Renal Tissue Oxygenation with Renal Arterial Stenosis

Abstract

Functional renal oxygen consumption, VrO2 is due to tubular reabsorption of sodium (TNa) in the proximal (∼67%) and distal(∼30%) nephrons, resulting in compartments (cortex/medulla) with distinct VrO2/TNa relationships. A progressive drop in renal blood flow (RBF) with renal arterial stenosis (RAS), disrupts O2 delivery, vital for reabsorption. The overall objective for the study is to determine the intra‐renal regional alterations in tissue oxygenation (PtO2) and theVrO2/TNa relationship in acute RAS. The hypothesis is RAS is accompanied by intra‐renal regional changes in oxygenation. Unilateral acute RAS was induced in 8 pigs by an extra‐vascular balloon. RBF and PtO2 were measured continuously with an ultrasound flow probe during baseline, RBF autoregulation and 3 sequential decreases in RBF, recovery, and furosemide administration. VrO2 was determined using Fick arterio‐venous differences. There were concomitant decreases in VrO2, and PtO2 throughout the occlusion periods. Medullary PtO2 changes were 35% more pronounced than cortical. This study suggests medullary decreases in PtO2 are more aggravated than cortical changes with reductions in RBF, accentuating the medulla's vulnerability to progressive RAS. Mild to moderately severe obstructions seem to preserve the tubular transport costs.Funding provided by NIH Grant (HL16496‐32), 2007 APS Porter Physiology Fellowship and the Mayo Foundation.