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)

The effect of indomethacin on protein excretion and on the synthesis of glomerular basement membrane (GBM) was studied during various stages of nephrotoxic nephritis (NTN) in the rat. Daily administration of indomethacin (4 mg/kg) was instituted 1, 6, or 21 days after the induction of NTN with 210, 240, or 268 microgram kidney-fixing antibodies (KFAb). Proteinuria in rats with nephritis induced by 210 microgram KFAb decreased under treatment with indomethacin regardless of the day on which treatment was started but was not affected by indomethacin in rats with clinically more severe nephritis induced with higher doses of KFAb. GBM synthesis was measured in vivo and in vitro by determination of the incorporation of 3H-proline into the GBM. NTN rats treated with indomethacin showed increased GBM synthesis early in the course of NTN, over and above an already increased synthesis. In the later phase of NTN indomethacin treatment did not affect GBM synthesis. The absence of a relationship between the effect of indomethacin on proteinuria and its effect on GBM synthesis clearly shows that the reduction of protein excretion occurring under indomethacin treatment is not mediated by alterations in the rate of GBM synthesis.
Nephron 1977
PMID:Effect of indomethacin on the synthesis of glomerular basement membrane and on proteinuria in rats with nephrotoxic nephritis. 88 86

Rats were injected with various amounts of bovine albumin (0.5, 1.0 and 1.75 g/24h), inducing thereby proteinuria ranging from 100 to 400 mg/24h. The glomerular oxygen uptake, dry weight and glucose-6-phosphate dehydrogenase (G-6-PHD) activity were measured on the 4th day of proteinuria and in a group of control animals. Oxygen uptake increased of +60%, expressed per glomerulus and of +25% when expressed per milligram dry weight and this increase was not different between the 3 groups of rats. Glomerular dry weight increased significantly in the 3 series. There was an highly significant relationship between glomerular dry weight and oxygen uptake, combining the 3 series together. G-6-PDH increased as expected from previous experiments and this increase was more marked for the more marked proteinuria. The relationship between G-6-PDH and QO2 was of borderline statistical significance (p=0.05). The glomerular hypertrophy, oxidative hyperactivity and increase in G-6-PDH activity are probably related to transcellular transport of protein.
Nephron 1977
PMID:Glomerular metabolism in protein-load proteinuria. 91 75

A 62-year-old white male suffering from plasmacytosis with monoclonal gammopathy developed gastrointestinal bleeding, microscopic hematuria, proteinuria and progressive azotemia. A renal biopsy demonstrated capillary wall thickening, mesangial hyperplasia, crescent formation and subepithelial humps. Serum immunoglobulin analysis showed IgG of lambda type. Serum complement, ANA, ASO titer and cryoglobulin were normal. It is suggested that proliferative glomerulonephritis with subepithelial humps should be added to forms of renal pathology that can be seen in plasma cell dyscrasias.
Nephron 1977
PMID:Proliferative glomerulonephritis in monoclonal gammopathy. 91 80

Renal biopsy and clinical data from 60 patients with extracapillary proliferation (crescent formation) in greater than or equal to 50% of glomeruli were correlated. Nephropathy was related to infection (15 cases) malignancy (4 cases) and trichlorethylene exposure (2 cases). Isolated proteinuria was found 0.5-20 years before biopsy in 16 patients. Outcome was significantly related to percentage of crescentic involvement. Oligoanuria and impaired function at presentation were bad prognostic signs but preceding infection was favourable. Diverse histological and immunofluorescent findings indicate that extracapillary glomerulonephritis is not a single entity. The clinical course is not always rapidly progressive.
Nephron 1976
PMID:The significance of extracapillary proliferation. Clinicopathological review of 60 patients. 124 62

Complementuria is a common finding in patients with heavy proteinuria from a variety of causes, and was detected in 23 out of 34 nephrotic subjects. Mean excretion of C3 and C4 in these patients was 49 +/- 22 and 14 +/- 3 mg/24h, respectively. The renal handling of complement appears to be largely molecular weight (MW) dependent, an inverse relationship between the sieving coefficient and MW of transferrin, IgG, C3, and C4 obtaining, in nephrotic patients irrespective of the nature of their glomerulopathy or degree of renal function. Furthermore, glomerular sieving of C3 and C4 was not significantly different in patients with immune glomerular injury associated with extensive glomerular complement deposition, from that in patients with non-immune glomerulopathy, suggesting that no unique mechanism exists for the transglomerular passage of complement from serum into the urine of the former group. The finding of a large increase of sieving of C3 and C4 in nephrotic patients with end-stage renal failure may indicate a failure by atrophic tubules to reabsorb and catabolize filtered complement.
Nephron 1976
PMID:Renal handling of the third (C3) and fourth (C4) components of the complement system in the nephrotic syndrome. 126 8

The human immunodeficiency virus (HIV) was recently suggested to be involved in generating kidney lesions in HIV-associated nephropathy (HIVN). The possibility that antiretroviral agents can slow down the usually explosive evolution of HIVN to end-stage renal failure (ESRF) has not been studied in many of the series of cases published. The present work is a retrospective analysis of 11 patients with histologically proven HIVN, 6 of whom were treated with zidovudine. Seven patients (group 1) either required dialysis at the outset, when HIVN was diagnosed, or progressed very fast to ESRF within 15-45 days. Two patients of this group were treated with zidovudine, but it had no effect on kidney function. In the remaining 4 patients (group 2), HIVN progressed more slowly than in group 1. All 4 patients were treated with zidovudine at an earlier stage of the disease than ESRF. Only 1 deteriorated to ESRF in 9 months. The 3 others, who did not have ESRF, were followed up for 13, 10 and 32 months, respectively. Although this is a preliminary study, its results do suggest that zidovudine can slow down the evolution of HIVN to ESRF. They highlight the need to screen HIV-positive patients regularly for proteinuria, in order to detect HIVN by renal biopsies at an early stage of renal lesion formation.
Nephron 1992
PMID:Nephropathy associated with infection by human immunodeficiency virus: a report on 11 cases including 6 treated with zidovudine. 130 Apr 39

Eicosapentaenoic acid (EPA) can induce a shift in prostaglandin and leukotriene synthesis. The effects of EPA supplementation of the diet on the progression of chronic renal failure (CRF) were evaluated in a model of 5/6 renal mass ablation in rats. After 30 or 60 days of CRF, elevation in single-nephron glomerular filtration rate due to an increase in glomerular plasma flow and hydraulic pressure was observed. These hemodynamic alterations were followed by a rise in proteinuria and glomerular sclerosis. EPA treatment for 30 or 60 days did not substantially modify the hemodynamic or morphological profiles induced by renal mass ablation. In the present non-immune model of CRF, preglomerular vasodilation with glomerular hyperperfusion and hypertension were responsible, at least in part, for the presence of proteinuria and glomerular sclerosis. No additional vasodilation was observed in the present model of CRF, and, thus, hemodynamic effects induced by EPA did not modify renal damage, in contrast to the EPA effects observed in immune-mediated models of CRF.
Nephron 1992
PMID:Effect of eicosapentaenoic acid on the progression of chronic renal failure in rats. 130 Apr 41

Compared to Wistar (WAG) rats, rats of the fawn-hooded (FH) strain have a high level of glomerular filtration rate (GFR) and urinary protein excretion (UpV). To investigate the possible role of vasoactive eicosanoids in this spontaneous model of hyperfiltration and proteinuria, we compared the urinary excretion of thromboxane-B2 (TxB2), 6-keto-prostaglandin (Pg)F1 alpha and PgE2 in male FH and WAG rats during normal ageing. All measurements were performed sequentially in the same animals 12, 24, 36, 48 and 60 weeks after weaning. Throughout the study, GFR was higher in FH rats as were the filtration fraction and UpV. From week 24, UpV in FH rats increased progressively. No elevations in UpV were observed in WAG rats. At weeks 12 and 24, the urinary excretion of TxB2, 6-keto-PgF1 alpha and PgE2 was 2-4 times higher in FH rats compared to WAG rats. With time, a shift in the urinary excretion from vasodilator to vasoconstrictor eicosanoids was observed, i.e., the excretion of PgE2 declined and that of TxB2 increased. Proteinuria in FH rats was positively correlated with TxB2 excretion and negatively correlated with PgE2 excretion. We conclude that in FH rats, early hyperfiltration coincides with enhanced urinary excretion of all eicosanoids. Subsequent progressive proteinuria is associated with an increase in TxB2 and a decrease in PgE2 excretion.
Nephron 1992
PMID:Enhanced urinary excretion of eicosanoids in fawn-hooded rats. 130 Apr 42

In 2 patients with the nephrotic syndrome, unsuspected solid tumors were found. One was a small cell lung carcinoma, accompanied with the syndrome of inappropriate ADH secretion. The other was a cancer of the breast with lymph node and bone metastases. In both, renal biopsy showed minimal change disease without immune complex deposits. There are only 14 other reported cases of paraneoplastic lipoid nephrosis complicating solid tumors. Such cases lead to the discussion on the respective roles of tumor cell gene product(s) inducing proteinuria and of lymphokine secretion by lymphocytes directed against the tumor itself. Cancer should be considered as a possible etiology of the minimal change nephrotic syndrome in the adult.
Nephron 1992
PMID:Minimal change nephrotic syndrome revealing solid tumors. 813 50

The effects of the reduction of neutrophils in glomeruli on the improvement of proteinuria and glomerular injuries were determined in the first (heterologous) phase of Masugi (nephrotoxic) nephritis. Male (6-week-old) WKA/Hkm rats were initially injected with 2.0 ml of a newly developed monoclonal antineutrophil antibody and then injected with 1.0 ml of nephrotoxins. This monoclonal anti-neutrophil antibody was found to have selectively reduced the number of neutrophils in the glomerular capillary lumen in cases of Masugi nephritis by light microscopy. Malondialdehyde (MDA) levels or superoxide dismutase (SOD) activities in renal tissues of such rats were also examined. However, there were no significant differences in the levels of proteinuria and the number of glomerular cells containing resident cells and infiltrated mononuclear cells in the first phase of Masugi nephritis with or without pretreatment with antineutrophil antibody. No significant differences were observed in the levels of MDA or SOD activities in renal tissues of Masugi nephritis with or without pretreatment with such an antibody either. It appeared that infiltration of neutrophils in the glomeruli might not be related to proteinuria and glomerular injuries in the first phase of Masugi nephritis. It was postulated that the massive proteinuria in the first phase of Masugi nephritis might be correlated with the activities of reactive oxygen species induced by the glomerular cells, i.e. glomerular resident cells and infiltrated mononuclear cells.
Nephron 1992
PMID:Correlation between reduction of polymorphonuclear leucocytes in glomeruli injected with a newly developed monoclonal antineutrophil antibody and proteinuria in Masugi nephritis. 133 43


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