URINARY ENZYMES IN ACUTE-RENAL-FAILURE

Intestinal-type alkaline phosphatase (IAP) has been localized to the S3 segment of the renal tubule in previous studies, a site believed to be particularly vulnerable to toxic and ischaemic damage. During a 17-month period a pilot study of the value of urinary enzyme measurements (IAP and tissue non-specific alkaline phosphatase-TNAP, using monoclonal antibody-based immunoassays, and N-acetyl-beta-glucosaminidase-NAG, using colorometric assay) in 50 prospectively followed cases of acute renal failure (ARF) was performed. Urinary enzymes were measured at initial evaluation ('start') and then each day for 14 days, with the highest enzyme value ('peak') also used for analysis. Patients were divided into prerenal (n = 16), renal (n = 28), postrenal (n = 6) categories according to standard criteria. Of the renal ARF patients 23 of 28 had acute tubular necrosis (ATN), 3 of 28 acute interstitial nephritis (AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50 had a fatal outcome and 1 of 50 was dialysis-dependent at discharge ('poor' prognosis group), while 31 of 50 survived hospital without becoming dialysis-dependent ('good' prognosis group). Median enzyme concentration were increased in 'poor' compared to 'good' prognosis patients: start IAP 3.2 versus 2.2 U/g creat (NS), start NAG 48.6 versus 13.7 (P<0.01), start TNAP 3.5 versus 0.9 (P<0.02). When renal ARF patients alone were analysed, only IAP (3.2 versus 1.3 U/g creat at start) and NAG (57.9 versus 7.8 U/g creat at start) were significantly increased in the poor compared to the good prognosis group. Peak values showed similar trends. Of all patients, five with a start IAP > 12 U/g creat died, and all survivors had a start IAP < 12, but 14 of 19 poor prognosis patients also had a start IAP < 12. All urinary enzymes were less in the postrenal group, but only the IAP significantly so. None of the enzymes were significantly different between prerenal and renal ARF groups. Urinary enzymes IAP, NAG, TNAP appear to be unhelpful in determining the site of renal injury in ARF, except for postrenal cases, where IAP was significantly lower. There were too few patients with AGN or AIN to test the hypothesis that the enzymes would be less in glomerular compared to tubular pathologies. Despite a low sensitivity, the start IAP may be a marker of outcome in ARF if the high positive predictive value for death is confirmed in larger studies.