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)

Acidic hydrolases were assayed in urines of 19 normal children, 33 children with idiopathic nephrotic syndrome of childhood (INS), 21 children with glomerulonephritides (GN) and 7 children with persistent proteinuria/hematuria, and in plasma of 10 children each with INS or GN. Both plasma and urinary acidic hydrolases were studied in intermittent orthostatic proteinuria. Cbeta-galactosidase and Cbeta-N-hexosaminidase were done in normals and children with active renal disease. Significantly (P less than 0.01) elevated urinary acidic hydrolases excretion in active renal diseases, both in INS and GN, returned to a normal range with regression of the diseases. Increased postural proteinuria was associated with normal urinary acidic hydrolases. Both beta-galactosidase and beta-N-hexosaminidase excretion was higher than similar mol wt proteins in normals and increased further in active renal diseases. The data suggests that increased urinary acidic hydrolases is related to the activity of the renal disease, and not to urinary WBC, hematuria or proteinuria. The likely source of urinary acidic hydrolases thus appears to be the injured renal parenchyma itself.
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PMID:Urinary acidic hydrolases in renal diseases in children. 10 80

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

Two lysosomal glycohydrolases, beta-galactosidase and beta-N-hexosaminidase which have been associated with kidney disease were measured in the urine of 110 youngsters with juvenile diabetes mellitus. The mean enzyme excretions in the diabetic group were intermediate between those of normal youngsters and those with active renal disease. Three youngsters with known kidney disease had elevations comparable to others in the diabetic group but no direct correlation could be shown between enzyme elevations and proteinuria or Addis count abnormalities. Positive correlations were seen between enzyme levels and indices of metabolic balance including blood sugar, cholesterol and triglycerides but not with urine sugar or ketones. Duration and estimated stage and control of diabetes also correlated with the urinary enzymes. These preliminary studies are consistent with the possibility that the excretion of these enzymes reflects the ongoing renal damage which occurs in most juvenile diabetics.
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PMID:Urinary acidic glycohydrolases as an index of kidney damage in juvenile diabetes mellitus. 11 9

The induction of nephrotoxic nephritis in rats with rabbit antibodies preparation results in proteinuria, hypoproteinemia and hyperlipidemia with little glomerular lesions. A study of some hydrolases in cortex and medulla on one hand and glomerular and tubules on the other, showed changes in the activities of following enzymes. 1) A 20-30 % decrease in Na+, K+ dependent ATP-ase in whole kidney. 2) A 20 % decrease in beta-galactosidase activity in glomerular and medulla. 3) A 20 % increase of arylsulphatase A activity in tubules. These results are discussed in the light of the present knowledge of sulphatide metabolism in kidney.
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PMID:[Experimental nephrotic syndrome in the rat. Biologic parameters and study of several hydrolases in different purified kidney fractions]. 20 50

The activity of beta-N-acetylglucosaminidase (NAG), beta-galactosidase, alpha-L-fucosidase, beta-glucuronidase, beta-glucosidase and alpha-mannosidase was determined in the urine of rats at progressive ages from newborn to old animals. The age-dependence of urinary creatinine, protein and pH values was also studied. Enzyme activity, related to urinary creatinine, was significantly higher in the newborn group than other ages. The excretion of NAG increased significantly in adult rats (3-6 months old) compared to young rats (1 month old). Most of the enzyme activities were diminished in old rats (25 months old). Increased proteinuria and creatinine excretion were observed in rats since 3 months of age. Age-related differences among enzyme activities therefore should be considered when these urinary glycosidases are to be studied in rats.
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PMID:Age-related excretion of six glycosidases in rat urine. 136 39

Mercury exposure and renal function parameters were examined in 68 dentists and 64 dental assistants. The levels of mercury in urine were low: only three individuals exceeded 20 micrograms/l. Increased excretion of urinary proteins and increased activity of urinary enzymes were observed. This enhanced prevalence of renal function changes appeared not to be related to the mercury urine level, age, sex, or smoking and drinking habits. Only for men was a positive relation between the level of mercury in urine and the activity of beta-galactosidase found. The proteinuria may be due to one or more potential nephrotoxic agents used in dental practice.
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PMID:Urinary mercury levels and early changes in kidney function in dentists and dental assistants. 313 45

Acute passive Heymann glomerulonephritis in rats induced heavy proteinuria and highly increased urinary activity of N-acetyl-beta-D-glucosaminidase, acid beta-galactosidase and acid phosphatase. The cortical activity of these acid hydrolases was increased essentially in the large lysosomes as demonstrated by subfractionation of the lysosome-rich mitochondrial-lysosomal fraction, by rate zonal centrifugation. Banding density of small lysosomes shifted or reduced to slightly lower value (1.225 g/ml), which is between the banding densities of small 'light' (1.20 g/ml) and small 'dense' lysosomes (1.235 g/ml) in normal rat kidney cortex. Labelled protein reabsorbed in the proximal tubule is recovered in these populations of small lysosomes as well as in the large lysosomes or 'protein droplets'. Glomerulonephritis also induced a new population of small 'light' lysosomes (density 1.185-1.195 g/ml) enriched in cathepsin D. The previously demonstrated morphological, biochemical, and physiological heterogeneity of renal lysosomes was confirmed and emphasized in the kidney cortex of glomerulonephritic rats. The main changes in the lysosomal populations appear to reflect the increased protein reabsorption as confirmed by the proteinuria.
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PMID:Changes in lysosome populations in the rat kidney cortex induced by passive Heymann glomerulonephritis. 313 21

The nephrotoxic potential of alpha-interferon (IFN alpha-2b) was analysed in 21 patients with chronic myeloid leukemia. As particularly sensitive parameters in the detection of subclinical renal injury we measured the excretion of the following urinary enzymes: lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), leucine arylaminidase (LAP), beta-galactosidase (GAL) and N-acetyl-beta-glucosaminidase (NAG). Additionally, protein excretion and urinary sediment were analysed. In 18 of 21 patients a significant increase in the excretion of LDH, LAP, GGT and NAG was found, in 6 patients there was an additional rise in the output of GAL. Eleven patients developed proteinuria up to 2 g/l, one patient excreted up to 9 g/l. Enzymuria and protein excretion decreased in all patients after reduction of the IFN alpha-2b dosage and disappeared in two patients following cessation of therapy. The high incidence of nephrotoxic events in patients with CML during IFN alpha-2b therapy might be mostly due to immunological or substance-specific effects.
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PMID:[Detection of nephrotoxicity of human alpha 2b interferon with special reference to the analysis of urine enzymes in patients with chronic myeloid leukemia]. 347 5

In humans a higher incidence of renal toxicity is seen in old than in young patients undergoing gentamicin therapy. To investigate whether the sensitivity of the old kidney to gentamicin is a function of age, separate from the adverse effects arising from declining renal excretory function, the nephrotoxicity of 12 daily injections of this antibiotic was measured in rats. Young (7-10 months) and old (25-28 months) rats, selected for minimal age-related nephropathy, received an initial dose of 30 or 50 mg of gentamycin/kg. Based on the plasma half-lives, subsequent doses for the high dose group were reduced as needed to equalize renal exposure to gentamicin. Urinary excretion of beta-galactosidase peaked by the second or third day of injections, while proteinuria was highest in the second week. The amount of microscopic renal tubular damage was dose-related and was greater in the old rats of each dose group. The increased sensitivity of old kidneys toward gentamycin toxicity, although small, thus appears to be in addition to any age-related decrease in renal elimination of the drug from plasma.
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PMID:Effect of aging on gentamicin nephrotoxicity and pharmacokinetics in rats. 716 27

We assayed plasma activities of beta-galactosidase, beta-hexosaminidase, alpha-fucosidase and alpha-galactosidase involved in degradation of the glycoprotein molecule in 110 insulin-dependent diabetics aged 3-1/2 to 19 years and compared them to a group of normal youngsters. We correlated the plasma enzyme activities with the duration, control and sequelae of insulin-dependent diabetes. Insulin-dependent diabetics had a significantly higher plasma activity of beta-hexosaminidase and alpha-mannosidase (p less than 0.01) and a significantly lower plasma activity of alpha-fucosidase and alpha-galactosidase (p less than 0.01). Of the 5 enzymes studied, only plasma beta-hexosaminidase correlated with fasting and postprandial blood sugar (p less than 0.01), cholesterol and triglycerides (p less than 0.05). Additionally, poor control of diabetes was also associated with a significantly higher plasma beta-hexosaminidase activity (p less than 0.01). Proteinuria or an abnormal Addis count suggestive of renal involvement was associated with various changes in plasma acidic hydrolases. These changes may be related to insulin deficiency rather than hyperglycemia and may be genetically determined.
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PMID:Plasma acidic glycohydrolases in insulin-dependent diabetes mellitus. 730 74


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