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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Mineralocorticoid receptor (MR) antagonists (MRA), also referred to as aldosterone blockers, are now well recognised for their clinical benefit in patients with heart failure with reduced ejection fraction (HFrEF). Recent studies have also shown MRA can improve outcomes in patients with ‘HFpEF’, where the ejection fraction is preserved but left ventriclar filling is reduced. While the MR is a steroid hormone receptor best known for anti-natriuretic actions on electrolyte homeostasis in the distal nephron, it is now estalished that the MR has many physiological and pathophysiological roles in the heart, vasculature and other non-epithelial tissue types. It is the impact of MR activation on these tissues that underpins the use of MRA in cardiovascular disease, in particular heart failure. This minireview will discuss the origins and the development of MRA and highlight how their use has evolved from the ‘potassium-sparing diuretics’ spironolactone and canrenone over 60 years ago, to the more receptor-selective eplerenone and most recently the emergence of new non-steroidal receptor antagonists esaxerenone and finerenone.

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