The Effect of Ischemia and Hypoxia on Renal Blood Flow, Energy Metabolism and Function in Vivo

Abstract

The kidneys play a major role in maintaining body homeostasis by regulating the concentration of many of the plasma constituents, and by eliminating all the metabolic wastes. These functions are mediated via two interdependent regulatory systems that govern the rate of glomerular function and tubular secretion and reabsorption. For these processes the kidneys utilize 10% of the whole body oxygen consumption¹. Thus, a decrease in oxygen availability causes many abnormalities in cell physiology such as: increase in mitochondrial NADH², ATP depletion, cell swelling, an increase in intracellular free calcium, acidosis, phospholipase and protease activation, oxidant injury, inflammatory response, a reduction in glomerular filtration rate (GFR)^{2, 3}, inducing acute renal failure (ARF). Furthermore, reperfusion itself is known to enhance renal cellular damage by formation of reactive oxygen species⁴. Short periods of ischemia will allow resynthesis of ATP, whereas, prolonged ischemia may cause irreversible loss of mitochondrial function, further impairing regeneration of ATP. Therefore, the rate of cell ATP recovery is dependent on the ability of the cell to survive ischemia and also on the duration of the ischemic period³.