4 (62 +/- 76 v 14 +/- 11 micrograms/ml, p less than 0.01), and platelet micro-aggregates (20 +/- 16 v 12 +/- 11%, p less than 0.01). There was no significant difference in fibrinogen and fibrinopeptide A levels, nor in 'in vitro' tests of platelet aggregation between the groups. Dilute whole blood clot lysis time was increased in the diabetic group v controls (6.4 +/- 2.6 v 4.8 +/- 0.5 hours, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet aggregation and coagulation factors in insulin dependent diabetics with and without microangiopathy. 295 Dec 19