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)

In order to investigate the renal function, a cross-sectional study was carried out on four groups of workers significantly exposed to a mixture of alicyclic and aliphatic C5-C7 hydrocarbons, to styrene, to a mixture mostly composed of toluene and xylenes and to chlorinated hydrocarbons, respectively. The study involved 438 workers. Exposure was characterized by means of urinary metabolites, or by means of environmental measures, when biological indicators were not available. The renal function impairment indicators included total proteinuria, albuminuria and urinary excretion of muramidase (E.C. 3.2.1.17) and beta-glucuronidase (E.C. 3.2.1.31). The trend of these parameters provides some evidence of renal damage due to occupational exposure to organic solvents and suggests that the lesions are mild and tubular rather than glomerular.
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PMID:Early indicators of renal damage in workers exposed to organic solvents. 660 22

Cadmium metallothionein (CdMT) nephrotoxicity was studied in rats injected i.p. with a single nonlethal dose of CdMT (0.6 mg of Cd per kg). Within 8 hr of CdMT injection, urine volume and urine sodium excretion were increased and sodium dodecyl sulfate gel electrophoresis of urine proteins showed that elevated levels of low molecular weight proteins were present in the urines of CdMT-treated rats. Urine RNAase activity was also elevated, approximately 7-fold, by CdMT but not by zinc metallothionein (ZnMT) or lysozyme at equivalent protein doses, demonstrating that a proteinuria indicative of proximal tubule cell dysfunction develops as an early response to CdMT exposure. Ultrastructural alterations were also present in animals injected with CdMT but not ZnMT or lysozyme. The earliest alterations occurred in the lysosome compartment of the cell. By 1 hr, the number of small lysosomes in renal proximal convoluted tubule cells increased significantly with no changes in other organelle compartments. By 4 and 8 hr, there was a further increase in lysosome number with a concomitant decrease in size and a marked increase in the number of small clear apical vacuoles. Lysosomal cathepsin D activity was decreased at 4 and 8 hr after CdMT injection, and in vitro studies indicated that this effect was not due to a direct inhibition of the enzyme by Cd++ or CdMT. Thus, both lysosome size and protease activity were rapidly altered by CdMT exposure. Studies of Cd binding in the kidney suggest that non-MT-bound Cd is an important factor in CdMT-associated toxicity. Approximately 97% of the Cd present in the cytoplasm at 1 hr was non-MT-bound. Prior induction of renal MT by treatment with zinc (20 mg of Zn per kg as ZnSO4, i.p. 16 hr before CdMT injection) markedly reduced non-MT binding of Cd++ in kidneys of treated animals and inhibited the alterations in urine volume and low molecular weight protein reabsorption induced by CdMT. These data suggest that acute CdMT exposure provides an excellent system for studying the mechanism of cadmium tubular proteinuria and that the intracellular renal MT pool plays a key role in regulating this process.
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PMID:Cadmium-Metallothionein nephropathy: relationships between ultrastructural/biochemical alterations and intracellular cadmium binding. 670 45

The presence of tubular involvement, as a marker for the detection of urinary tract infection (UTI) site, was examined in 19 patients with pyelonephritis and in 15 patients with cystitis or asymptomatic bacteriuria. The urinary excretion of four markers of tubular proteinuria, beta 2-microglobulin (beta 2M), lysozyme (LZ), lactic dehydrogenase isoenzyme V (LAD-5) and N-acetyl-beta D-glucosaminidase (NAG), was investigated. LAD-5 appeared particularly valuable for the early detection of upper UTI. However, the overall diagnostic accuracy appeared to be further strengthened using, besides LAD-5, one additional variable. A set of simple and noninvasive biochemical tests on urine samples can reliably help to identify the site of UTI.
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PMID:Contribution of four markers of tubular proteinuria in detecting upper urinary tract infections. A multivariate analysis. 675 51

We prospectively evaluated concentrations of beta-D-galactosidase, alpha-L-fucosidase, beta-D-N-acetylglucosaminidase, and lysozyme in urine from normal subjects, ambulatory patients with cystic fibrosis (CF), and CF patients with previously normal renal function who were receiving intravenous aminoglycoside (AG) therapy. Enzyme activities were generally low or negligible in subjects not receiving AG. Enzymuria was documented during 12 of 13 AG treatment courses and most frequently involved beta-D-N-acetylglucosaminidase excretion. In nine courses, enzymuria occurred in the absence of proteinuria or elevations of blood urea nitrogen and serum creatinine. In three courses attended by enzymuria and evidence of nephrotoxicity, neither the time of appearance nor the magnitude of enzymuria was different from that of nonnephrotoxic patients. In two of these three treatment courses, enzymuria preceded clinical evidence of nephrotoxicity of 16 and 5 days, and in the third course enzymuria and elevation of blood urea nitrogen and serum creatinine occurred simultaneously. We conclude that enzymuria is not a reliable predictor of nephrotoxicity due to AG in CF patients and is not an indication of discontinue AG therapy.
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PMID:Are measurements of urine enzymes useful during aminoglycoside therapy? 679 92

Gentamicin and other aminoglycoside antibiotics in high doses may produce proteinuria and other signs of nephrotoxicity. Proteinuria may result from general renal damage or may reflect alterations in specific steps in the renal handling of proteins. To distinguish between these two possibilities, experiments were designed to quantify the effects of nephrotoxic doses of several aminoglycosides on the renal handling of proteins in the isolated perfused rat kidney with the cationic low-molecular-weight protein lysozyme as a representative protein. Each aminoglycoside was administered ip to male Wistar rats (30 mg/kg/day) for 7 days. Lysozyme and 125I-lysozyme were added to the perfusate to achieve a lysozyme perfusate concentration of about 100 mg/liter. Clearances of inulin and lysozyme, release of tyrosine and trichloroacetic acid-soluble radioactive metabolites into the perfusate, and the glomerular sieving coefficient of lysozyme were determined. Scanning and transmission electron microscopy indicated that gentamicin and tobramycin decreased the number and diameter of the endothelial fenestrae of the glomerular capillaries. Concurrently, gentamicin and tobramycin decreased the glomerular sieving coefficient of lysozyme from 0.8 to 0.6 and 0.5, respectively. Netilmicin did not affect the percentage reabsorption of lysozyme whereas gentamicin and tobramycin decreased lysozyme reabsorption from 71.7 to 35.4 and 34.4% of the filtered load, respectively. Lysozyme degradation, estimated by the release of tyrosine into the perfusate during a 150-min perfusion period, was decreased from a control value of 12 mumol/liter to 4.43 and 4.65 mumol/liter in kidneys from rats treated with gentamicin and tobramycin, respectively. This study demonstrates that polycationic aminoglycosides may affect several processes involved in renal handling of lysozyme including glomerular permeability, tubular reabsorption, and intracellular proteolytic degradation.
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PMID:Effects of aminoglycosides on glomerular permeability, tubular reabsorption, and intracellular catabolism of the cationic low-molecular-weight protein lysozyme. 684 78

To evaluate the effect of improved metabolic control on kidney function, urinary excretion rate of beta-2-microglobulin, lysozyme, and gamma-glutamyltransferase were evaluated in nine poorly controlled, newly diagnosed diabetic patients before and during treatment. In six poorly controlled insulin-dependent nephropathic diabetic patients, besides the parameters cited above, urinary albumin excretion rate and IgG/transferrin clearance ratio were further investigated to estimate the permeability and the selectivity of glomerular barrier during conventional treatment and after improvement of the metabolic control by a glucose-controlled insulin infusion system (GCIIS). The improved glycemic control resulted in a significant reduction of urinary beta-2-microglobulin and lysozyme excretion in all diabetic patients. Significant decreases of urinary albumin excretion and of IgG/transferrin clearance ratio (indicating a more selective proteinuria) during strict metabolic control were also observed in nephropathic diabetic patients. The reduction of urinary beta-2-microglobulin and lysozyme excretion indicates that a tubular reabsorptive dysfunction, reversible with the amelioration of glycemic control, can be observed in poorly controlled, newly diagnosed and in insulin-dependent nephropathic diabetic patients during conventional treatment. In the latter patients, the permeability and the selectivity properties of glomerular barrier also improved during GCIIS.
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PMID:Kidney function after improved metabolic control in newly diagnosed diabetes and in diabetic patients with nephropathy. 692 32

The presence and significance of monocytes in the glomerular lesions of 13 renal specimens obtained from ten patients with systemic lupus erythematosus-associated nephritis were studied. The monocytes were identified by the presence of intracytoplasmic lysozyme, as demonstrated by immunoperoxidase staining on paraffin-embedded tissue. Eight specimens obtained from six patients displayed monocytes. These were found most often associated with mesangial hypercellularity, and their appearance fluctuated with it. There was a positive correlation between the number of lysozyme-positive cells and the amount of proteinuria. We conclude that monocytes contribute to the endocapillary hypercellularity and affect protein filtration in lupus nephritis.
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PMID:Presence of monocytes in systemic lupus erythematosus-associated glomerulonephritis: marker study and significance. 697 91

The evolution of proteinuria in rabbits with experimentally induced chronic serum sickness was followed up longitudinally by analytical and quantitative assays. The results suggest that sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) is a more sensitive index of kidney malfunction than are total-protein assays or the quantitation of albumin and lysozyme. In some rabbits that showed abnormal proteinuria by SDS-PAGE, no histologic evidence of pathologic damage or of deposition of immune complexes in the kidneys was found. This suggests that SDS-PAGE may detect functional alterations at early stages of kidney damage when the lesions are either undetectable or reversible. In one rabbit that was killed after normalization of the proteinuria, immunofluorescence tests indicated deposition of C3, IgG, and fibrinogen, but there was no histologic evidence of kidney damage.
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PMID:Experimental model of chronic serum sickness. Relationships between proteinuria, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and glomerular and extraglomerular renal pathology. 699 Aug 90

In two patients who had malignant histiocytosis, renal involvement was present at an early stage of their diseases and consisted clinically of proteinuria and renal failure. The associated renal lesion was characterized by a diffuse and global endocapillary hypercellularity of the glomeruli imputable to atypical cells occluding the capillary loops. Immunoglobulins were absent from this lesion. The atypical cells were positively identified by lysozyme immunoperoxidase study as malignant histiocytes. It is suggested that renal biopsy complemented by marker study could play a role in the diagnosis of malignant histiocytosis.
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PMID:Renal involvement in malignant histiocytosis. An immunoperoxidase marker study. 702 27

The glomerular filtration rate (creatinine clearance), glomerular permeability (qualitative and quantitative proteinuria), tubular reabsorption (k-lambda chains of immunoglobulins and lysozyme) and indexes of tubular cell lysis (alpha-glucosidase and gamma-glutamyltranspeptidase) were measured in the urine of 10 patients with moderate, uncomplicated essential hypertension during placebo therapy and after captopril given at increasing doses of 25, 50, 100 and 200 mg twice daily, the first three doses being given for 3 days and the last one for 4 weeks in all patients and for an additional 6 months in 5 patients. During placebo therapy, proteinuria was absent in eight patients and detectable (glomerular and selective) in two; selective proteinuria appeared in two and a decrease in selectivity was observed in two patients with previous proteinuria after 4 weeks of captopril therapy. No proteinuria was detectable in the five patients followed up to 6 months, not even in the one in whom a decrease in glomerular selectivity had occurred after 4 weeks. The glomerular filtration rate was unchanged as were lysozyme and gamma-glutamyltranspeptidase values, while light chains were always undetectable. Alpha-glucosidase showed some increase; however, increments were transient and always much lower than those observed with known tubular toxic drugs. These data show that under our experimental conditions captopril caused no evident changes in glomerular and tubular function.
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PMID:Effect of captopril on renal function in patients with essential hypertension. 704 2


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