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)

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

The post-exercise urine samples from 122 long-distance runners showed evident abnormalities upon microscopic examination in 95% of all subjects. Proteinuria, alone or with microscopic hematuria, was frequently found. Macroscopic hematuria was a rare occurrence. The urine samples collected in 30 runners before, immediately after the race, and 6, 12, 24, 36, and 48 h later showed a significant post-race decrease in the osmolarity and a significant increase in gamma-glutamyl transferase and N-acetyl-beta-glucosaminidase enzyme activity. Plasma renin activity and plasma aldosterone, determined before and after the race in nine runners, showed a significant increase in the post-race samples. The abnormal urinary findings disappeared in all cases within 24-36 h. It can be concluded that urinary abnormalities are very common after exercise. These abnormalities are most often of a "renal" origin, probably due to a temporary hemodynamic impairment, partially of glomerular but principally of tubular function.
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PMID:Exercise-induced urinary abnormalities in long-distance runners. 615 14

The renal function of a population of workers occupationally exposed to mercury in the chlor-alkali industry has been examined and compared to that of a population of workers with no occupational exposure to mercury. Measurement of specific urinary proteins and enzymes have been carried out on each individual on three separate occasions and have been complemented by blood plasma measurements at the final visit. Under the conditions of exposure to mercury sustained in this study, there is no evidence of an increased prevalence of renal dysfunction as indicated by enzyme and protein measurements. The urinary concentration of the low molecular weight protein, beta 2-microglobulin, is significantly lower in the mercury-exposed group than in the control group. In contrast to recently published literature, no relationship is seen between urinary mercury concentration and the appearance of high molecular weight protein in urine. A small increase in the prevalence of higher activities of the urinary enzyme N-acetyl-beta-glucosaminidase and gamma glutamyl transferase is observed when the urinary mercury concentration exceeds 100 micrograms/g creatinine. A small increase in the prevalence of raised urinary N-acetyl-beta-glucosaminidase activity is observed when the duration of exposure to mercury exceeds ten years. The pattern of proteinuria has been characterised in a total of sixteen individuals from both populations; a low molecular weight proteinuria is seen in three individuals from the control group whilst a high molecular weight proteinuria is seen in the remainder (seven in the control and six in the mercury group).
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PMID:An evaluation of renal function in workers occupationally exposed to mercury vapour. 635 40

Renal function tests were performed in 101 unselected patients who had been on lithium for two weeks to 12 years. None had a recorded episode of lithium intoxication. The glomerular filtration rate (GFR), was not correlated with the cumulative dose of lithium or the duration of use of other psychotropic drugs. Nine patients had creatinine clearances lower than predicted; in six of these, no cause was identified and the small reductions in GFR may have been related to lithium use. Urinary concentrating ability (Umax) declined with age, and total dose of lithium received. Although the concurrent use of neuroleptics did not significantly reduce the Umax, the total duration of treatment with these drugs showed a negative correlation. The results suggest that prolonged use of neuroleptics, particularly in patients treated with lithium, may be responsible for an irreversible reduction in urine concentrating ability. Microalbuminuria was present in 40 per cent of the patients, although the rate of albumin excretion was not correlated with duration of use of psychotropic drugs. beta 2 microglobulin excretion was only raised in nine of these patients, suggesting that increased glomerular permeability rather than impaired proximal tubular protein reabsorption was responsible for the proteinuria. The urinary excretion of beta 2 microglobulin and N-acetyl-beta-glucosaminidase were slightly increased in small numbers of patients, indicating little evidence for proximal tubular damage. Increased NAG excretion did not correlate with reduced distal tubular function. However, there was a tendency to higher urinary beta 2 microglobulin excretion in patients with a reduced Umax.
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PMID:Renal function during lithium treatment. 648 19

The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.
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PMID:Increased ammoniagenesis and the renal tubular effects of potassium depletion. 651 81

Anti-rat glomerular basement membrane (GBM) rabbit serum was produced by immunizing rabbits with the supernatant substance of trypsin-digested rat GBM. Nephritis was induced in rats by a single intravenous administration of 0.25 ml of anti-serum and changes in pathohistological and biochemical parameters during the process of the disease were investigated in comparison with those of Masugi nephritis and the modified type of Masugi nephritis previously reported. In light microscopic studies, histological changes seen in the kidneys closely resembled those of typical human glomerulonephritis. Changes such as hypercellularity, adhesion between capillary wall and Bowman's capsule, crescent formation and hyalinization in glomeruli and interstitial infiltration were the most pronounced on the 30th day after the anti-serum injection. In immunofluorescent studies, a linear fixation of rabbit IgG was observed along the GBM from the 1st day and the staining of a certain intensity was preserved throughout the experimental periods. A linear staining with anti-rat IgG serum was recognized from the 10th day. The fixation of fibrinogen was also seen in not only the glomerular capillary walls, but also in Bowman's space after the 10th day. Proteinuria significantly increased from the 1st day, reached a peak of 12 times the control level, and thereafter gradually decreased. The patterns of progress of urinary alkaline phosphatase and N-acetyl-beta-glucosaminidase activities were much the same as those seen in cases of proteinuria and the levels at their peak times were about 10 and 3 times control levels, respectively. Plasma urea nitrogen level transiently increased on the 5th day and then reverted to the control level by the 30th day. Plasma cholesterol levels were significantly high from the 5th to the 20th days. It is concluded that glomerular damages in this model are more severe, so-called, "nephritic type" and continue for longer periods than in cases of Masugi nephritis, however, do not differ in degree and duration from findings in the modified type of Masugi nephritis.
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PMID:[Pharmacological studies on experimental nephritic rats (11). Changes in pathohistological and biochemical parameters in anti-rat GBM rabbit serum-induced nephritis (author's transl)]. 728 45

To study the role of lysosomal enzymes in glomeruli, we examined specific activities of lysosomal hydrolases in isolated glomeruli and, for comparison in isolated tubules, from rat kidney cortex of normal animals and animals with puromycin aminonucleoside nephrosis (PAN). Nephrotic syndrome was induced in rats by a single intraperitoneal injection of aminonucleoside and the rats were sacrificed at the time of peak proteinuria. Colloidal iron staining of renal cortex demonstrated decreased staining for the epithelial polyanion in animals with PAN. Lysosomal enzymes were determined by fluorogenic and colorimetric methods. In normal kidney, total specific activities of cathepsin beta 1, beta-2-fucosidase, acetyl-beta-glucosaminidase, and arylsulfatase were lower in glomeruli compared with tubules and with tissue slices of the same kidney. Total activity of acid phosphatase was higher in glomeruli than tubules. In glomeruli of PAN rats, there were lower activities of N-acetyl-beta-glucosaminidase, D-fucosidase, beta-glucosidase, beta-glucoronidase, and arylsulfatase compared with control rats. Activity of acid phosphatase, on the other hand, was higher in glomeruli of PAN than control rats. All differences were statistically significant. These studies demonstrate that (1) activities of lysosomal enzymes in normal glomeruli and in glomeruli of nephrotic rats have a property distinct from the rest of the kidney, and (2) the specific activities of lysosomal hydrolases are altered in glomeruli of rats with PAN. These studies suggest that changes in activities of lysosomal enzymes may be related to pathogenesis of this glomerulopathy.
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PMID:Activities of lysosomal enzymes in isolated glomeruli. Alterations in experimental nephrosis. 732 25

The kidney can be considered as both culprit and victim in the hypertensive process. Deranged renal function contributes to the development of arterial hypertension and of secondary vascular damage at the glomerular and arteriolar level and accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans from the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by hyperuricaemia and increased urinary excretion of enzymes such as N-acetyl-beta-glucosaminidase and proteins such as albumin and beta 2-microglobulin. Later, a progressive fall in glomerular filtration rate, sometimes accompanied by proteinuria, can be observed if high blood pressure persists.
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PMID:Renal damage in hypertension. 760 39

Sixty-eight cases of non-insulin dependent diabetes mellitus (NIDDM) complicated with nephropathy were randomly divided into two groups: treated group, 35 cases treated with alcohol extraction of Abelmoschus manihot, Gliclazide and Captopril tablets; control group, 33 cases treated with Gliclazide and Captopril tablets, over a period of 8 weeks. The total effective rate in treated and control group were 83.87% and 31.03%(P < 0.01), urinary micro-albumin were 31.7 mg/L and 76.3 mg/L (P < 0.05), proteinuria were 0.41 g/24h and 0.77 g/24h (P < 0.01), blood beta 2-microglobulin were 3317.8 ng/ml and 3473.1 ng/ml (P < 0.05), urinary beta 2-microglobulin were 367.2 ng/ml and 641.5 ng/ml (P < 0.01), urinary N-acetyl-beta-glucosaminidase (NAG) were 26.3 u/L and 66.7 u/L (P < 0.01), plasma lipid peroxide (LPO) were 6.13 nmol/L and 8.78 nmol/L (P < 0.05), and plasma superoxide anion were 8.36 kcpm and 10.42 kcpm respectively (P < 0.05). It was suggested that Abemoschus manihot alcohol extraction could eliminate oxygen free radicals, alleviate renal tubular-interstitial diseases, improve renal function and reduce proteinuria.
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PMID:[Clinical observation on diabetic nephropathy treated with alcohol of Abelmoschus manihot]. 764 Apr 95

We investigated potential renal functional impairment induced by chronic use of anti-epileptic drugs (AEDs) in 79 epileptic children. They were divided into five groups: valproic acid (VPA) monotherapy where the serum concentration (SC) of VPA was no less than 60 micrograms/ml (VPA [SC > or = 60]) (15 cases), VPA monotherapy where the SC VPA was less than 60 micrograms/ml (VPA [SC < 60]) (29 cases), phenobarbital monotherapy (PB) (7 cases), carbamazepine monotherapy (CBZ) (16 cases), and polytherapy containing VPA (12 cases). Urinalysis (proteinuria and hematuria) and serum creatinine were normal except for two cases of proteinuria and two cases of hematuria. The level of urinary excretion of N-acetyl-beta-glucosaminidase (u-NAG) was high in 29% of all patients, and 47% of VPA (SC > or = 60), 38% of CBZ, 25% of polytherapy, and 24% of VPA (SC < 60) groups. There was a significant positive correlation between serum concentration of VPA and u-NAG/urinary creatinine (u-Cr). The level of guanidinoacetic acid (u-GAA) excreted in the urine was normal except in one patient. U-NAG/u-Cr may be a more sensitive marker than u-GAA/u-Cr for renal functional impairment in AED therapy.
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PMID:Urinary N-acetyl-beta-glucosaminidase and guanidinoacetic acid levels in epileptic patients treated with anti-epileptic drugs. 769 90


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