The following is the summary of “Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill” published in the December 2022 issue of Critical care by Hu, et al.

Acute kidney injury, or AKI, is common in critically ill patients. The pathophysiology of this condition has been attributed to inadequate oxygenation of the renal medullary tissue. However, in large mammalian models of critical disease, hypoxia in the renal medullary tissue can be recognized before biochemical evidence of acute kidney injury (AKI). This lends credence to the use of medullary hypoxia as a pathophysiological biomarker for the early detection of imminent AKI, which, in turn, makes it possible to stop the condition’s progression. 

The idea that the urinary oxygen tension (PuO²) of the bladder, which can only be measured non-invasively, can provide a reliable estimate of the oxygen tension (tPO²) of the renal medullary tissue, which can only be measured invasively, is supported by evidence from research involving both animals and humans. In addition, treatments that alter medullary tPO² cause changes in bladder PuO² that are equivalent to those modifications. Clinical research has demonstrated that the oxygen concentration in the bladder correlates with the heart’s output. This concentration rises in response to an increase in cardiopulmonary bypass (CPB) flow and means arterial pressure. 

Patients undergoing cardiac surgery that involves CPB have been subjected to clinical observational studies, which have revealed that the patient’s bladder PuO² has predictive significance for subsequent AKI. Therefore, continuous bladder PO² shows potential as a new clinical tool for monitoring the adequate oxygenation of the renal medullary, which has implications for the diagnosis and prevention of medullary hypoxia and, as a result, acute kidney injury (AKI).

Source: ccforum.biomedcentral.com/articles/10.1186/s13054-022-04230-7