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Renal Oxygenation in Ischemic Acute Kidney Injury
Author(s) -
Bourgette Ryan,
Pham Hai,
Hepokoski Mark,
Thomson Scott,
Singh Prabhleen
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1217.17
Subject(s) - oxygenation , renal blood flow , kidney , renal function , ischemia , renal ischemia , medicine , chemistry , reabsorption , hypoxia (environmental) , oxygen , blood flow , hemodynamics , renal sodium reabsorption , cardiology , endocrinology , reperfusion injury , organic chemistry
There are unique features of renal oxygenation that render the kidney susceptible to oxygen demand‐supply mismatch and hypoxia, which are implicated in the pathogenesis of kidney imjury. Renal oxygen consumption by oxidative metabolism is closely coupled to and driven by tubular transport, which is linked to the filtered solute load and GFR. Hence, tubular transport is among the principal determinants of intrarenal oxygenation. We examined the early and late changes in renal oxygenation in ischemic AKI. We subjected rats to renal ischemia‐reperfusion (IR, bilateral pedicle clamp x 1h) or sham ischemia. After 4 or 24 hrs, rats were examined for oxygen delivery (renal blood flow), oxygen consumption (QO2) and GFR measurements and other hemodynamic measurements. At 4 and 24 hours post IR, GFR was significantly lower in the IR group ( Fig) vs. shams (*p<0.005). Renal blood flow (RBF) or mean arterial pressure (MAP) were not different between shams and IR at either the 4 hr or 24 hr time point. QO2 was variable but 3 times higher in IR compared to shams at 4 hrs, and QO2 factored for GFR was significantly higher at this time point, *p<0.01. At 24 hr time point, QO2 was similar between shams and IR, but QO2 factored for GFR was much higher in the IR group(#p=0.06). Our findings demonstrate an unchanged renal oxygen delivery but high oxygen consumption despite low GFR and filtered sodium. This is remarkable since the need for ATP for reabsorption of filtered Na is the major driver of renal oxygen consumption, indicating an uncoupling between tubular transport and metabolism in ischemic AKI. These findings were pronounced at the early stages after IR, less so, but persistent at 24 hrs. The underlying mechanisms for these findings and changes in tubular mitochondrial oxidative metabolism, cellular metabolic and survival pathways are being investigated. Support or Funding Information National Institute of Diabetes and Digestive and Kidney Diseases Grant K08‐DK‐084305 (P. Singh), Veterans Affairs (VA) Merit Award BX002175 (P. Singh), the University of Alabama at Birmingham‐University of California San Diego O'Brien Center (P30‐DK‐079337).Renal hemodynamics and oxygenation at 4 and 24 hours after IR