Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia

摘要

Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O2 delivery, and O2 consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O2 delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O2. Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O2 consumption decreased proportionally to O2 delivery during the graded stenosis (19 ± 10.8, 48.2 ± 9.1, 58.9 ± 4.7 vs. 15.1 ± 5, 35.4 ± 3.5, 57 ± 2.3%, respectively) while arterial venous O2 differences were unchanged. Acute RAS produced a sharp reduction in O2 efficiency for sodium reabsorption (P < 0.01). Cortical decreases are exceeded by medullary decreases during stenosis (34.8 ± 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O2 delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.