Are the native kidneys responsible for erythrocytosis in renal allorecipients?
The development of erythrocytosis following renal transplantation has been reported to be caused by a number of factors. These include acute and chronic rejection, hydronephrosis and renal artery stenosis. In this study, seven patients were noted to have erythrocytosis with hematocrits ranging between 53.5 and 66%. Serum erythropoietin levels were elevated and ranged between 11 and 60 mU/ml with a mean of 31.9 mU/ml in six of seven patients. Selective catheterization of veins of native and transplanted kidneys in three patients revealed mean serum levels of 40.9 and 13.0 mU/ml, respectively. This suggests that excess erythropoietin is being produced from the diseased native kidneys. Bilateral nephrectomy in one patient cured erythrocytosis and dropped systemic levels of erythropoietin (EP) to 6.1 mU/ml. In four of the remaining five patients, hematocrits came down spontaneously to within normal over a 1- to 3-year period. Consequently, it appears that in a number of transplant patients the retained diseased kidneys, having lost all excretory and concentrating function, may remain capable of functioning as endocrine erythropoietin-producing organs.
D004921:Erythropoietin / Q000096:biosynthesis; D006400:Hematocrit; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D016030:Kidney Transplantation; D011086:Polycythemia / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D011183:Postoperative Complications / Q000097:blood / Q000503:physiopathology*; D014184:Transplantation, Homologous
D004921:Erythropoietin