Renal Adaptation to Anemia

Abstract

Renal adaptation to anemia was studied in dogs that had been bled repeatedly during a week to produce hematocrit values of between 12 and 21%. Total renal blood flow was unaltered despite a significant increase in cardiac output. Total renal oxygen consumption was within normal limits, but the Po 2 of cortical tissue was significantly reduced. Glomerular filtration rate and therefore filtered sodium load were reduced. These alterations were interpreted as resulting from preglomerular vasoconstriction together with a decrease in postglomerular vascular resistance, the latter perhaps a consequence chiefly of the diminished blood viscosity. Sodium reabsorption in relation to filtered sodium load was unimpaired in anemic animals; actually the sodium excretion factor was lower than in normal animals. It is concluded that the maintenance of normal renal function in the anemic animal is obtained by a decrease in work load (i.e. reduced glomerular filtration rate) and more efficient oxygen extraction related to increased blood tissue Po 2 gradient. Increased titers of erythropoiesis-stimulating substance could be demonstrated in these anemic animals. It is suggested that the low cortical tissue Po 2 is responsible for the release of this factor.