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073, P?=?0.209), or donor risk index (Spearman's r?=?0.015, P?=?0.801). In a multivariate model adjusting for recipient factors, male donor (P?=?0.016), increasing warm ischemic time (P?=?0.002) and the presence of >30% macrovesicular steatosis on ��time zero�� biopsy (P? http://www.selleckchem.com/products/bmn-673.html (P?=?0.231), and hypertension (P?=?0.285) was not different between the AKI and non-AKI patients. Thirty-four percent of patients who developed AKI compared to 15.7% of patients who did not develop AKI received renal sparing immunosuppression from immediately following liver transplantation (P? http://www.selleck.cn/products/incb024360.html (P?=?0.019), ��5 units red cells intra-operatively http://www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html (P?=?0.005), intra-operative inotropes (P?=?0.008), and sepsis during the postoperative period (P?=?0.007) were associated with the development of AKI. Donor and graft variables associated with peri-operative AKI on univariate analysis are outlined in Table?2. AKI patients were more likely to have a donor ��65-year old (P?=?0.017), >30% macrovesicular steatosis on ��time-zero�� biopsy (P?=?0.032) or a cold ischemic time >12?h (P?=?0.050). The donor risk index was higher in patients who developed AKI compared to patients who did not (P?=?0.041). Peak serum AST demonstrated a significant correlation with peak peri-operative serum creatinine (Spearman's r?=?0.283, P?