Post-transplant hypertension remains an important risk factor for cardiovascular mortality and graft function. There are multiple mechanisms responsible for post-transplant hypertension. The details of these mechanisms are poorly understood. Steroids, acute and chronic rejection, recurrent renal disease, native kidney disease, and renal artery stenosis have all been implicated in causing post-transplant hypertension. With the addition of cyclosporine, a known hypertensive agent, to the immunosuppressive armamentarium, the evaluation of post-transplantation hypertension has become difficult. Presently, medical therapy is initially directed toward the complications of cyclosporine nephrotoxicity. Empirically, converting enzyme inhibitors are added to the antihypertensive regimen. Further management is aimed at identification of specific causes of post-transplant hypertension. Unfortunately, because of the multifactorial etiology of post-transplant hypertension and a lack of detailed information about the mechanisms, medical and surgical therapy are often unrewarding. Further study is needed to clarify the mechanisms involved in post-transplant hypertension, and thus direct therapy.