In this study factors possibly contributing to the development of erythrocytosis after renal transplantation (PTE) were analyzed. Out of 131 transplanted patients nine developed PTE (mean hemoglobin 17. 9 +/- 0.3 g/dl) 2 to 27 months after transplantation (group 1) and were compared to the nine with normal hemoglobin concentration (mean hemoglobin 12.4 +/- 0.2 g/dl, control group 2). The study was performed about two years after transplantation (25 +/- 3.9 months group 1 and 23.7 +/- 2.6 months group 2). Immunosuppressive therapy given in standard doses consisted of cyclosporine, azathioprine and prednisone. At the onset of the study no difference in renal graft function was noted between the groups (for group 1 sCr = 111.7 +/- 10.4 micromol/l and for group 2 sCr = 154.6 +/- 27.6 micromol/l). The mean serum immunoreactive erythropoietin (Epo) levels were significantly higher in PTE patients compared to control group of patients (33.9 +/- 4.6 mU/ml vs 21.6 +/- 2.5 mU/ml, p = 0.03). In addition, the ratio between observed to expected (O/E) Epo, a useful index in assessing Epo secretion in renal transplant patients, was ten times higher for group 1 than for group 2 (Median value 10.0 vs. 1.05). Spontaneous growth of Burst-forming unit- erythroid (BFU-E) in peripheral blood was detected in 5 out of 9 patients from group 1 and none in patients from group 2 (p = 0.04). Burst Promoting Activity (BPA) in Phytohemagglutinine Stimulated Leukocytes Condition Medium (PHA-LCM) from patients blood were higher in the PTE patients than in controls. Whole blood cyclosporine levels were higher in group 1 than in group 2 throughout the first 30 weeks after transplantation. It was concluded that sustained erythropoiesis after correction of renal anemia by kidney transplantation, leading to PTE could be explained as a consequence of increased levels of Epo and BPA and increased sensitivity of early erythroid progenitors to these stimulators induced by high cyclosporine levels.