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Hyperchloremic acidosis is associated with acute kidney injury after abdominal surgery.
Nephrology 2017 September
AIM: Hyperchloremic acidosis may have an important role as a precursor of acute kidney injury (AKI) in the hyperchloremic environment induced by chloride-rich fluids, but this remains unclear. We tested the hypothesis that hyperchloremic acidosis assessed by the Stewart approach is associated with postoperative AKI.
METHODS: A historical cohort study was conducted in adult patients who had normal renal function preoperatively and required admission to the intensive care unit after elective abdominal surgery. The Risk, Injury, Failure, Loss of kidney function, End stage kidney disease (RIFLE) classification was used for definition of AKI.
RESULTS: Of 206 patients (144 male, 69.9%) included in the study, 42 (20.4%) had postoperative AKI (AKI group) and 164 (79.6%) did not (non-AKI group). Base excess-chloride (BE-Cl) and strong ion difference (SID, approximated as Na-Cl) decreased, and the chloride level on postoperative day 1 increased compared with preoperative values in both groups (P < 0.05). In the AKI group, BE-Cl and SID were lower, and chloride was higher than in the non-AKI group (P < 0.05). The intraoperative load of chloride ions in fluids increased the risk of postoperative AKI (P < 0.01). In multivariate logistic regression analysis, postoperative BE-Cl < -7 mEq/L (i.e. SID <31 mEq/L) was an independent risk factor for AKI (odds ratio; 2.8, 95% CI; 1.2-6.4, P = 0.01). In the AKI group, stays in the intensive care unit and in hospital were longer than those in the non-AKI group (P < 0.05).
CONCLUSION: Hyperchloremic acidosis is associated with postoperative AKI, and this may be attenuated by reducing the intraoperative chloride load.
METHODS: A historical cohort study was conducted in adult patients who had normal renal function preoperatively and required admission to the intensive care unit after elective abdominal surgery. The Risk, Injury, Failure, Loss of kidney function, End stage kidney disease (RIFLE) classification was used for definition of AKI.
RESULTS: Of 206 patients (144 male, 69.9%) included in the study, 42 (20.4%) had postoperative AKI (AKI group) and 164 (79.6%) did not (non-AKI group). Base excess-chloride (BE-Cl) and strong ion difference (SID, approximated as Na-Cl) decreased, and the chloride level on postoperative day 1 increased compared with preoperative values in both groups (P < 0.05). In the AKI group, BE-Cl and SID were lower, and chloride was higher than in the non-AKI group (P < 0.05). The intraoperative load of chloride ions in fluids increased the risk of postoperative AKI (P < 0.01). In multivariate logistic regression analysis, postoperative BE-Cl < -7 mEq/L (i.e. SID <31 mEq/L) was an independent risk factor for AKI (odds ratio; 2.8, 95% CI; 1.2-6.4, P = 0.01). In the AKI group, stays in the intensive care unit and in hospital were longer than those in the non-AKI group (P < 0.05).
CONCLUSION: Hyperchloremic acidosis is associated with postoperative AKI, and this may be attenuated by reducing the intraoperative chloride load.
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