Experimental Renal Erythrocytosis. I. Effects of Pressure and Vascular Interference.

I HE ASSOCIATION of renal neoplasms with erythrocytosis is now well known, although the mechanism by which the erythrocytosis develops remains obscure. The possibility is present that the tumor cells themselves secrete an erythropoietic principle which, by its action on the bone marrow, leads to erythrocytosis. Erythrocytosis is, at times however, associated with single or multiple renal cysts or with hydronephrosis; here, the secretion of a stimulatory substance by cellular components of the lesion itself can almost certainly be excluded. In such cases the possibility may be considered that the pressure exerted by the expanding lesion’, be it a tumor, renal cyst or hydronephrosis, on the surrounding renal parenchyma results in the secretion of an erythropoietic principle by the renal parenchyma. It has been well established that the kidney is the main site of erythropoietin production or activation (Jacobson’). However, no experimental evidence exists to show that erythrocytosis results from various renal lesion’s. Van Lessen et al2 demonstrated increased erythropoietic activity in the blood collected from the renal vein of a dog after partial ligation of the vein and Takaku et a13 found elevations of erythropoietin levels in animals in which the renal artery had been constricted. The present study was designed to test the hypothesis that pressure exerted on normal renal parenchyma may result in erythrocytosis and also to determine the possible role of renal blood vessels and of erythropoietin in its production.