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)

Immunologic mechanisms of proteinuria were investigated in guinea pigs (GP) injected with sheep antiserum (NTS) to GP glomerular basement membrane (GBM). Linear deposition of sheep gamma 1 and gamma 2 IgG led to a prompt but transient (36 hr) increase in albumin excretion from control values of 0.026 +/- 0.013 mg/hr to maximal values of 26+/-12.1 mg/rh at six hours without detectable histologic or electron microscopic changes except for decreased staining for glomerular polyanion and epithelial cell foot process fusion. GBM permeability to anionic ferritin was not increased during proteinuria. Anti-GBM antibody deposits did not fix GP C3 or C4 in vivo or in vitro. NTS-induced proteinuria was the same in guinea pigs that were normal, greater than 95% depleted of C3 through C9, genetically deficient in C4, and depleted of circulating polymorphonuclear leukocytes (PMN). Prior administration of antihistamines, steroids, azathioprine, colchicine, indomethacin, heparin, aprotinin (Trasylol), and niridazole also failed to reduced proteinuria. Initial proteinuria subsided by 36 hr, did not recur despite linear deposition of GP gemma 1 and gemma 2 after day seven, and antibody to GMB-bound sheep globlin. In the GP nephrotoxic nephritis model, anti-GBM antibody deposits apparently mediate increased permeability to albumin by a currently undefined mechanism which is independent of complement, PMN, and other know mediators of inflammation.
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PMID:Complement-independent nephrotoxic nephritis in the guinea pig. 1 57

The central lipid abnormality in essential fatty acid deficiency (EFAD) is the lack of availability of arachidonic acid. To examine the role of total eicosanoid's biosyntheses in the pathology and pathophysiology of glomerulonephritis, EFAD was induced in weanling rats, which were then subjected to antiglomerular basement membrane antibody (NTS)-induced injury in adulthood. Glomerular dynamics (as assessed by micropuncture), quantitative histology, and eicosanoid generation rates were measured at two hours and two weeks post-NTS, and compared to those of standard diet-fed (STD) controls. Two hours post-NTS, and despite the occurrence of proteinuria in both EFAD and STD animals, glomerular dynamics were essentially normal in EFAD rats, whereas STD animals had reduced values for glomerular filtration rate (GFR) and renal plasma flow rate (RPF). At two weeks, severe histologic changes were observed in STD animals including mesangial and stalk hypercellularity, moderate sclerosis, and interstitial nephritis, coupled with heavy proteinuria and reduced GFR and RPF. In dramatic contrast, EFAD rats displayed totally normal glomerular structures and functions. In parallel, glomerular generation rates of prostaglandin E2 and thromboxane A2 were suppressed markedly in EFAD rats. Thus, EFAD confers complete protection against the histopathologic and functional sequelae of immune-initiated injury in the glomerulus. The data suggest that the initial wave of complement-induced neutrophil infiltration (with resultant proteinuria) is not sufficient to perpetuate injury into the more destructive chronic phases. The results provide strong impetus for the design of more specific interventional therapies targeting the various enzymes and products of arachidonic acid metabolism in the attempts to control glomerular inflammation.
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PMID:Essential fatty acid deficiency normalizes function and histology in rat nephrotoxic nephritis. 161 38

Effect of exercise on rats with renal injury was studied. Nephritis was induced in rats by injection of anti-GBM antibody followed by ligation of a branch of the left renal artery after nephrectomy of the right kidney. Moderate daily treadmill exercise was forced on these experimental rats for ten weeks. Sedentary nephritic rats that received the same treatment described above served as controls. The sedentary nephritic rats suffered progressively increasing proteinuria during the time course of the experiment, whereas the nephritic rats with daily treadmill exercise experienced less proteinuria. Mild proteinuria was induced by daily treadmill exercise forced on non-nephritic rats that had received only nephrectomy of the right kidney, but no NTS injection. Light microscopy and immunofluorescence microscopy revealed severe glomerular injury in the sedentary nephritic rats, however, less glomerular injury was seen in nephritic rats with treadmill exercise. Serum cholesterol level was higher in the sedentary rats than in the rats with daily treadmill exercise. The results suggest that daily exercise by nephritic rats will not aggravate renal injury.
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PMID:[Effect of exercise on rats with renal injury]. 163 31

Two types of experimental GN induced by immunological procedures. Heymann-type AIC-GN and NTN, were treated with anticoagulant agents. Dipyridamole, aspirin, ticlopidine or batroxobin was administered either to rats with AIC-GN for 14 to 28 days or to NTN rats 2 days prior to injection with NTS and 14 to 21 days thereafter. A significant decrease in the amount of urinary protein was observed only in rats treated with 12.5 to 50.0 mg/kg dipyridamole daily, whereas no significant decrease in proteinuria was observed in either AIC-GN or NTN rats treated with the other agents. Histopathologically, no improvement in the light and electron microscopic findings was noted in AIC-GN rats treated with these agents, even with dipyridamole. On the other hand, in NTN rats, light and electron microscopic study of the kidneys from rats sacrificed 30 to 60 min after NTS injection revealed that platelet aggregation and inflammatory changes in the glomeruli were remarkable reduced in rats pretreated with 56.4 mg/kg aspirin or 50.0 mg/tg triclopidine daily, but no difference in the renal lesions between rats treated with aspirin or triclopidine and control animals were observed 2 weeks after NTS injection. No histological improvement was observed in rats pretreated with dipyridamole. It would be reasonable to conclude from these results that the favorable effect of dipyridamole on proteinuria is not related to its antiplatelet activity and that platelet aggregation is not essential to the development of renal lesions in rat AIC-GN and NTN. (J Lab Clin Med 99:428, 1982.)
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PMID:Effects of various antiplatelet drugs and defibrinating agent on experimental glomerulonephritis in rats. 646 69

1 The effects of aspirin, prednisolone, and indomethacin on nephrotoxic serum nephritis in rats was studied. The nephritis was induced by a single intravenous injection of nephrotoxic serum (NTS, rabbit anti-serum against the water-soluble renal antigen of the rat). The injection of NTS induced the heterologous phase of proteinuria (within a day after NTS injection) and then the autologous phase (5 to 7 days after NTS injection). The effect of drugs given before the NTS (i.e. prophylactically) or after the NTS (i.e. therapeutically) was investigated. 2 Aspirin, which was given orally at doses of 150 and 250 mg/kg daily from the day before NTS injection, suppressed the development of proteinuria in both the heterologous and the autologous phase, and lowered the serum cholesterol level towards the normal level. Aspirin (250 mg/kg daily, orally) had no significant effect against the established proteinuria in the autologous phase. 3 Prednisolone, which was given orally at doses of 3 and 5 mg/kg daily from the day before NTS injection, elevated the proteinuria in the heterologous phase, while inhibiting the development of proteinuria in the autologous phase. Prednisolone (5 mg/kg daily, orally) was ineffective against established proteinuria in the autologous phase. 5 Indomethacin (3 mg/kg daily, orally) did not exert any significant effect on proteinuria in either the heterologous or the autologous phase.
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PMID:Effects of aspirin, prednisolone and indomethacin on nephrotoxic serum nephritis in the rat. 707 88

The Mer receptor tyrosine kinase is strongly expressed in the glomerulus. We wondered if this molecule might modify immune-mediated glomerular disease through its functions as a receptor for apoptotic cells and immunoregulatory molecule. Mer-knockout (KO) mice showed decreased survival rate and greatly increased proteinuria and serum urea levels compared to wild type (WT) mice by day 3 after injection of NTS. Their glomeruli were hyperplastic and later became necrotic. In the glomerulus of WT mice, a significant increase of Mer expression was observed. Apoptotic bodies were evident in NTS-treated Mer-KO kidneys, but not in normal controls. NTS-treated Mer-KO mice had massive neutrophil infiltration and inflammatory cytokine expression. Mer thus has a critical role in attenuating renal inflammation, both as a receptor for apoptotic cells and as a molecule that downregulates inflammation.
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PMID:A protective role of Mer receptor tyrosine kinase in nephrotoxic serum-induced nephritis. 2044 50