Factors predisposing to post-renal transplant erythrocytosis. A prospective matched-pair control study

• Published in: Clinical nephrology Vol. 45; no. 2; p. 83
• Main Authors: Kessler, M, Hestin, D, Mayeux, D, Mertes, P M, Renoult, E
• Format: Journal Article
• Language: English
• Published: Germany 01-02-1996
• Subjects: Adult; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Case-Control Studies; Causality; Female; Humans; Immunosuppressive Agents - therapeutic use; Kidney Transplantation; Male; Middle Aged; Polycythemia - diagnosis; Polycythemia - drug therapy; Polycythemia - epidemiology; Postoperative Complications - diagnosis; Postoperative Complications - drug therapy; Postoperative Complications - epidemiology; Prevalence; Prospective Studies; Risk Factors; Sex Factors; Treatment Outcome
• ISSN: 0301-0430

We conducted a prospective study on 81 consecutive patients who had a kidney transplant with graft function for over 3 months to evaluate the prevalence of erythrocytosis following renal transplantation (PTE) and its potential risk factors. True PTE was defined as a RBC mass > 120% of the theoretical value allowing for sex, weight and height. 18 patients (22.2%) developed PTE (RBC mass = 157 +/- 21%) with no evidence of polycythemia vera (PV), or secondary polycythemia due to reduced arterial oxygen, kidney or hepatic tumors. PTE was more common in males (p = 0.041) and less common in patients treated with recombinant erythropoietin (rHEPO) prior to transplantation. 18 non-polycythemic patients (Hb 12.6 +/- 1.3 g/dl) matched for sex, age and renal function were used as case controls. Fewer PTE patients were transfused post-transplantation (p = 0.026). At the time of diagnosis, mean serum EPO was normal and similar to that of controls. PTE patients had lower serum ferritin (p = 0.005) and more commonly received iron supplementation when PTE occurred (p = 0.003). Other clinical factors did not differ significantly between the two groups. Two patients had a thrombotic event, 6 recovered spontaneously and 11 were successfully treated with angiotensin-converting enzyme inhibitors (ACEI). The normalization of Hb, hematocrit and RBC mass in ACEI treated patients was accompanied by a decline in serum EPO (p = 0.008). We conclude that true erythrocytosis is prevalent in cyclosporine-treated renal transplant patients. PTE seems to be an idiopathic erythrocytosis. Pretransplant rHEPO treatment may limit PTE by blunting the increased sensitivity of erythroid precursors to EPO and iron supplementation, which stimulates the development of PTE. ACEI treatment is effective and safe.