Renal Adaptation to Anemia

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 Po2 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 Po2 gradient. Increased titers of erythropoiesis-stimulating substance could be demonstrated in these anemic animals. It is suggested that the low cortical tissue Po2 is responsible for the release of this factor.

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