Abstract

Multiple forms of acute and chronic kidney disease are associated with renal tissue hypoxia. This has led to the proposition that renal hypoxia is not just a consequence of kidney disease, but rather a primary pathogenic event. Using telemetric technology to chronically measure the partial pressure of oxygen (PO2), we recorded cortical PO2 during the early stages of development of chronic kidney disease (CKD) in conscious rats. Male Wistar rats underwent 5/6 subtotal nephrectomy (n = 4) or sham (n = 4) surgery. After an initial increase, cortical PO2 values decreased in the first 2 weeks after induction of CKD and thereafter remained stable for the subsequent 6 weeks with an average reduction of 42 ± 12% compared to baseline. Sham operation had little effect on cortical PO2. The decrease in tissue PO2 in the remnant kidney occurred before proteinuria and uremia suggesting that hypoxia precedes the symptoms of CKD and therefore could be a major driver of the subsequent pathology. This is consistent with the hypothesis that kidney hypoxia is central in the pathogenesis of CKD.Grant Funding Source: EU, FP7, Marie Curie Actions, International Outgoing Fellowship

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