Elevation of red blood cell count (post -transplant erythrocytosis-PTE) develops in more than 15% of kidney transplant recipients, generally within two years after transplant. PTE may potentially increase the risk of thrombosis in vital organs. The cause of PTE is uncertain and may be due to signaling between erythropoietin and angiotensin. Erythropoietin is a protein growth factor produced by the kidneys that is required for the production of red blood cells. Recent studies suggest that another protein, angiotensin and its receptor appear to play a role in the pathogenesis of PTE. Others have shown that inhibition of angiotensin converting enzyme reduces circulating erythropoietin and angiotensin signaling pathways may be an important part of the mechanism of PTE. Our objective is to examine the signal transduction pathways through which angiotensin modulates red blood cell proliferation and the mechanism by which these pathways contribute to PTE. Blood will be drawn from 45 adults. The blood will be processed and studied to determine a) the expression of angiotensin receptor in red blood cell precursor from patients with PTE; b) the proliferatic ve response of red blood cell progenitors from patients with or without PTE to angiotensin; and c) the plasma level of Ac-SDPK (a factor involved in red blood cell production) in patients with PTE.
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