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)

Spontaneously hypertensive rats (SHR) were injected with streptozotocin (STZ-SHR) to induce diabetes. The effect of DP-1904, a thromboxane A2 synthetase inhibitor, on diabetic nephropathy was then studied by administering it for 5 months (1 or 10 mg/kg). DP-1904 did not affect renal 6-keto prostaglandin (PG)F1 alpha production in STZ-SHR, but markedly inhibited renal thromboxane (TX) B2 production, so that the 6-keto PGF1 alpha/TXB2 ratio was significantly increased (P less than 0.05). STZ-SHR showed significant uraemia and proteinuria, plus increases in urinary gamma-glutamyl-transpeptidase and urinary N-acetyl-beta-glucosaminidase. DP-1904 significantly decreased (P less than 0.01) the urinary changes. STZ-SHR also showed an increase in mesangial periodic acid-Schiff-positive substance and in relative renal weight, both of which were significantly inhibited by DP-1904 (P less than 0.05). Thus, DP-1904 inhibited both TXB2 production and the progression of renal damage in STZ-SHR.
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PMID:A thromboxane A2 synthetase inhibitor retards hypertensive rat diabetic nephropathy. 135 Sep 91

Previous metabolic studies in rats have suggested in vivo formation of the acrolein-glutathione (acrolein-GSH) adduct following administration of the highly reactive alpha, beta-unsaturated aldehyde acrolein. Early studies by several investigators demonstrated that similar compounds such as alpha, beta-unsaturated aldehyde-cysteine adducts have toxic (carcinostatic) activity against Ehrlich ascites tumor cells implanted in mice. The current studies investigated the in vivo toxicity associated with the acrolein-GSH adduct in the male Sprague-Dawley rat. The 1:1 acrolein-GSH adduct was synthesized and characterized by physical-chemical methods. Rats given the acrolein-GSH adduct intravenously at 0.5 or 1 mmol/kg developed nephrotoxicity characterized by glucosuria, proteinuria, elevation in serum urea nitrogen, and gross and histologic changes of the kidney. The toxicity was not affected by pretreatment of rats with pyrazole, an alcohol dehydrogenase inhibitor; disulfiram, an inhibitor of aldehyde dehydrogenases; or probenecid, a renal organic anion transport inhibitor. Administration of a similar but nonaldehydic glutathione conjugate, S-n-propylglutathione, did not result in nephrotoxicity in the rat. The nephrotoxicity induced by the acrolein-GSH adduct was inhibited by acivicin, a gamma-glutamyl-transpeptidase inhibitor. These results indicate that the acrolein-GSH adduct requires processing through the first step of the renal mercapturic acid synthesis pathway to be activated to a toxic species.
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PMID:Nephrotoxicity of the 1:1 acrolein-glutathione adduct in the rat. 147 Nov 52

The brush border of the proximal tubule of human kidney consists of peripheral, integral as well as of transmembranous antigens. Peripheral (surface) antigens are associated with the presence of 5-7 nm globular particles sensitive to limited proteolysis; particles were found to contain a multienzyme complex and exhibited strong affinity towards ConA and WGA. PM-antigens can be solubilized from different portions of PM by differential treatment with proteases and detergents. Labelled antisera against isolated surface glycoproteins reveal a specific reaction with luminal PM of the proximal tubule only, supporting their value for quantitative image analysis (histometry) of kidney tissue sections and for screening of tissue-proteinuria. PM were capable of binding cationic serumproteins (esp. immunoglobulin) and certain O/K-antigens from E.coli, where adhesion was observed on peripheral and intrinsic PM-antigens as well. Major markers of the distal tubule are Tamm-Horsfall protein (cytoplasmic compartment) and a PNA-binding glycoprotein originating from the luminal PM. PM from renal adenocarcinoma exhibit not the globular surface structure found in renal PM, show low immunogenicity, a modulation in the glycosylation pattern of the marker gamma-Glu-transpeptidase and are characterized by a marked depletion of normally differentiated renal antigens. Due to solubilization experiments the presence of cryptic antigens are likely. In addition common determinants between cancer antigens and distinct proteins of the distal tubule and placental trophoblast became apparent.
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PMID:[Characterization of membrane antigens from human kidney and renal adenocarcinoma]. 639 70

Rats were injected intraperitoneally with saline or fumonisin B1 (FB1) at doses of 7.5 and 10.0 mg FB1/kg for 4 days. For each day of dosing, 24-hr urine samples were collected and analyzed for creatinine and protein content and the enzymes gamma-glutamyl-transpeptidase, lactate dehydrogenase, and N-acetyl-beta-D-glucosaminidase. Twenty-four hours after the last dose, animals were killed and kidneys removed for ion transport measurement and histopathology. Significant increases in urine volume and decreases in urine osmolality were observed in both FB1 dose groups. Creatinine excretion was decreased only in the 10 mg FB1/kg group on the final day of the study. Urine protein excretion was elevated in both treated groups and found to be due primarily to high-molecular-weight proteins indicative of increased glomerular permeability. Enzymuria, a marker of tubular cell damage, was also observed with increases in the urinary excretion of all three enzymes measured. In renal cortical slices tubular transport of the anion p-aminohippuric acid was reduced by 75-80% and cationic transport of tetraethylammonium was reduced by 40% in the FB1-treated animals. While these results suggest significant alterations in renal function, only minor histopathologic changes were observed in the kidneys of both dose groups. Results of the present study indicate that urine volume, proteinuria, enzymuria, and ion transport are sensitive indicators of early FB1-induced nephrotoxicity.
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PMID:The effects of fumonisin B1 on several markers of nephrotoxicity in rats. 764 15

Ten patients, mean age 51.50 +/- 3.03 years, with degenerative rheumatism on NSAID treatment without any sign of renal disease, and 11 control subjects, mean age 43.50 +/- 1.51 years, were studied. NSAID treatment was of 11.30 +/- 5.60 weeks duration in average, with ibuprofen, naproxen, or indomethacin. Urinary excretion of three specific renal tubular enzymes--AAP: alanine-amino-peptidase, GGT: gamma-glutamyl-transpeptidase, and beta-NAG: beta-N-acetyl-glucosaminidase, were determined in 8-h overnight urine samples, as well as GFR creatinine clearance/1.73 m2, urinary volume/8 h, specific gravity of the urine, proteinuria and glucosuria. In the group treated with NSAIDs, urinary excretion of the enzymes was significantly higher than in the control group--AAP: 1414.20 +/- 317.60, 864.20 +/- 94.42, p < 0.00001; GGT: 8034.6 +/- 1378.55, 5095.64 +/- 614.40, p < 0.00001, and beta-NAG: 1644.60 +/- 299.97, 964.82 +/- 142.00, p < 0.00001. Patients on NSAID treatment showed abnormal urinary excretion of AAP in 7/10 cases, of GGT in 6/10, and of beta-NAG in 7/10 cases. Duration of the treatment did not correlate with the urinary excretion of the enzymes. Age was in correlation with the urinary excretion of the enzymes only in the control group, r = 0.52, p < 0.005 for AAP, r = -0.43, p < 0.02 for GGT, and r = -0.23, p < 0.05 for beta-NAG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of three specific renal tubular enzymes in patients treated with nonsteroidal anti-inflammatory drugs (NSAID). 809 99

The authors investigated renal damage in 46 chlorine-alkaly plant workers (mean age was 38.8 +/- 5.7 years) under conditions of continued occupational exposure to metallic mercury vapour. The mercury unexposed control group consisted of 32 workers who works in the plant area. Significantly low of serum globulin level was found in exposed evaluated group compared with control subjects (P < 0.001). The serum globulin level was in correlation with urine mercury level (P < 0.001). Analyses of urine chemistry indicated that exposed workers had cell death produces in sediment urine as the most common signs (P < 0.001). The proteinuria was found in 4 out 32 and high level of gamma-glutamyl-transpeptidase in 8 out 32 exposed workers to high mercury level workers. Additionally, disuria and ejaculatory pain as symptoms occurred without evidence of urological disease. Mercury induced nephropathy usually associated with proteinuria, but is not with renal insufficiency.
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PMID:[Chronic occupational mercury exposure in renal damage in workers in the chlorine-alkali electrolysis industry]. 1452 21