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.; Harrop, Gerard K.; Ngo, Jennifer P.; Evans, Roger G.

doi:10.1093/ndt/gfy047

Cited by 67 publications

(105 citation statements)

References 44 publications

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“…Furthermore, most patients requiring diagnostic evaluation of AKI are in critical care settings, connected to monitoring and life-maintaining equipment that preclude bedside usage of MRI. A more feasible and promising technology for the early real-time detection of evolving medullary hypoxia and for assessing the risk of hypoxic AKI is a continuous determination of urinary pO 2 at the catheter tip, as recently shown in the settings of cardiac surgery [80].…”

Section: Renal Functional Imagingmentioning

confidence: 99%

Why Have Detection, Understanding and Management of Kidney Hypoxic Injury Lagged behind Those for the Heart?

Abassi

Rosen

Lamothe

et al. 2019

JCM

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The outcome of patients with acute myocardial infarction (AMI) has dramatically improved over recent decades, thanks to early detection and prompt interventions to restore coronary blood flow. In contrast, the prognosis of patients with hypoxic acute kidney injury (AKI) remained unchanged over the years. Delayed diagnosis of AKI is a major reason for this discrepancy, reflecting the lack of symptoms and diagnostic tools indicating at real time altered renal microcirculation, oxygenation, functional derangement and tissue injury. New tools addressing these deficiencies, such as biomarkers of tissue damage are yet far less distinctive than myocardial biomarkers and advanced functional renal imaging technologies are non-available in the clinical practice. Moreover, our understanding of pathogenic mechanisms likely suffers from conceptual errors, generated by the extensive use of the wrong animal model, namely warm ischemia and reperfusion. This model parallels mechanistically type I AMI, which properly represents the rare conditions leading to renal infarcts, whereas common scenarios leading to hypoxic AKI parallel physiologically type II AMI, with tissue hypoxic damage generated by altered oxygen supply/demand equilibrium. Better understanding the pathogenesis of hypoxic AKI and its management requires a more extensive use of models of type II-rather than type I hypoxic AKI.

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Section: Renal Functional Imagingmentioning

confidence: 99%

Why Have Detection, Understanding and Management of Kidney Hypoxic Injury Lagged behind Those for the Heart?

Abassi

Rosen

Lamothe

et al. 2019

JCM

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“…Computational models of renal oxygenation also predict medullary hypoxia during CPB 9‐12 . Furthermore, risk of AKI is associated with indices of intra‐operative renal hypoxia, as assessed by urinary oxygen tension (PO 2 ) 13‐15 or near infrared spectroscopy 16,17 . Thus, strategies aimed at improving renal oxygenation during CPB have the potential to mitigate post‐operative AKI.…”

Section: Introductionmentioning

confidence: 99%

Influence of blood haemoglobin concentration on renal haemodynamics and oxygenation during experimental cardiopulmonary bypass in sheep

et al. 2020

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Aim Blood transfusion may improve renal oxygenation during cardiopulmonary bypass (CPB). In an ovine model of experimental CPB, we tested whether increasing blood haemoglobin concentration [Hb] from ~7 g dL−1 to ~9 g dL−1 improves renal tissue oxygenation. Methods Ten sheep were studied while conscious, under stable isoflurane anaesthesia, and during 3 hours of CPB. In a randomized cross‐over design, 5 sheep commenced bypass at a high target [Hb], achieved by adding 600 mL donor blood to the priming solution. After 90 minutes of CPB, PlasmaLyte® was added to the blood reservoir to achieve low target [Hb]. For the other 5 sheep, no blood was added to the prime, but after 90 minutes of CPB, 800‐900 mL of donor blood was given to achieve a high target [Hb]. Results Overall, CPB was associated with marked reductions in renal oxygen delivery (−50 ± 12%, mean ± 95% confidence interval) and medullary tissue oxygen tension (PO2, −54 ± 29%). Renal fractional oxygen extraction was 17 ± 10% less during CPB at high [Hb] than low [Hb] (P = .04). Nevertheless, no increase in tissue PO2 in either the renal medulla (0 ± 6 mmHg change, P > .99) or cortex (−19 ± 13 mmHg change, P = .08) was detected with high [Hb]. Conclusions In experimental CPB blood transfusion to increase Hb concentration from ~7 g dL−1 to ~9 g dL−1 did not improve renal cortical or medullary tissue PO2 even though it decreased whole kidney oxygen extraction.

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“…There is accumulating evidence for an important role of renal tissue hypoxia, particularly in the medulla, in the pathophysiology of this form of AKI 3 . Renal medullary hypoxia during CPB is predicted from computational models of renal oxygenation, 4,5 has been observed in experimental models of CPB, 6‐9 and can be inferred from the observation of reduced urinary oxygen tension (pO 2 ) during CPB in patients 10‐12 . Moreover indices of intra‐operative renal hypoxia in patients, generated from near‐infrared spectroscopy 13,14 or measurement of urinary pO 2 , 10‐12 are associated with development of post‐operative AKI.…”

Section: Introductionmentioning

confidence: 99%

Reversal of renal tissue hypoxia during experimental cardiopulmonary bypass in sheep by increased pump flow and arterial pressure

et al. 2020

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Aim Renal tissue hypoxia during cardiopulmonary bypass could contribute to the pathophysiology of acute kidney injury. We tested whether renal tissue hypoxia can be alleviated during cardiopulmonary bypass by the combined increase in target pump flow and mean arterial pressure. Methods Cardiopulmonary bypass was established in eight instrumented sheep under isoflurane anaesthesia, at a target continuous pump flow of 80 mL·kg−1 min−1 and mean arterial pressure of 65 mmHg. We then tested the effects of simultaneously increasing target pump flow to 104 mL·kg−1 min−1 and mean arterial pressure to 80 mmHg with metaraminol (total dose 0.25‐3.75 mg). We also tested the effects of transitioning from continuous flow to partially pulsatile flow (pulse pressure ~15 mmHg). Results Compared with conscious sheep, at the lower target pump flow and mean arterial pressure, cardiopulmonary bypass was accompanied by reduced renal blood flow (6.8 ± 1.2 to 1.95 ± 0.76 mL·min−1 kg−1) and renal oxygen delivery (0.91 ± 0.18 to 0.24 ± 0.11 mL·O2 min−1 kg−1). There were profound reductions in cortical oxygen tension (PO2) (33 ± 13 to 6 ± 6 mmHg) and medullary PO2 (31 ± 12 to 8 ± 8 mmHg). Increasing target pump flow and mean arterial pressure increased renal blood flow (to 2.6 ± 1.0 mL·min−1 kg−1) and renal oxygen delivery (to 0.32 ± 0.13 mL·O2 min−1kg−1) and returned cortical PO2 to 58 ± 60 mmHg and medullary PO2 to 28 ± 16 mmHg; levels similar to those of conscious sheep. Partially pulsatile pump flow had no significant effects on renal perfusion or oxygenation. Conclusions Renal hypoxia during experimental CPB can be corrected by increasing target pump flow and mean arterial pressure within a clinically feasible range.

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Urinary hypoxia: an intraoperative marker of risk of cardiac surgery-associated acute kidney injury

Abstract: Low urinary PO2 during adult cardiac surgery requiring CPB predicts AKI, so may identify patients in which intervention to improve renal oxygenation might reduce the risk of AKI.

Cited by 67 publications

References 44 publications

Why Have Detection, Understanding and Management of Kidney Hypoxic Injury Lagged behind Those for the Heart?

Why Have Detection, Understanding and Management of Kidney Hypoxic Injury Lagged behind Those for the Heart?

Influence of blood haemoglobin concentration on renal haemodynamics and oxygenation during experimental cardiopulmonary bypass in sheep

Reversal of renal tissue hypoxia during experimental cardiopulmonary bypass in sheep by increased pump flow and arterial pressure

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