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Intra‐Operative Urinary Hypoxia During Cardiac Surgery on Cardiopulmonary Bypass Predicts Later Development of Acute Kidney Injury
Author(s) -
Evans Roger G.,
Zhu Michael Z.,
Smith Julian A.,
Harrop Gerard K.,
Thrift Amanda G.,
Cochrane Andrew D.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.698.5
Subject(s) - medicine , cardiopulmonary bypass , acute kidney injury , urinary system , cardiac surgery , creatinine , hypoxia (environmental) , catheter , anesthesia , lipocalin , cardiology , urology , surgery , oxygen , chemistry , organic chemistry
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 (UPO 2 ) reflect changes in medullary PO 2 . Therefore, we evaluated the relationship between intra‐operative UPO 2 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. UPO 2 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. UPO 2 fell during surgery, particularly during CPB. The lowest (nadir) UPO 2 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 UPO 2 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). UPO 2 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 PO 2 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 UPO 2 during cardiac surgery requiring CPB is strongly associated with later development of AKI. Continuous intra‐operative monitoring of UPO 2 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.