Absolute concentration of urinary endogenous β‐glucuronidase determined by an ELISA method as a sensitive but non‐specific indicator for active renal parenchymal damage

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Abstract
Objective To demonstrate that the absolute concentration, instead of the activity, of urinary endogenous P‐glucuronidase is a better indicator for active renal parenchymal damage. Materials and methods 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 β‐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 β‐glucuronidase and bilirubin in the urine were also detected. Results The urinary p‐glucuronidase activity was affected by certain inhibitors (d‐glucaro‐1, 4‐lactone), intrinsic substrates (conjugated bilirubin) and bacterial β‐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 β‐glucuronidase concentration (X ng/umol creatinine) was significantly correlated with its maximal velocity (Y nmol/ min/μmol creatinine): Y = 0.003 + 0.103X. Contrary to blood urea nitrogen, which increases with the increase in serum creatinine, the urinary β‐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 β‐glucuronidase. Conclusion The absolute concentration of the urinary β‐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.