Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial renal biopsies for glomerular culture, histochemical staining for beta-glucuronidase, electron microscopy (EM) and light microscopy, were used to study macrophage involvement in experimental chronic immune complex (IC) glomerulonephritis (GN) induced in rabbits by daily intravenous injections of bovine serum albumin (BSA). In the 26 animals studied, proliferative GN of variable severity was induced, with mild disease in 5 animals, moderate proliferation in 15 and crescentic GN in 6. Macrophages first appeared in glomerular culture outgrowths during the 2nd and 3rd weeks, coincident with the onset of proteinuria and rising serum creatinine concentration. Large numbers of macrophages (in excess of 20 per glomerulus) were seen by the 5th weeks and persisted to the 9th week. The number of macrophages in outgrowths was not significantly greater in animals with crescentic disease. EM demonstrated macrophages in capillary loops, and in glomeruli with crescents, macrophages could be seen in the urinary space. Histochemical staining for beta-glucuronidase also demonstrated macrophages in the glomerular tuft and in crescents when present. These results indicate that macrophages constitute a considerable proportion of the glomerular hypercellularity seen in chronic IC glomerulonephritis.
Nephron 1982
PMID:Involvement of the macrophage in experimental chronic immune complex glomerulonephritis. 621 16

In the early phase of hemodialysis progressive decreases in some enzyme activities in the leukocyte homogenate, neutrophil granule fraction and postgranular supernatant were found with concomitant rise in plasma beta-glucuronidase activity, which is indicative of the release of neutrophil granule factors into the extracellular environment. Intravenous infusion of human neutrophil granule products to rabbits induced profound transient neutropenia. The results suggest that the release of neutrophil granule factors in the early period of hemodialysis may be a possible cause of hemodialysis neutropenia.
Nephron 1984
PMID:Release of neutrophil granule factors during early period of hemodialysis: a possible cause of hemodialysis neutropenia. 671 2

Nephrotoxicity was evaluated in 37 patients receiving aminoglycosides by serial urinary measurements of the low-molecular weight protein beta 2-microglobulin (beta 2m) and the proximal tubular enzymes N-acetyl-glucosaminidase and beta-glucuronidase. Clinical nephrotoxicity, with a rise in serum creatinine greater than 20% of the baseline value, was diagnosed in 15 of 30 evaluable patients. The laboratory diagnosis of nephrotoxicity, defined as a two-fold increase in beta 2m, N-acetylglucosaminidase and beta-glucuronidase, was confirmed in 11/15 patients. Additionally, there were 3 patients in whom there was definitive laboratory nephrotoxicity in the absence of a rise in serum creatinine. The laboratory diagnosis of nephrotoxicity could be made 4.1--5.5 days prior to significant elevation in serum creatinine. The data suggest that beta 2m and enzyme studies are predictors of nephrotoxicity.
Nephron 1981
PMID:Aminoglycoside nephrotoxicity and its predictability. 702 43