#ExpBio - Urine Oxygen and Acute Kidney Injury

Apr 24 2017 Published by under [Medicine&Pharma], ExpBio 2017

Original source: ajprenal.physiology.org/content/284/3/F433

All nephrologists know that acute kidney injury (AKI) commonly complicates heart surgery, especially if patients require cardiopulmonary bypass (CPB). AKI increases morbidity and mortality in this setting, so heading it off could improve patient outcomes.

AKI in this setting usually occurs due to acute tubular necrosis, when low oxygen in the outer medulla of the kidney (see image at right) damages proximal tubular cells. Patients often require support with dialysis until these cells can repopulate in a few weeks.

At present, detecting medullary hypoxia is a guessing game. Did the patient get hypoxia? Did the blood pressure drop? How long were they on CPB?

Probe sits just above catheter tip

Experimental evidence from animals showed that the pressure of oxygen in the urine (UO2) correlates with medullary hypoxia. A surgical group wondered if UO2 during operations might predict AKI in heart surgery patients requiring CPB. UO2 can be measured with a fiber-optic probe inside the urinary catheter all of these patients have placed before the cutting begins (see diagram).

Their study included 35 adult patients, with 14 developing AKI (defined as rise in creatinine). The lowest intra-operative UO2 was 50% lower in patients who developed AKI than those who did not (p=0.02). Worse levels of UO2 had even greater predictive value for AKI. However, no level of UO2 completely eliminated AKI risk.

Continuous monitoring of UO2 can be done and may provide additional information about renal risk during heart surgery with CPB. As a pediatric nephrologist, I wonder about it's use in other conditions with high risk for AKI.


IntraOperative Urinary Hypoxia During Cardiac Surgery on Cardiopulmonary Bypass Predicts Later Development of Acute Kidney Injury

Roger G. Evans1, Michael Z. Zhu1,2, Julian A. Smith2, Gerard K. Harrop1, Amanda G. Thrift3, Andrew D. Cochrane2. 1Cardiovascular Disease Program, Biosciences Discovery Institute and Department of Physiology, Monash University, Melbourne, Australia, 2Department of Surgery (School of Clinical Sciences), Monash University and Department of Cardiothoracic Surgery, Monash Health, Clayton, Australia, 3Department of Medicine (School of Clinical Sciences) at Monash Health, Monash University, Clayton, Australia

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 intraoperative UPO2 and the development of AKI after cardiac surgery requiring cardiopulmonary bypass (CPB). From January 2015 to July 2016, thirty-five adult patients undergoing onpump cardiac surgery were prospectively enrolled. UPO2 was continuously recorded intraoperatively via a fiberoptic 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 intraoperative 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 4.5fold [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 7.3fold [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 intraoperative monitoring of UPO2 is simple and relatively noninvasive. It may provide a realtime 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.

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