Absolute concentration of urinary endogenous β‐glucuronidase determined by an ELISA method as a sensitive but non‐specific indicator for active renal parenchymal damage
- 1 January 1995
- journal article
- Published by Wiley in British Journal of Urology
- Vol. 75 (1), 78-84
- https://doi.org/10.1111/j.1464-410x.1995.tb07239.x
Abstract
To demonstrate that the absolute concentration, instead of the activity, of urinary endogenous beta-glucuronidase is a better indicator for active renal parenchymal damage. Urine samples were obtained from 143 adult patients comprising 60 control subjects with no evidence of urinary tract disease and 83 patients with serum creatinine > 1.5 mg/dL. The absolute concentration of urinary endogenous beta-glucuronidase was determined by an enzyme-linked immunosorbant assay (ELISA) method recently developed by us. The maximal velocity of the enzyme was determined by the enzyme kinetic method. The bacterial beta-glucuronidase and bilirubin in the urine were also detected. The urinary beta-glucuronidase activity was affected by certain inhibitors (D-glucaro-1, 4-lactone), intrinsic substrates (conjugated bilirubin) and bacterial beta-glucuronidase present in the urine. Its concentration, determined by the ELISA method, was not interfered with by such factors. When those urine samples which were contaminated with bacteria and/or bilirubin were excluded, the beta-glucuronidase concentration (X ng/mumol creatinine) was significantly correlated with its maximal velocity (Y nmol/min/mumol creatinine): Y = 0.003 + 0.103X. Contrary to blood urea nitrogen, which increases with the increase in serum creatinine, the urinary beta-glucuronidase activity and its concentration reached a peak at a serum creatinine of 1.6-3.0 mg/dL and declined at higher serum creatinine levels. Episodic elevation of serum creatinine due to acute insult to the kidney or flare up of disease activity was often preceded by an increase in the level of urinary beta-glucuronidase. The absolute concentration of the urinary beta-glucuronidase was not affected by several factors in the urine which interfere with its activity, and was a sensitive indicator for renal parenchymal damage, particularly in the early stage when the disease is active.Keywords
This publication has 22 references indexed in Scilit:
- Inhibition of β-glucuronidase in Human Urine by Ascorbic AcidHuman & Experimental Toxicology, 1990
- d-Glucaro-1,4-lactone: Its excretion in the bile and urine and effect on the biliary secretion of β-glucuronidase after oral administration in ratsHepatology, 1989
- Monitoring glomerular function in diabetic nephropathyAmerican Journal Of Medicine, 1983
- Chronic progressive renal disease: Rate of change of serum creatinine concentrationKidney International, 1977
- A SIMPLE METHOD OF ESTIMATING PROGRESSION OF CHRONIC RENAL FAILUREThe Lancet, 1976
- Urinary excretion of β-glucuronidase in protein-calorie malnutritionClinica Chimica Acta; International Journal of Clinical Chemistry, 1973
- Urinary -glucuronidase activity in renal diseaseArchives of Internal Medicine, 1973
- Bilharzia and bladder cancer. An investigation of urinary β-glucuronidase associated with S. haematobium infectionTransactions of the Royal Society of Tropical Medicine and Hygiene, 1972
- Multiple Range and Multiple F TestsBiometrics, 1955
- The Determination of Enzyme Dissociation ConstantsJournal of the American Chemical Society, 1934