OBJECTIVE: To examine the dynamic and potentially synergistic influence of warm ischemia time (WIT) and excisional volume loss (EVL) on predicted rates of postpartial acute kidney injury (AKI) across a range of tumor complexities, and to investigate whether these modifiable variables sensitize the kidney to each other's damaging influence. MATERIALS AND METHODS: We retrospectively reviewed 1245 patients between 2006 and 2016 with bilateral kidneys and enhancing renal masses in our single-institution robotic partial nephrectomy (PN) database. EVL was calculated as the difference between specimen and tumor volume based on pathologic measurements. Multivariate logistic regressions, followed by marginal effects, were run to examine the interaction of ischemia type, EVL, and radius, exophytic/endophytic properties, nearness of deepest tumor portion to collecting system or sinus, anterior/posterior and location relative to polar line score on rates of AKI. RESULTS: We found a significant interaction effect of WIT and log EVL on predicted AKI (P < .001). Each doubling of EVL caused a 4.03% and 8.46% increased probability of AKI for WIT of <25 and >25 minutes, respectively. At an EVL of >5.5 cm3, prolonged WIT had statistically greater odds of causing AKI. These predicted effects on AKI were amplified for increasing radius, exophytic/endophytic properties, nearness of deepest tumor portion to collecting system or sinus, anterior/posterior and location relative to polar line scores (P < .001). CONCLUSION: Although the adverse functional effects of WIT and parenchymal volume loss during PN have previously been described in isolation, our findings suggest that their influence on AKI is synergistic, especially in complex tumors. As such, additional attention should be given to limiting warm ischemia and maximizing surgical precision to avoid a "double hit" on postoperative renal function.
OBJECTIVE: To examine the dynamic and potentially synergistic influence of warm ischemia time (WIT) and excisional volume loss (EVL) on predicted rates of postpartial acute kidney injury (AKI) across a range of tumor complexities, and to investigate whether these modifiable variables sensitize the kidney to each other's damaging influence. MATERIALS AND METHODS: We retrospectively reviewed 1245 patients between 2006 and 2016 with bilateral kidneys and enhancing renal masses in our single-institution robotic partial nephrectomy (PN) database. EVL was calculated as the difference between specimen and tumor volume based on pathologic measurements. Multivariate logistic regressions, followed by marginal effects, were run to examine the interaction of ischemia type, EVL, and radius, exophytic/endophytic properties, nearness of deepest tumor portion to collecting system or sinus, anterior/posterior and location relative to polar line score on rates of AKI. RESULTS: We found a significant interaction effect of WIT and log EVL on predicted AKI (P < .001). Each doubling of EVL caused a 4.03% and 8.46% increased probability of AKI for WIT of <25 and >25 minutes, respectively. At an EVL of >5.5 cm3, prolonged WIT had statistically greater odds of causing AKI. These predicted effects on AKI were amplified for increasing radius, exophytic/endophytic properties, nearness of deepest tumor portion to collecting system or sinus, anterior/posterior and location relative to polar line scores (P < .001). CONCLUSION: Although the adverse functional effects of WIT and parenchymal volume loss during PN have previously been described in isolation, our findings suggest that their influence on AKI is synergistic, especially in complex tumors. As such, additional attention should be given to limiting warm ischemia and maximizing surgical precision to avoid a "double hit" on postoperative renal function.