Posttransplant erythrocytosis (PTE) is an often-recognized but poorly understood complication of renal transplantation. Defined as a persistently elevated hematocrit (> 0.51), it occurs most commonly during the first 2 years posttransplant in hypertensive males with excellent allograft function. Its consequences are disputed, but may include increased risk of thromboembolic events. Traditionally, PTE has been thought to reflect excess erythropoietin production, of either native kidney or allograft origin, and to abate spontaneously with time. More recent data indicate that factors other than erythropoietin may be involved in the pathogenesis of PTE and that spontaneous resolution is relatively uncommon. Standard treatments have included serial phlebotomy and native kidney nephrectomy. It now appears that PTE also can be managed safely and effectively with converting enzyme inhibitors, a development that challenges our previous understanding of PTE and offers new avenues for investigating its pathogenesis.