Predicting oxygen tension along the ureter

Lee, Chang Joon; Gardiner, Bruce S.; Evans, Roger G.; Smith, David W.

doi:10.1152/ajprenal.00122.2021

Cited by 7 publications

(8 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of the caveats for the understanding of relationship between urinary and medullary PO 2 is that it may be cofounded by several factors. A concern arising from experimental and computational models is that systemic arterial oxygen tension (PaO 2 ) may affect ureteric and bladder wall oxygenation which, in turn, may influence PuO 2 [ 7 – 10 ]. Experimental observations in anesthetized rabbits suggested that oxygen exchange within the urinary tract is slow and is unlikely to be a major confounder of the relationship between renal medullary tissue PO 2 and PuO 2 [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of changes in inspired oxygen fraction on urinary oxygen tension measurements

Osawa

Cutuli

Yanase

et al. 2022

ICMx

Self Cite

View full text Add to dashboard Cite

Background Continuous measurement of urinary PO2 (PuO2) is being applied to indirectly monitor renal medullary PO2. However, when applied to critically ill patients with shock, its measurement may be affected by changes in FiO2 and PaO2 and potential associated O2 diffusion between urine and ureteric or bladder tissue. We aimed to investigate PuO2 measurements in septic shock patients with a fiberoptic luminescence optode inserted into the urinary catheter lumen in relation to episodes of FiO2 change. We also evaluated medullary and urinary oxygen tension values in Merino ewes at two different FiO2 levels. Results In 10 human patients, there were 32 FiO2 decreases and 31 increases in FiO2. Median pre-decrease FiO2 was 0.36 [0.30, 0.39] and median post-decrease FiO2 was 0.30 [0.23, 0.30], p = 0.006. PaO2 levels decreased from 83 mmHg [77, 94] to 72 [62, 80] mmHg, p = 0.009. However, PuO2 was 23.2 mmHg [20.5, 29.0] before and 24.2 mmHg [20.6, 26.3] after the intervention (p = 0.56). The median pre-increase FiO2 was 0.30 [0.21, 0.30] and median post-increase FiO2 was 0.35 [0.30, 0.40], p = 0.008. PaO2 levels increased from 64 mmHg [58, 72 mmHg] to 71 mmHg [70, 100], p = 0.04. However, PuO2 was 25.0 mmHg [IQR: 20.7, 26.8] before and 24.3 mmHg [IQR: 20.7, 26.3] after the intervention (p = 0.65). A mixed linear regression model showed a weak correlation between the variation in PaO2 and the variation in PuO2 values. In 9 Merino ewes, when comparing oxygen tension levels between FiO2 of 0.21 and 0.40, medullary values did not differ (25.1 ± 13.4 mmHg vs. 27.9 ± 15.4 mmHg, respectively, p = 0.6766) and this was similar to urinary oxygen values (27.1 ± 6.17 mmHg vs. 29.7 ± 4.41 mmHg, respectively, p = 0.3192). Conclusions Changes in FiO2 and PaO2 within the context of usual care did not affect PuO2. Our findings were supported by experimental data and suggest that PuO2 can be used as biomarker of medullary oxygenation irrespective of FiO2.

show abstract

Section: Introductionmentioning

confidence: 99%

Effects of changes in inspired oxygen fraction on urinary oxygen tension measurements

Osawa

Cutuli

Yanase

et al. 2022

ICMx

Self Cite

View full text Add to dashboard Cite

show abstract

“…Whilst bladder tPO 2 could contaminate bladder PuO 2 measurement, it appears that the oxygen diffusion between bladder tPO 2 and bladder PuO 2 contributes little to final bladder PuO 2 value, which is chiefly influenced by the PuO 2 of urine entering the bladder from the ureter [ 30 ]. This ureteric PuO 2 value is in turn determined by the time available for oxygen diffusion between ureteric wall and the urine (a function of the transit time of each bolus of urine and the bolus volume) [ 75 ]. Consequently, the major confounders of the relationship between renal medullary (or pelvic ureteric) PuO 2 and bladder PuO 2 appear to be the patient’s systemic oxygenation and their rate of urine flow.…”

Section: Limitationsmentioning

confidence: 99%

“…Thus, as urine flow becomes greater, the error in the estimate of medullary PO 2 generated by measurement of urinary PO 2 becomes less. In contrast, as urine flow becomes less and a patient becomes progressively hyperoxemic or hypoxemic, the error becomes greater [ 75 ]. Therefore, in a clinical setting, estimating medullary oxygenation directly from measurement of urinary PO 2 is probably most useful when patients have a normal or high urine flow.…”

Section: Limitationsmentioning

confidence: 99%

“…The most sophisticated model developed to date predicts the existence of a family of linear relationships between bladder PuO 2 and pelvic ureteric PuO 2 for any given set of input conditions of urine flow and systemic arterial PO 2 in human patients (Fig. 4 ) [ 75 ]. Thus, it should be technically possible to predict renal medullary tPO 2 in real time based on continuous measurement of bladder PuO 2 , provided accurate and real-time measurements of urine flow and arterial PO 2 are available.…”

Section: Limitationsmentioning

confidence: 99%

“…

Fig. 4 Contour plot of urine flow, bladder PuO 2 and pelvic PuO 2 under modelling conditions of A normoxia (PaO 2 = 90 mmHg) and B hyperoxia (PaO 2 = 300 mmHg) and other assumptions as per Lee et al [ 75 ]. Figure reproduced with permission …”

Section: Limitationsmentioning

confidence: 99%

See 2 more Smart Citations

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

Lankadeva

Yanase

et al. 2022

Crit Care

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Urinary oxygen tension and its role in predicting acute kidney injury: A narrative review

Wang,

Song,

Wang

et al. 2024

Journal of Clinical Anesthesia

View full text Add to dashboard Cite

Predicting oxygen tension along the ureter

Cited by 7 publications

References 74 publications

Effects of changes in inspired oxygen fraction on urinary oxygen tension measurements

Effects of changes in inspired oxygen fraction on urinary oxygen tension measurements

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

Urinary oxygen tension and its role in predicting acute kidney injury: A narrative review

Contact Info

Product

Resources

About