Urinary enzymes in acute renal failure

Intestinal-type alkaline phosphatase (IAP) has been localizedto the S3 segment of the renal tubule in previous studies, asite believed to be particularly vulnerable to toxic and ischaemicdamage. During a 17-month period a pilot study of the valueof urinary enzyme measurements (IAP and tissue non-specificalkaline phosphatase—TNAP, using monoclonal antibody-basedimmunoassays, and N-acetyl-beta-glucosaminidase—NAG, usingcolorometric assay) in 50 prospectively followed cases of acuterenal failure (ARF) was performed. Urinary enzymes were measuredat initial evaluation (‘start’), and then each dayfor 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 tostandard criteria. Of the renal ARF patients 23 of 28 had acutetubular necrosis (ATN), 3 of 28 acute interstitial nephritis(AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50had a fatal outcome and 1 of 50 was dialysis-dependent at discharge(‘poor’ prognosis group), while 31 of 50 survivedhospital without becoming dialysis-dependent (‘good’prognosis group). Median enzyme concentration were increased in ‘poor’compared to ‘good’ prognosis patients: start IAP3.2 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 patientsalone 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 significantlyincreased in the poor compared to the good prognosis group.Peak values showed similar trends. Of all patients, five witha start IAP>12 U/g creat died, and all survivors had a startIAP<12, but 14 of 19 poor prognosis patients also had a startIAP<12. All urinary enzymes were less in the postrenal group,but only the IAP significantly so. None of the enzymes weresignificantly different between prerenal and renal ARF groups. Urinary enzymes IAP, NAG, TNAP appear to be unhelpful in determiningthe site of renal injury in ARF, except for postrenal cases,where IAP was significantly lower. There were too few patientswith AGN or AIN to test the hypothesis that the enzymes wouldbe less in glomerular compared to tubular pathologies. Despitea low sensitivity, the start IAP may be a marker of outcomein ARF if the high positive predictive value for death is confirmedin larger studies.