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)

Amylase/creatinine clearance ratio (CAm/CCr), urinary protein concentration and urinary protein pattern were studied in 102 samples from 27 patients with acute pancreatitis and in 46 controls. Raised CAm/CCr, proteinuria and a tubular protein pattern were present in 74, 56 and 96% of the patients, respectively. However, CAm/CCr and proteinuria and CAm/CCr and tubular protein pattern were not correlated. These results do not support the suggestion that an elevated CAm/CCr in acute pancreatitis is due to generalized tubular protein reabsorption failure presenting with tubular proteinuria.
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PMID:Amylase/creatinine clearance ratio and tubular proteinuria in acute pancreatitis. 9 20

Creatinine, total protein, albumin and beta2-microglobulin were measured in the urine of fifteen healthy women before and after strenuous short-term exercise. The heavy intermittent load produced an increased urinary excretion of total protein, albumin and beta2-microglobulin, while creatinine was unaffected. The renal clearance of albumin and beta2-microglobulin showed very high values after stopping the exercise. However, 45 min after the end of exercise, total protein returned to initial values while albumin and beta2-microglobulin remained high. The urinary ratio between beta2-microglobulin and albumin is higher in urine collected after exercise than in normal proteinuria. This implies that post-exercise proteinuria is of glomerular and tubular origin.
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PMID:Renal glomerular and tubular impairment during strenuous exercise in young women. 9 13

The proteinuria rate and the relative clearances of beta 2-microglobulin, orosomucoid, albumin, transferrin and IgG were measured in forty-two workers exposed to cadmium and in seventy-seven control workers. A tubular type proteinuria with an increased excretion of beta 2-microglobulin and often also a glomerular type proteinuria with an increased excretion of orosomucoid, albumin, transferrin and IgG were observed mainly in workers exposed to cadmium for more than 25 years and whose cadmium concentration in blood exceeded 1 microgram Cd/100 ml and that in urine 10 microgram Cd/g creatinine. The glomerular dysfunction was also suggested by an increased plasma level of beta 2-microglobulin and creatinine. Both tubular and glomerular impairments occurred with the same prevalence and were not necessarily associated. The increased release of beta-galactosidase by the kidney suggested that cadmium can damage some epithelial cells.
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PMID:Renal excretion of proteins and enzymes in workers exposed to cadmium. 11 May 96

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.
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PMID:Effects of dietary cadmium on rhesus monkeys. 11 86

Twenty-two cancer patients were treated with streptozotocin (SZN) in six weekly intravenous doses of 1.0-1.5 g/m2. The results of the initial courses of therapy include 3 complete and 2 partial responses, 11 patients with no change, 4 with progression, and 2 deaths due to tumor progression. Three additional deaths also due to tumor progression occurred in previously responding patients. All responses were in patients with pancreatic tumor. Toxicity consisted of transient proteinuria in 11/15 patients, transient azotemia in 11/18 patients, marked reduction of creatinine clearance in 1 patient, burning pain at site of injection, nausea, and vomiting in 20/22 patients, change of FBS from pretherapy to post-therapy of at least 10 mg/100 ml in 11/17 patients, significantly decreased platelet count in 1/22 patients, decreased Hgb in 2/22 patients, and duodenal ulcer in 2/22 patients. A reduced dosage schedule and combination with other drugs known to be effective in pancreatic tumors deserves further investigations.
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PMID:Streptozotocin therapy in 22 cancer patients. 12 12

Antibody-dependent cell-mediated cytotoxicity (ADCMC) was studied retrospectively in 20 long-term (1.3-11 years) renal allograft recipients. The serum of all seven patients having persistent proteinuria greater than 1 g/24 hr exhibited positive ADCMC activity to donor lymphocytes. All 11 patients having a negative ADCMC test had normal levels of urinary protein (mean + 0.28 +/- 0.06 (SE) g/24 hr). Two patients had a positive ADCMC test but had normal urinary proteins and no evidence of chronic rejection. In the ADCMC positive group, the mean serum creatinine values were significantly higher and the mean creatinine clearance values were significantly lower than in the ADCMC negative group. There was no significant positive correlation between the presence of ADCMC and the number of HL-A mismatches identified or the response to donor lymphocytes in mixed lymphocyte culture tests in the two groups. Two patients had transplant nephrectomy and histologically showed both glomerular and arterial lesions of chronic rejection. Post-transplant ADCMC activity showed a significant correlation with proteinuria, decreased creatinine clearance, and elevated serum creatinine, and suggests that the chronic rejection syndrome may be related to ADCMC activity in the recipient.
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PMID:Antibody-dependent cellular cytotoxicity and chronic renal allograft rejection. 13 84

A prospective study was carried out in 25 patients following visceral angiography using, on average, 3.5 (2.3 to 4.3) ml/kg. of sodium methyl glucamine diatrizoate 76%. No significant changes were found in the liver enzymes (SGTP, LDH and alkaline phosphatase). On the other hand, there was a significant but temporary rise of serum creatinine from 0.9 +/- 0.2 mg% to 1.2 +/- 0.3 mg% as well as transient proteinuria (7 cases) and microhaematuria (6 cases). With the usual contrast doses for visceral angiography, the kidney appears to be the critical organ. In order to reduce the risks of renal complications, contrast doses should be kept to below 4 ml/kg. if possible; angiography should be carried out only if the patient is well hydrated and the indications for angiography should be particularly stringent if there is previous renal damage.
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PMID:[Evaluation of hepatic and renal function after visceral angiography (author's transl)]. 15 51

Eleven rabbits were given bovine serum albumin i.v., in daily doses of 25 mg. Renal biopsy was performed on the 30th, 60th and 100th day of treatment and the specimens were subjected to light-, electron-microscopic and immunofluorescent studies, so as to follow up the dynamics of the glomerular process. Proteinuria and the serum creatinine and BUN levels were also measured. By the 100th day of treatment mesangioproliferative glomerulopathy had developed in 7, membranoproliferative glomerulopathy in 3 cases and membraneous glomerulopathy in 1 case. On the 30th day of treatment exudative glomerulopathy was demonstrable in the majority of the cases (in 9 animals). It is suggested that the earliest stage of the various glomerulopathies, regardless of their type, is marked by exudative lesions. The heaviest proteinuria was found in membraneous and membranoproliferative glomerulopathies. Changes in the serum creatinine and BUN levels indicative of a deteriorating renal function were noted in the membranoproliferative cases. The results are correlated with clinical observations of human glomerulopathies.
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PMID:Experimental glomerular lesions induced by chronic immune complex formation. II. Pathomorphological analysis. 15 42

Streptozotocin (STZ) has shown antitumor activity against various tumors in man, but the clinical usefulness of this drug has been limited, mainly because of renal and gastrointestinal toxicity. Nineteen patients with advanced cancer of various types were given a mean dose of 3.4 g/m2 of STZ by continuous iv infusion over 5-6 days each month for one or two monthly cycles. Basic serum and urine studies were performed immediately before and after each treatment cycle. Following STZ treatment, no significant changes in BUN or creatinine were seen. Four patients in whom initial tests for proteinuria were negative developed grade 1 or 2+ proteinuria after completion of the treatment cycle. No myelosuppression or renal failure was observed. Six patients had no nausea or vomiting, seven patients had nausea only, three patients had nausea and vomiting which were well-controlled with antiemetics, and three patients had uncontrollable nausea and vomiting. Confusion, lethargy, and depression were noted in five patients who had no prior central nervous system abnormalities; these effects appeared during treatment or in the immediate posttreatment period. Two patients with diffuse non-Hodgkin's lymphoma had complete remission, while several other patients had documented improvement. Although central nervous system toxicity may be a limiting factor, prolonged STZ infusions may have significant clinical promise.
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PMID:Continuous streptozotocin infusion: a phase I study. 16 Aug 36

The nephrotoxicities of gentamicin and three other experimental aminoglycosides were compared at a single 60 mg. per kilogram per day dose in rats. Renal function, lysosomal enzymuria, and antibiotic concentrations in plasma, urine, and renal tissue were measured at regular intervals throughout the course of treatment. Kidney tissue was examined by light and electron microscopy in animals killed at intervals throughout the period of antibiotic administration. Proteinuria and enzymuria were early indicators of nephron dysfunction, whereas endogenous creatinine clearance declined later in the course of treatment. All animals were killed 24 hours after a previous antibiotic injection and displayed sustained renal tissue antibiotic concentrations which were 5 to 10 times higher than those in serum or urine. When assayed separately, renal cortical tissue had a fivefold greater antibiotic concentration than renal medulla. Light microscopy displayed necrosis of the pars convoluta of the proximal tubule. Electron microscopy revealed appearance of cytosegrosomes with myeloid bodies. It is possible that impaired cytoplasmic degradation of sequestered organelle membranes, resulting from aminoglycoside accumulation, is responsible for the myeloid body formation and subsequent tubular necrosis.
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PMID:Experimental aminoglycoside nephrotoxicity. 16 76


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