Urinary Hypoxia: An Intraoperative Marker of Risk of Cardiac Surgery-associated Acute Kidney Injury

Zhu, Michael Z.L.; Martin, Andrew; Cochrane, Andrew; Smith, Julian A.; Thrift, Amanda G; Ngo, Jennifer P.; Harrop, Gerard K.; Evans, Roger G.

doi:10.1016/j.hlc.2018.04.119

Cited by 16 publications

(59 citation statements)

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“…They also accord with clinical observations of urinary hypoxia (as a surrogate marker of medullary hypoxia) during CPB . Indeed, urinary hypoxia during CPB, or at any time during cardiac surgery, independently predicts development of post‐operative AKI, supporting the concept that hypoxia in the renal medulla is a major factor in the development of cardiac surgery‐associated AKI. This combination of modelling with experimental and clinical studies is a prime example of how computational models can drive translational research.…”

Section: Renal Oxygenation: What Are the Critical Questions Mathematisupporting

confidence: 82%

“…These findings have most recently been confirmed in a clinically relevant large animal model of CPB . They also accord with clinical observations of urinary hypoxia (as a surrogate marker of medullary hypoxia) during CPB . Indeed, urinary hypoxia during CPB, or at any time during cardiac surgery, independently predicts development of post‐operative AKI, supporting the concept that hypoxia in the renal medulla is a major factor in the development of cardiac surgery‐associated AKI.…”

Section: Renal Oxygenation: What Are the Critical Questions Mathematisupporting

confidence: 78%

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Renal oxygenation: From data to insight

et al. 2020

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Computational models have made a major contribution to the field of physiology. As the complexity of our understanding of biological systems expands, the need for computational methods only increases. But collaboration between experimental physiologists and computational modellers (ie theoretical physiologists) is not easy. One of the major challenges is to break down the barriers created by differences in vocabulary and approach between the two disciplines. In this review, we have two major aims. Firstly, we wish to contribute to the effort to break down these barriers and so encourage more interdisciplinary collaboration. So, we begin with a “primer” on the ways in which computational models can help us understand physiology and pathophysiology. Second, we aim to provide an update of recent efforts in one specific area of physiology, renal oxygenation. This work is shedding new light on the causes and consequences of renal hypoxia. But as importantly, computational modelling is providing direction for experimental physiologists working in the field of renal oxygenation by: (a) generating new hypotheses that can be tested in experimental studies, (b) allowing experiments that are technically unfeasible to be simulated in silico, or variables that cannot be measured experimentally to be estimated, and (c) providing a means by which the quality of experimental data can be assessed. Critically, based on our experience, we strongly believe that experimental and theoretical physiology should not be seen as separate exercises. Rather, they should be integrated to permit an iterative process between modelling and experimentation.

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Section: Renal Oxygenation: What Are the Critical Questions Mathematisupporting

confidence: 82%

Section: Renal Oxygenation: What Are the Critical Questions Mathematisupporting

confidence: 78%

Renal oxygenation: From data to insight

et al. 2020

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“…This is greater than the commonly used flow rate in adult humans of w2.4 L min -1 m -2 . 19 Sheep were also cooled by w3 C on bypass, in line with standard practice for coronary artery bypass graft surgery at our associated center. 19 Consequently, mixed venous SO 2 on CPB was w76%, within the target range for clinical perfusion.…”

Section: Discussionmentioning

confidence: 99%

“…19 Sheep were also cooled by w3 C on bypass, in line with standard practice for coronary artery bypass graft surgery at our associated center. 19 Consequently, mixed venous SO 2 on CPB was w76%, within the target range for clinical perfusion. 15 We also rendered sheep relatively hypercapnic on CPB to promote dilation of renal resistance arteries.…”

Section: Discussionmentioning

confidence: 99%

Strategies that improve renal medullary oxygenation during experimental cardiopulmonary bypass may mitigate postoperative acute kidney injury

Lankadeva

Cochrane

Marino

et al. 2019

Kidney International

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Renal medullary hypoxia may contribute to cardiac surgery-associated acute kidney injury (AKI). However, the effects of cardiopulmonary bypass (CPB) on medullary oxygenation are poorly understood. Here we tested whether CPB causes medullary hypoxia and whether medullary oxygenation during CPB can be improved by increasing pump flow or mean arterial pressure (MAP). Twelve sheep were instrumented to measure whole kidney, medullary, and cortical blood flow and oxygenation. Five days later, under isoflurane anesthesia, CPB was initiated at a pump flow of 80 mL kg -1 min -1 and target MAP of 70 mm Hg. Pump flow was then set at 60 and 100 mL kg -1 min -1 , while MAP was maintained at approximately 70 mm Hg. MAP was then increased by vasopressor (metaraminol, 0.2-0.6 mg/min) infusion at a pump flow of 80 mL kg -1 min -1 . CPB at 80 mL kg -1 min -1 reduced renal blood flow (RBF), -61% less than the conscious state, perfusion in the cortex (-44%) and medulla (-40%), and medullary PO 2 from 43 to 27 mm Hg. Decreasing pump flow from 80 to 60 mL kg -1 min -1 further decreased RBF (-16%) and medullary PO 2 from 25 to 14 mm Hg. Increasing pump flow from 80 to 100 mL kg -1 min -1 increased RBF (17%) and medullary PO 2 from 20 to 29 mm Hg. Metaraminol (0.2 mg/min) increased MAP from 63 to 90 mm Hg, RBF (47%), and medullary PO 2 from 19 to 39 mm Hg. Thus, the renal medulla is susceptible to hypoxia during CPB, but medullary oxygenation can be improved by increasing pump flow or increasing target MAP by infusion of metaraminol.A KI occurs in more than 20% of adult patients after cardiac surgery requiring CPB. 1 The ability to decrease the risk of AKI associated with cardiac surgery is hampered by our lack of knowledge of the effects of CPB on renal perfusion and oxygenation. 2 Evolving evidence shows that renal medullary hypoxia contributes to the development of AKI. 3,4 Mathematical models predict renal medullary hypoxia during CPB, 5,6 and medullary hypoxia has been observed in a rat model of CPB 7 and in a pilot study of 2 pigs subjected to CPB. 8 However, there have been no systematic investigations of renal global and regional (i.e., cortical and medullary) perfusion and oxygenation in a clinically relevant large animal model of CPB. Furthermore, although evidence shows that goaldirected perfusion can mitigate risk of postoperative AKI 9-11 and that the increase in renal fractional oxygen extraction during CPB can be alleviated by increasing pump flow, 12,13 the potential for perfusion conditions to be

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“…It is not feasible to routinely or directly measure renal medullary tissue oxygen tension (PO 2 ) in humans. However, it is possible to measure the PO 2 of bladder urine in patients with an indwelling bladder catheter . In a pioneering study, Kainuma et al continuously measured bladder urinary PO 2 (uPO 2 ), in patients undergoing cardiac surgery requiring cardiopulmonary bypass (CPB), using polargraphic electrodes .…”

Section: Introductionmentioning

confidence: 99%

Factors that confound the prediction of renal medullary oxygenation and risk of acute kidney injury from measurement of bladder urine oxygen tension

et al. 2019

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Aim: Urinary oxygen tension (uPO 2 ) may provide an estimate of renal medullary PO 2 (mPO 2 ) and thus risk of acute kidney injury (AKI). We assessed the potential for variations in urine flow and arterial PO 2 (aPO 2 ) to confound these estimates. Methods: In 28 sheep urine flow, uPO 2 , aPO 2 and mPO 2 were measured during development of septic AKI. In 65 human patients undergoing cardiac surgery requiring cardiopulmonary bypass (CPB) uPO 2 and aPO 2 were measured continuously during CPB, and in a subset of 20 patients, urine flow was estimated every 5 minutes. Results: In conscious sheep breathing room air, uPO 2 was more closely correlated with mPO 2 than with aPO 2 or urine flow. The difference between mPO 2 and uPO 2 varied little with urine flow or aPO 2 . In patients, urine flow increased abruptly from 3.42 ± 0.29 mL min −1 to 6.94 ± 0.26 mL min −1 upon commencement of CPB, usually coincident with reduced uPO 2 . During hyperoxic CPB high values of uPO 2 were often observed at low urine flow. Low urinary PO 2 during CPB (<10 mm Hg at any time during CPB) was associated with greater (4.5-fold) risk of AKI. However, low urine flow during CPB was not significantly associated with risk of AKI. Conclusions: uPO 2 provides a robust estimate of mPO 2 , but this relationship is confounded by the simultaneous presence of systemic hyperoxia and low urine flow.Urine flow increases and uPO 2 decreases during CPB. Thus, CPB is probably the best time to use uPO 2 to detect renal medullary hypoxia and risk of post-operative AKI. K E Y W O R D Sacute kidney injury, cardiac surgery, cardiopulmonary bypass, hypoxia, sepsis 2 of 12 | NGO et al.

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Urinary Hypoxia: An Intraoperative Marker of Risk of Cardiac Surgery-associated Acute Kidney Injury

Cited by 16 publications

References 0 publications

Renal oxygenation: From data to insight

Renal oxygenation: From data to insight

Strategies that improve renal medullary oxygenation during experimental cardiopulmonary bypass may mitigate postoperative acute kidney injury

Factors that confound the prediction of renal medullary oxygenation and risk of acute kidney injury from measurement of bladder urine oxygen tension

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