Intra‐Operative Urinary Hypoxia During Cardiac Surgery on Cardiopulmonary Bypass Predicts Later Development of Acute Kidney Injury

Abstract

Renal medullary hypoxia may be a common pathway in the development of acute kidney injury (AKI). There are no validated methods to detect medullary hypoxia in patients. However, experimental findings indicate that changes in urinary oxygen tension (UPO2) reflect changes in medullary PO2. Therefore, we evaluated the relationship between intra‐operative UPO2 and the development of AKI after cardiac surgery requiring cardiopulmonary bypass (CPB). From January 2015 to July 2016, thirty‐five adult patients undergoing on‐pump cardiac surgery were prospectively enrolled. UPO2 was continuously recorded intra‐operatively via a fiber‐optic probe deployed through the lumen of the urinary catheter, with the end of the probe at the catheter tip, where it was in contact with bladder urine. UPO2 fell during surgery, particularly during CPB. The lowest (nadir) UPO2 was most frequently observed during the rewarming phase of CPB, or shortly after weaning from CPB (n=25, 71%). Fourteen patients (40%) developed AKI as defined by an increase in serum creatinine from baseline of either > 26.5 μmol/L (0.3 mg/dL) within 48 hours or > 50% within 5 days. Nadir intra‐operative UPO2 was lower in patients who later developed AKI (8.5 ± 1.6 mmHg, mean ± SE) than in those who did not (16.5 ± 4.2 mmHg, P = 0.02). UPO2 below 10 mmHg at any time during surgery was associated with a 4.5‐fold [95% confidence limits 1.6 – 19.1] greater risk of AKI (P = 0.03). Furthermore, urinary PO2 below 15 mmHg for longer than the median time for all patients (5.6 min per hour of surgery) was associated with a 7.3‐fold [1.8 – 35.1] greater risk of AKI (P = 0.01) and an area under the receiver operator curve of 0.73 [0.56 – 0.90] (P = 0.03). We conclude that low UPO2 during cardiac surgery requiring CPB is strongly associated with later development of AKI. Continuous intra‐operative monitoring of UPO2 is simple and relatively non‐invasive. It may provide a real‐time biomarker of risk of AKI. Early detection of risk of AKI may in‐turn provide a window of opportunity to intervene and thus avoid development of AKI in patients undergoing cardiac surgery.