N-acetyl-beta-D-glucosaminidase urinary excretion as an early indicator of kidney damage in rheumatoid arthritis patients starting on parenteral gold and Depo-Medrone/placebo injections.

Abstract

The purpose of the study was to determine the effect of initiation of gold therapy on glomerular and tubular integrity. Urine albumin was used as a marker of glomerular damage. N-acetyl-beta-D-glucosaminidase (NAG) urinary excretion served as an indicator of proximal tubular damage. This study was an adjunct to a clinical trial that investigated the safety and the efficacy of Depo-Medrone during the induction phase of gold therapy. The NAG activities and albumin levels in the urine of 36 patients with active rheumatoid arthritis treated with sodium aurothiomalate weekly up to a total of 1 g were investigated. NAG was assayed in 565 early morning urine samples of these patients at weekly intervals for 24 weeks. The mean NAG level rose from 50.2 nmol/mg of creatinine on entry to peak NAG excretion of 120.4 nmol/mg of creatinine at week 4 and then fell to 56.3 nmol/mg of creatinine at week 24. Urinary albumin was assayed in 252 early morning urine samples at monthly intervals during gold treatment. Values greater than 20 mg/l were observed in 7.5% of urine samples. Microalbuminuria was present in 9% of patients at baseline. Two patients who were withdrawn because of proteinuria and macroalbuminuria had normoalbuminuria on entry. We conclude that raised levels of NAG associated with tubular damage are more frequent than glomerular damage on entry to, and during, treatment with gold salts.