Urinary actin, interleukin-6, and interleukin-8 may predict sustained arf after ischemic injury in renal allografts

Abstract

Background:Cellular damage and inflammation after ischemia contribute to sustained acute renal failure (ARF). Methods:To quantify cellular damage and inflammation in postischemic ARF and identify markers of renal functional outcome, urine specimens from 40 renal allograft recipients, including 30 cadaveric (9 “sustained ARF” and 21 “recovery” subjects) and 10 living donor allografts (“LD”), were analyzed for actin, γ-glutamyl transpeptidase (GGTP), lactate dehydrogenase (LDH), interleukin–6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) during the first posttransplant week. Results:On day 0, urinary actin, GGTP, IL-6, and IL-8 were elevated in recipients destined to have sustained ARF compared with those destined to recover. Median values per gram of urine creatinine in the sustained ARF, recovery, and LD groups were 263.9, 0.0, and 0.0 μg for actin; 5000.0, 892.9, and 5555.6 U for GGTP; 193.1, 27.2, and 10.5 ng for IL-6; and 382.0, 17.8, and 18.5 ng for IL-8, respectively. In contrast, urinary LDH and TNF-α increased in recipients with recovering function compared with those who had sustained ARF. The corresponding median values were 36.7 and 16.3 U (recovery versus sustained ARF) for LDH, and 18.4 and 7.6 ng (LD versus sustained ARF) for TNF-α. Computational analyses using the Receiver Operating Characteristic Curve found that elevated urinary actin, IL-6, and IL-8 on day 0 were strong predictors of sustained ARF, where the calculated areas under the curve were 0.75, 0.91, and 0.82, respectively. Conclusion:Increased urinary actin, IL-6, and IL-8 may be useful markers for the prediction of sustained ARF after ischemia.