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

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

To assess their potential value as early indicators of gentamicin-induced kidney damage, lysosomal hydrolases were measured in the 24-h urines of rats receiving 30 or 60 mg of gentamicin per kg per day for 15 days. Proteinuria, urine osmolality, blood urea nitrogen, and creatinine clearance were also measured. Kidney tissue was examined by both light and electron microscopy. Beta-galactosidase, beta-n-acetyl-hexosaminidase, and alpha-fucosidase were sensitive indicators and were significantly elevated above control values by day 3 at both doses (P < 0.01). Proteinuria, urine osmolality, and tests reflecting glomerular filtration rate were later indicators of nephron damage. Changes by light microscopy were detected on day 5. Necrosis was most prominent in the proximal convoluted tubules on day 10. Electron microscopy revealed numerous cytosomes with myeloid bodies within the proximal tubular epithelium on day 5. Lysosomal enzymuria appears to be an early manifestation of gentamicin nephrotoxicity and may possibly be related to the lysosomal abnormalities seen on electron microscopy.
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PMID:Enzymuria in gentamicin-induced kidney damage. 113 89

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

The relationship between proteinuria and glomerular polyanion (GPA) charge has been studied in a model of experimental cadmium (Cd) nephropathy. Female Sprague-Dawley rats were administered Cd in drinking water for up to 18 months. From month 2, the animals showed an elevation of albuminuria preceding by about 6 months the rise of urinary beta 2-microglobulin and IgG. The nephrotoxic action of Cd was not readily detectable on the basis of the urinary output of beta-N-acetylglucosaminidase, alanine aminopeptidase and lactate dehydrogenase. These enzymes showed either little variation or were affected late in the intoxication process. Administration of Cd for 12 or 18 months did not impair the GFR. The glomerular origin of the albuminuria induced by Cd was demonstrated by estimating the glomerular filtration of rat or human (injected intravenously) albumin in rats whose tubular reabsorption had been blocked by a saturating dose of cytochrome C. The GPA charge was assessed by measuring the binding of the cationic dye, Alcian blue (AB), to membranes of isolated glomeruli. The sialic and sulfate content of these membranes was also determined. The Cd induced-albuminuria was negatively correlated (r = -0.73; n = 37) with the AB binding to glomerular membranes, their sialic acid content (r = -0.39) but not with their sulfate content (r = -0.15). A negative correlation (r = -0.62; n = 37) was also observed between the albuminuria and red blood cell membrane negative charges largely contributed by sialic acid. All these observations can be interpreted as the evidence that Cd enhances the glomerular filtration of proteins through a GPA depletion involving mainly sialic acid.
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PMID:Loss of glomerular polyanion correlated with albuminuria in experimental cadmium nephropathy. 151 26

As shown in studies of 123 patients with various nephropathies, activities of alpha-glucosidase and N-acetyl-beta-D-hexosaminidase in urine of the patients correlated with severity and stages of these diseases; at the same time, simultaneous estimation of both enzymatic activities in urine was shown to be more informative in diagnostic of kidney impairments. Low values of correlation coefficient (r = 0.35 +/- 0.09) between daily excretion of protein and the activity of neutral alpha-glucosidase in urine showed that the enzyme activity did not depend on proteinuria and was independent test for kidney impairment. Estimation of alpha-glucosidase activity could be used for control of the therapy; the enzymatic activity in urine correlated distinctly with the clinico-laboratory patterns of the patients studied.
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PMID:[Diagnostic value of determining neutral alpha-glucosidase and N-acetyl-beta-D-hexosaminidase activity in the urine in kidney pathology]. 294 5

The urinary excretion of beta-hexosaminidase in relation to creatinine was studied during one year in 30 consecutive patients with polycystic kidney disease (S-creatinine 75-1 000 micro mol/l) and 30 healthy controls. The excretion of beta-hexosaminidase was significantly increased in the patients and was positively correlated to S-creatinine and to the relative increase in S-creatinine during the year of the study. No correlation was found between the enzyme excretion and age, mean blood pressure, number of antihypertensive drugs, proteinuria or pyuria. A significant rise in beta-hexosaminidase excretion was observed in two patients with acute cyst bleeding and/or kidney infarction.
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PMID:Urinary beta-hexosaminidase excretion in polycystic kidney disease. 646 Apr 26

The urinary excretion of beta-hexosaminidase was studied in different forms of proteinuria. Patients with tubular proteinuria showed a very large increase in beta-hexosaminidase only in the acute stage of the renal disease, while patients with chronic tubular dysfunction did not show any greater degree of beta-hexosaminidase excretion. The same findings were noted in glomerular disease, in which patients with a very high degree of disease activity showed a marked increase in enzyme excretion. There was a good correlation between enzyme excretion and level of proteinuria. In Bence-Jones proteinuria it seems possible to determine the grade of renal injury caused by the light chain.
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PMID:Urinary excretion of beta-hexosaminidase in different forms of proteinuria. 677 40

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

The activity of beta-N-acetylglucosaminidase (beta-NAG) was determined in 41 workers of a chemical plant, exposed to metallic mercury, and in 10 controls. In addition, a routine urine examination was performed and the level of creatinine was measured in serum. The mercury excretion in urine in the exposed workers exceeded admissible biological concentrations three times, on average. In the group exposed to mercury the beta-NAG activity in urine was significantly higher than in the a control group. Several cases of trace proteinuria and microscopic haematuria were found in the exposed group. A mean beta-NAG activity in urine was significantly higher in those cases than in other persons. The study proved the usefulness of determinations of the beta-NAG activity in urine in assessing nephrotoxicity in workers exposed to metallic mercury.
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PMID:[Beta-n-acetylglucosaminidase in urine as a sign of kidney damage in workers exposed to metallic mercury]. 800 20


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