Urinary Oxygen Pressure in Renal Parenchymal and Vascular Disease

Leonhardt, Kurt O.

doi:10.1001/jama.1965.03090170023008

Cited by 16 publications

(5 citation statements)

References 15 publications

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“…4B) [34]. Indeed, based on their findings, Leonhardt and Landes concluded that urinary P O2 “reflects the interstitial P O2 in the medulla” [35], again in contrast to our conclusion. These discrepancies suggest that there may be fundamental differences in renal hemodynamics and medullary oxygenation between the rat and larger animals like sheep and human.…”

Section: Discussioncontrasting

confidence: 72%

“…4b ). Indeed, on the basis of their findings, Lenhardt & Landes (1965 ) concluded that urinary P \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$_{\rm O2}$\end{document} ‘reflects the interstitial P \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$_{\rm O2}$\end{document} in the medulla,’ again in contrast to our conclusion. These discrepancies suggest that there may be fundamental differences in renal haemodynamics and medullary oxygenation between the rat and larger animals like sheep and human.…”

Section: Discussionmentioning

confidence: 99%

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Renal medullary and urinary oxygen tension during cardiopulmonary bypass in the rat

Sgouralis

Evans

2016

Math Med Biol

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Renal hypoxia could result from a mismatch in renal oxygen supply and demand, particularly in the renal medulla. Medullary hypoxic damage is believed to give rise to acute kidney injury, which is a prevalent complication of cardiac surgery performed on cardiopulmonary bypass (CPB). To determine the mechanisms that could lead to medullary hypoxia during CPB in the rat kidney, we developed a mathematical model which incorporates (i) autoregulation of renal blood flow and glomerular filtration rate, (ii) detailed oxygen transport and utilization in the renal medulla, and (iii) oxygen transport along the ureter. Within the outer medulla, the lowest interstitial tissue PO2, which is an indicator of renal hypoxia, is predicted near the thick ascending limbs. Interstitial tissue PO2 exhibits a general decrease along the inner medullary axis, but urine PO2 increases significantly along the ureter. Thus, bladder urinary PO2 is predicted to be substantially higher than medullary PO2. The model is used to identify the phase of cardiac surgery performed on CPB that is associated with the highest risk for hypoxic kidney injury. Simulation results indicate that the outer medulla’s vulnerability to hypoxic injury depends, in part, on the extent to which medullary blood flow is autoregulated. With imperfect medullary blood flow autoregulation, the model predicts that the rewarming phase of CPB, in which medullary blood flow is low but medullary oxygen consumption remains high, is the phase in which the kidney is most likely to suffer hypoxic injury.

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Section: Discussioncontrasting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Renal medullary and urinary oxygen tension during cardiopulmonary bypass in the rat

Sgouralis

Evans

2016

Math Med Biol

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“…Furthermore, pelvic ureteric PuO 2 increased with hydration, although the response time was delayed in patients with reduced renal perfusion (e.g. sepsis or shock) [ 38 ], whilst hypertonic saline infusion reduced pelvic ureteric PuO 2 , presumably due to the increased medullary oxygen consumption associated with salt loading [ 39 ]. Both pelvic PuO 2 and bladder PuO 2 were reported to rise with increasing inspired fraction of oxygen, although the response was sluggish in disease states such as pyelonephritis or azotemia [ 38 ].…”

Section: Experimental Studies In Animalsmentioning

confidence: 99%

“…sepsis or shock) [ 38 ], whilst hypertonic saline infusion reduced pelvic ureteric PuO 2 , presumably due to the increased medullary oxygen consumption associated with salt loading [ 39 ]. Both pelvic PuO 2 and bladder PuO 2 were reported to rise with increasing inspired fraction of oxygen, although the response was sluggish in disease states such as pyelonephritis or azotemia [ 38 ]. Additionally, the investigators reported that PuO 2 was altered with agents that affect sympathetic tone, in a manner independent of urine flow [ 37 ].…”

Section: Experimental Studies In Animalsmentioning

confidence: 99%

“…Finally, the implications of disease states of the kidney for measurements of bladder PuO2 remain to be fully elucidated, as recent clinical studies have been performed largely on patients without established kidney disease [ 55 – 58 ]. Furthermore, an elevated ureteric PuO 2 has been noted in established hydronephrosis and could also occur with renal cysts, due to medullary thinning and the influence of renal cortical oxygenation on measurements [ 38 ]. Nevertheless, it remains possible that trends in bladder PuO 2 could still be useful as a reflection of the adequacy of medullary oxygenation.…”

Section: Limitationsmentioning

confidence: 99%

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Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill

Lankadeva

Yanase

et al. 2022

Crit Care

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Acute kidney injury (AKI) is common in the critically ill. Inadequate renal medullary tissue oxygenation has been linked to its pathogenesis. Moreover, renal medullary tissue hypoxia can be detected before biochemical evidence of AKI in large mammalian models of critical illness. This justifies medullary hypoxia as a pathophysiological biomarker for early detection of impending AKI, thereby providing an opportunity to avert its evolution. Evidence from both animal and human studies supports the view that non-invasively measured bladder urinary oxygen tension (PuO2) can provide a reliable estimate of renal medullary tissue oxygen tension (tPO2), which can only be measured invasively. Furthermore, therapies that modify medullary tPO2 produce corresponding changes in bladder PuO2. Clinical studies have shown that bladder PuO2 correlates with cardiac output, and that it increases in response to elevated cardiopulmonary bypass (CPB) flow and mean arterial pressure. Clinical observational studies in patients undergoing cardiac surgery involving CPB have shown that bladder PuO2 has prognostic value for subsequent AKI. Thus, continuous bladder PuO2 holds promise as a new clinical tool for monitoring the adequacy of renal medullary oxygenation, with its implications for the recognition and prevention of medullary hypoxia and thus AKI.

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