Posttransplantation hypertension can be caused by:

A. Rejection.

B. Cyclosporine nephrotoxicity.

C. Renal transplant artery stenosis (RTAS).

D. Recurrent disease in the allograft. 

DISCUSSION: Both acute and chronic rejection may result in hypertension. The former causes acute fluid retention and plugging of peritubular capillaries with inflammatory cells. This may progress to intimal swelling and medial necrosis and eventuate in ischemia secondary to endothelial proliferation and obliteration of small vessels. Chronic rejection, thought to be related to protracted humoral injury, results in obliteration of capillaries via the development of intimal hyperplasia. Cyclosporine has a vasoconstrictive effect which, through activation of the renin-angiotensin system, may lead to hypertension. RTAS is responsible for hypertension in 4% to 12% of renal allograft recipients. It responds well to percutaneous angioplasty. A careful trial of angiotensin-converting enzyme inhibitors may be diagnostic of RTAS. Recurrent disease such as membranoproliferative glomerulonephritis and focal glomerular sclerosis may result in significant hypertension in renal allograft recipients.