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 possible tubulotoxicity of drugs can be judged with the help of the excretion of tubular membrane proteins in the urine. The brush border of the proximal tubular epithelia which react particularly sensitive to toxic influences contains surface antigens which easily release themselves from the membrane core membrane under pathological conditions and become provable in the urine by means of biochemical and immunological methods as signs of an early structural cell damage. Apart from these soluble membrane proteins which above all correspond to enzymes such as alanine aminopeptidase and gamma-glutamyl transpeptidase in severe lesions high molecular brush border fragments transformed to vesicles can appear. The clinical relevance of a pathological tissue proteinuria (histuria) of proteins of renal membranes is among others explained at the instance of the renal effects of cytostatics, antibiotics and x-ray contrast medias.
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PMID:[Assessment of drug nephrotoxicity by the excretion of tubule-specific membrane antigens and enzymes]. 614 70

Chronic mercuric chloride intoxication in an aged horse given 0.8 mg Hg/kg/day for 14 weeks was manifest by signs of progressive respiratory difficulty and renal disease. The effects were not self-limiting after mercury was withdrawn, and the animal was destroyed six weeks later. Renal function changes included heavy glycosuria, modest proteinuria, phosphaturia, reduced urine osmolality, gradually increasing urine production, reduced glomerular filtration rate, and terminally, azotemia. The condition bore similarities to the Fanconi syndrome in man. Urinary gamma-glutamyl transpeptidase, alkaline phosphatase and amino-aspartate transferase activities were inconsistent indicators of tubular damage in random samples at this dose rate. The pathologic response was characterized by extensive granulomatous infiltration throughout the lungs, in particular, and to a lesser extent in the kidneys, liver and bone marrow. The renal changes included this marked interstitial reaction and proximal tubular degeneration. Mercury levels were negligible in the lungs and highest in the renal cortex. The granulomatous reaction was not encountered in previous mercury toxicity studies in horses and may indicate an individual sensitivity to the agent.
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PMID:Some effects of chronic mercuric chloride intoxication on renal function in a horse. 621 26

The effect of puberty on aspirin-induced renal necrosis in female Sprague-Dawley rats was observed. Rats aged 31 days were unaffected by aspirin administration, but 55-day-old rats showed segmental cortical tubular necrosis after a single dose of 1000 mg/kg of aspirin. Urinary gamma-glutamyl transpeptidase (gamma-GT) and proteinuria were useful non-invasive indicators of these necrotic changes.
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PMID:Age-related susceptibility to aspirin-induced nephrotoxicity in female rats. 662 43

Cysteinyl leukotrienes (LT) play an important role in the development of experimental glomerulonephritis (GN). We have partially purified and characterized LTC4 synthase, the enzyme responsible for cysteinyl LT formation, from rat renal microsomes and have investigated this enzyme activity in nephritic rats. LTC4 formation, measured in vitro, was linear for > 10 min at 25 degrees C in the presence of 50 mM serine borate (an inhibitor of gamma-glutamyl transpeptidase), with Km values for LTA4 and GSH of 56 microM and 8.5 mM, respectively. Detergent solubilization and anion-exchange chromatography of microsomal proteins resulted in a 7-fold increase in enzyme specific activity. Enzymatic and immunoblot analysis demonstrated that cytosolic and microsomal glutathione S-transferase (GST) activities were distinct from LTC4 synthase activity. Comparison of LTC4 synthase activity in nephritic rats over 21 days revealed an initial increase over the first 24 h following injection of nephrotoxic sera, followed by a subsequent decline until day 7 and a gradual recovery by day 21. Inhibition of LT biosynthesis with MK-0591 (10 mg kg-1 d-1) reduced GN-associated proteinuria by 72% (P < 0.05). These results suggest a potential mechanism for enhanced cysteinyl LT formation in the development of experimental GN and further support their causal role in the etiology of this disease.
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PMID:Renal leukotriene C4 synthase: characterization, partial purification and alterations in experimental glomerulonephritis. 782 26

Urinary enzymes N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transpeptidase (gamma-GT) are sensitive markers of specific renal cell damage. Excessive urinary amino acid excretion may also be an indicator of renal tubular damage. We have evaluated urinary excretion of NAG, gamma-GT and 37 amino acids, phospholipids and dipeptides in 30 children (aged 2.3-18.1 years) with nephrotic syndrome (NS), 23 with minimal change nephrotic syndrome (MCNS), 7 with focal segmental glomerulosclerosis (FSGS) and 16 healthy age-matched controls. Nine MCNS patients were in relapse and 14 in remission. Enzyme activity is expressed as micromoles per milligram urinary creatinine. In FSGS, NAG excretion correlated with the following: blood urea nitrogen (BUN) (r = 0.8), serum protein (r = 0.57), serum cholesterol (r = 0.85), serum albumin (r = -0.68) and proteinuria (r = 0.56). In FSGS the gamma-GT excretion was not significantly different from MCNS in remission or in relapse. In FSGS, gamma-GT excretion correlated with the following: BUN (r = 0.48), serum creatinine (r = -0.66), serum protein (r = -0.54), serum albumin (r = -0.68) and serum cholesterol (r = 0.87). Compared with controls, the urinary excretion of 5 amino acids was increased in FSGS patients as a possible indicator of tubular damage. The value for 7 amino acids was reduced in MCNS patients. Urinary amino acid excretion was not different from controls for the other amino acids in either FSGS or MCNS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The differential diagnostic value of urinary enzyme and amino acid excretion in children with nephrotic syndrome. 791 41

2-Br-(diglutathion-S-yl)hydroquinone (2-Br-(diGSyl)HQ) is a potent nephrotoxicant, causing glucosuria, enzymuria, proteinuria, elevations in blood urea nitrogen, and severe histological alterations to renal proximal tubules at doses of 10-15 mumol/kg. In contrast, 2-Br-3-(glutathion-S-yl)hydroquinone (2-Br-3-(GSyl)HQ) is substantially less nephrotoxic than 2-Br-(diGSyl)HQ and requires a dose of at least 50 mumol/kg to cause modest elevations in blood urea nitrogen concentrations. The reason or reasons for this difference in potency is unclear, but since inhibition of renal gamma-glutamyl transpeptidase (gamma-GT) prevents 2-Br-(diGSyl)HQ-mediated nephrotoxicity, metabolism of these conjugates by the kidney must play an important role. To address this question we have compared the metabolism and toxicity of 2-Br-(diGSyl)HQ and 2-Br-3-(GSyl)HQ in the in situ perfused rat kidney (ISPRK). Following infusion of 20 mumol 2-Br-3-(GSyl)HQ into the right renal artery of male Sprague Dawley rats, a total of 23.5 +/- 1.9% (mean +/- SE) of the dose was accounted for in urine and bile over a period of 180 min. 2-Bromo-3-(cystein-S-yl)hydroquinone and 2-bromo-3-(N-acetylcystein-S-yl)hydroquinone were identified in urine, and unchanged 2-Br-3-(GSyl)HQ was identified in urine and bile. The product arising from the oxidative cyclization of 2-bromo-3-(cystein-S-glycine)hydroquinone, 2H-(3-glycine)-7-hydroxy-8-bromo-1,4-benzothiazine, was also identified in urine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolism and toxicity of 2-bromo-(diglutathion-S-yl)-hydroquinone and 2-bromo-3-(glutathion-S-yl)hydroquinone in the in situ perfused rat kidney. 795 22

Proteinuria, and renal tubular casts and epithelial cells in urine sediment, are commonly observed in both complicated and uncomplicated babesiosis, but do not necessarily reflect or predict renal failure. This study investigated the presence and degree of renal damage in canine babesiosis. Renal function and integrity were evaluated using serum urea and creatinine, serum electrolytes (sodium and potassium), fractional clearance of sodium (FcNa) and potassium (FcK), urine enzyme activity of gamma-glutamyl transpeptidase and alkaline phosphatase, urine protein:creatinine ratio, and urinalysis. One control group (n = 10) and 3 groups of babesiosis cases were studied: mild uncomplicated (n = 10), severe uncomplicated (n = 11), and complicated (n = 9). All babesiosis groups showed well-concentrated urine. Mean serum urea was elevated in the severe and complicated groups, and was significantly different from the control group. There was no statistically significant difference between the groups for creatinine, although the complicated group had a mean value above the normal reference range. Hypokalaemia was uncommon in all the groups. Hyperkalaemia was present in only 2 dogs in the complicated group. Marginal hyponatraemia was present in a minority of dogs in all groups. The serum electrolytes were not significantly different between groups. There was no overall elevation, nor any statistically significant difference in both the FcNa and FcK between the groups. Only 1 dog, in the complicated group, showed marked enzymuria. Proteinuria was a common finding and was significantly different between the severe and complicated groups and the control group. Some dogs in all groups had renal tubular epithelial cells in the urinary sediment, which increased in severity from the mild to the complicated groups and was significantly different from the control group. This study demonstrated that minimal renal damage occurs more often in canine babesiosis than significant damage or acute renal failure.
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PMID:Renal involvement in dogs with babesiosis. 1156 13

It was shown that development of the Guerin carcinoma and introduction of cisplatin led to the damage of the kidneys of rats that was confirmed by a relative increase of weight, proteinuria, change of gamma-glutamyl transpeptidase and lactate dehydrogenase activity in the urea and tissue homogenates of the kidneys, by a decrease of relative reabsorption and glomerular filtration. Introduction of nanoliposomal forms of the rhenium cluster compounds led to normalization of above mentioned diagnostic indexes and to reduction of the toxic cisplatin influence that was confirmed by biochemical and morphological investigations.
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PMID:[Changes of the state of rat kidneys under guerin carcinoma development and use of cytostatics]. 2286 Apr 3

Karyomegalic interstitial nephritis is a rare cause of hereditary chronic interstitial nephritis, described for the first time over 40 years ago.A 36-year-old woman, of Turkish origin, presented with chronic kidney disease and high blood pressure. She had a history of recurrent upper respiratory tract infections but no familial history of nephropathy. Physical examination was unremarkable. Laboratory tests showed serum creatinine at 2.3 mg/dL with an estimated glomerular filtration rate of 26 mL/min/1.73m, and gamma-glutamyl transpeptidase and alkaline phosphatase at 3 and 1.5 times the upper normal limit. Urinalysis showed 0.8 g/day of nonselective proteinuria, microscopic hematuria, and aseptic leukocyturia. Immunological tests and tests for human immunodeficiency and hepatitis B and C viruses were negative. Complement level and serum proteins electrophoresis were normal. Analysis of the renal biopsy showed severe interstitial fibrosis and tubular atrophy. Numerous tubular cells had nuclear enlargement with irregular outlines, hyperchromatic aspect, and prominent nucleoli. These findings were highly suggestive of karyomegalic interstitial nephritis, which was further confirmed by exome sequencing of FAN1 gene showing an identified homozygous frameshift mutation due to a one-base-pair deletion in exon 12 (c.2616delA).The present case illustrates a rare but severe cause of hereditary interstitial nephritis, sometimes accompanied by subtle extrarenal manifestations. Identification of mutations in FAN1 gene underscores recent insights linking inadequate DNA repair and susceptibility to chronic kidney disease.
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PMID:Karyomegalic Interstitial Nephritis: A Case Report and Review of the Literature. 2719 44


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