Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill
Abstract 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 justi...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-12-01
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| Series: | Critical Care |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s13054-022-04230-7 |
| _version_ | 1811292119940202496 |
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| author | Raymond T. Hu Yugeesh R. Lankadeva Fumitake Yanase Eduardo A. Osawa Roger G. Evans Rinaldo Bellomo |
| author_facet | Raymond T. Hu Yugeesh R. Lankadeva Fumitake Yanase Eduardo A. Osawa Roger G. Evans Rinaldo Bellomo |
| author_sort | Raymond T. Hu |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-04-13T04:39:33Z |
| format | Article |
| id | doaj.art-58bf57457a5a416b992cc0e630c6e547 |
| institution | Directory Open Access Journal |
| issn | 1364-8535 |
| language | English |
| last_indexed | 2024-04-13T04:39:33Z |
| publishDate | 2022-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Critical Care |
| spelling | doaj.art-58bf57457a5a416b992cc0e630c6e5472022-12-22T03:02:02ZengBMCCritical Care1364-85352022-12-012611910.1186/s13054-022-04230-7Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically illRaymond T. Hu0Yugeesh R. Lankadeva1Fumitake Yanase2Eduardo A. Osawa3Roger G. Evans4Rinaldo Bellomo5Department of Anaesthesia, Austin HealthDepartment of Critical Care, Melbourne Medical School, The University of MelbourneDepartment of Intensive Care, Austin HospitalCardiology Intensive Care Unit, DF Star HospitalPre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of MelbourneDepartment of Critical Care, Melbourne Medical School, The University of MelbourneAbstract 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.https://doi.org/10.1186/s13054-022-04230-7Acute kidney injuryUrine oximetryRenal medullary hypoxiaCritical care |
| spellingShingle | Raymond T. Hu Yugeesh R. Lankadeva Fumitake Yanase Eduardo A. Osawa Roger G. Evans Rinaldo Bellomo Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill Critical Care Acute kidney injury Urine oximetry Renal medullary hypoxia Critical care |
| title | Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| title_full | Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| title_fullStr | Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| title_full_unstemmed | Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| title_short | Continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| title_sort | continuous bladder urinary oxygen tension as a new tool to monitor medullary oxygenation in the critically ill |
| topic | Acute kidney injury Urine oximetry Renal medullary hypoxia Critical care |
| url | https://doi.org/10.1186/s13054-022-04230-7 |
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