Gaciong Z, Koziak K, Jarzyło I, Ludwicki K, Malanowska S, Paczek L, Szmidt J, Wałaszewski J, Lao M
Transplantation Institute, Warsaw Medical School, Poland.
Ann Transplant. 1996;1(1):29-33.
We studied production of erythropoietin (EPO) in long-term renal allograft recipients with posttransplant erythrocytosis (PTE). Among 951 recipients we found 74 patients with persistent elevation of hematocrit (Htc) value (female > 50%, male > 55%). However, only 63.5% of them had increased red-cell mass ( = "true" erythrocytosis). In all recipients with PTE known causes of secondary erythrocytosis were not found. EPO titer in peripheral blood was significantly higher in recipients with PTE (median 13.5 mIU/mL, range: 0.1-71.5 mIU/mL) as compared to healthy blood donors (median 5.75 mIU/mL, range: 0.1-19.5 mIU/mL) but not different from the group of renal allograft recipients without PTE (median 13.0, range 0.1-71.7 mIU/mL). However, EPO level measured in pretransplant sera was significantly higher in patients who developed PTE (median 16.4 mIU/mL, range: 1.0-281.2 mIU/mL) than in recipients without PTE (median 8.3, range: 1.0-50.3 mIU/mL). A significant difference in EPO level between systemic and effluent blood from native kidneys was found in 6 out of 14 recipients with PTE who underwent catheterization. After phlebotomy patients with PTE responded with higher increase in peak EPO titer than healthy blood donors (527 +/- 473% versus 194.5 +/- 44.2%, p < 0.05). Our results suggest that PTE develops spontaneously due to increased EPO production. Despite elevated EPO levels, regulation of EPO release remains preserved.
