Initial Experience with Sodium Acetate as a Renoprotective Agent During Robotic Partial Nephrectomy

In animal models, sodium acetate has been shown to protect against acute kidney injury (AKI) via activation of the hypoxia-inducible factor pathway. We report our clinical experience with sodium acetate as an intraoperative renoprotective agent in patients undergoing robotic partial nephrectomy.

Retrospective review of a single-surgeon experience using intraoperative sodium acetate infusion (SAI; 150 mEq at 200 mL/h) during partial nephrectomies. Primary outcomes included rates of AKI as defined by established standardized criteria (i.e., KDIGO [Kidney Disease: Improving Global Outcomes], RIFLE [Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease]). Propensity score matching without replacement was used to balance baseline characteristics between groups. Subsequent association between SAI and AKI events was assessed using logistic regression analysis in the matched cohort.

Overall, SAI did not impact postoperative renal function based on serum creatine level or glomerular filtration rate. On logistic regression analysis of the matched cohort, the administration of intraoperative SAI was associated with a 58% and 61% lower odds of AKI on postoperative day 1 based on the RIFLE (p = 0.06, CI 0.17-1.03) and KDIGO (p = 0.05, CI 0.15-1.01) criterion for AKI, respectively. In the subset of patients who had pre-existing chronic kidney disease (CKD), SAI was associated with significantly lower rates of AKI using both the RIFLE (p = 0.01) and KDIGO (p < 0.05) criteria.

Perioperative SAI did not confer a statistically significant renoprotective effect for all patients undergoing partial nephrectomy. However, it may reduce the odds of postoperative AKI based on the RIFLE/KDIGO criterion, particularly in patients with pre-existing CKD. Further research is warranted to determine the clinical impact of sodium acetate as a renoprotective agent.