Oxygen Tension of the Urine and Renal Structures

Leonhardt, Kurt O.; Landes, Ralph R.

doi:10.1056/nejm196307182690301

Cited by 110 publications

(43 citation statements)

References 9 publications

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“…Notably, Leonhardt et al reported that urinary P O2 decreases along the ureter, in direct contradiction with our model’s prediction, which indicates a substantial increase (see Fig. 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.…”

Section: Discussioncontrasting

confidence: 99%

“…In contrast, substantially higher medullary tissue P O2 (~30 mmHg) has been reported in unanesthetized sheep [6]. Similarly high renal pelvic urine P O2 values have been reported in anesthetized dogs (27 mmHg) [46] and in humans (28 mmHg) [34]. Notably, Leonhardt et al reported that urinary P O2 decreases along the ureter, in direct contradiction with our model’s prediction, which indicates a substantial increase (see Fig.…”

Section: Discussioncontrasting

confidence: 74%

“…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. For example, given the low tissue P O2 in the inner medulla (~10 mmHg) [14], it seems unlikely that pelvic urinary P O2 can rise to 50 mmHg, the value measured in human [34]. To reconcile these differences, one would need a better understanding of the anatomic structures and of renal and medullary blood flow autoregulation in humans.…”

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: 99%

Section: Discussioncontrasting

confidence: 74%

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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“…In studies of anesthetized human volunteers [55], the PuO 2 is fairly constant under normal conditions. The PuO 2 decreases in states of volume depletion and increases following volume re-expansion.…”

Section: Assessment Of Kidney Oxygenation and Metabolismmentioning

confidence: 99%

Physiological Biomarkers of Acute Kidney Injury: A Conceptual Approach to Improving Outcomes

Okusa

Jaber

Doran

et al. 2013

Contributions to Nephrology

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The past 5–10 years have brought significant advances in the identification and validation of novel biochemical biomarkers in the prevention and treatment of acute kidney injury (AKI). These biochemical biomarkers remain research tools but we anticipate that soon they will be employed in clinical practice. A Consensus Conference held by the Acute Dialysis Quality Initiative (ADQI) recently reviewed the evidence, and identified gaps and a research agenda. Furthermore, at this meeting was the birth of an initiative to comprehensively identify new opportunities to characterize the physiological changes during the course of AKI based upon a conceptual framework for the detection and monitoring of renal ischemia-reperfusion injury. This framework includes a transition from monitoring physiological biomarkers of adequate renal perfusion, to pathophysiologic biomarkers of renal hypoperfusion, and finally biomarkers of kidney cell structural injury/damage. Techniques to measure physiological changes in AKI include several physiological variables that might be used in an interactive way to supplement clinical information and biochemical damage biomarkers in the diagnosis and management of AKI. This review summarizes the spectrum of physiological parameters and potential new physiological methods that enable identification of high-risk patients for AKI, facilitate early diagnosis, and differential diagnosis to guide therapeutic management and prognostication. Finally, we propose a research agenda for the next 5 years to facilitate the development and validation of physiological biomarkers in AKI.

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“…Murphy et al (1963) have shown a definite increase in the directly measured renal blood-flow during sustained haemorrhagic hypotension in dogs, without having increased the blood-volume. Leonhardt and Landes (1963) found that infusion of mannitol in six dehydrated patients increased the partial pressure of oxygen in the urine from a mean of 29 mm. to a mean of 67 mm.…”

mentioning

confidence: 97%

Mannitol Therapy in Oliguria of Acute Onset

Eliahou¹

1964

BMJ

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Oxygen Tension of the Urine and Renal Structures

Cited by 110 publications

References 9 publications

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

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

Physiological Biomarkers of Acute Kidney Injury: A Conceptual Approach to Improving Outcomes

Mannitol Therapy in Oliguria of Acute Onset

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