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Determinants of kidney oxygen consumption and their relationship to tissue oxygen tension in diabetes and hypertension
Uppsala University, Sweden .
Georgetown University, DC, USA .
University of California San Diego, CA, USA.
Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Health Sciences.
2013 (English)In: Clinical and experimental pharmacology & physiology, ISSN 0305-1870, E-ISSN 1440-1681, Vol. 40, no 2, 123-137 p.Article, review/survey (Refereed) Published
Abstract [en]

The high renal oxygen (O2) demand is associated primarily with tubular O2 consumption (Qo2) necessary for solute reabsorption. Increasing O2 delivery relative to demand via increased blood flow results in augmented tubular electrolyte load following elevated glomerular filtration, which, in turn, increases metabolic demand. Consequently, elevated kidney metabolism results in decreased tissue oxygen tension. The metabolic efficiency for solute transport (Qo2/TNa) varies not only between different nephron sites, but also under different conditions of fluid homeostasis and disease. Contributing mechanisms include the presence of different Na+ transporters, different levels of oxidative stress and segmental tubular dysfunction. Sustained hyperglycaemia results in increased kidney Qo2, partly due to mitochondrial dysfunction and reduced electrolyte transport efficiency. This results in intrarenal tissue hypoxia because the increased Qo2 is not matched by a similar increase in O2 delivery. Hypertension leads to renal hypoxia, mediated by increased angiotensin receptor tonus and oxidative stress. Reduced uptake in the proximal tubule increases load to the thick ascending limb. There, the increased load is reabsorbed, but at greater O2 cost. The combination of hypertension, angiotensin II and oxidative stress initiates events leading to renal damage and reduced function. Tissue hypoxia is now recognized as a unifying pathway to chronic kidney disease. We have gained good knowledge about major changes in O2 metabolism occurring in diabetic and hypertensive kidneys. However, further efforts are needed to elucidate how these alterations can be prevented or reversed before translation into clinical practice.

Place, publisher, year, edition, pages
Blackwell Publishing , 2013. Vol. 40, no 2, 123-137 p.
Keyword [en]
diabetes, hypertension, hypoxia, kidney, oxygen consumption, tissue oxygenation
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-89738DOI: 10.1111/1440-1681.12034ISI: 000314244300009OAI: oai:DiVA.org:liu-89738DiVA: diva2:609743
Note

Funding Agencies|Swedish Science Council - Medicine||National Institutes of Health (NIH)|HL089583HL068686R01DK-28602|OBrien Kidney Center for Acute Kidney Injury|P30DK-079337|Department of Veterans Affairs Research Service||

Available from: 2013-03-07 Created: 2013-03-05 Last updated: 2017-12-06

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Palm, Fredrik

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