Hypertension in the Kidney Transplant Recipient

Abstract

Hypertension is a prevalent problem in kidney transplant recipients that is known to be a “traditional” risk factor for ASCVD leading to premature allograft failure and death. Donor, transplant and recipient factors impact hypertension risk. Blood pressure control after transplantation is inversely associated with GFR. Calcineurin inhibitors, the most commonly used class of immunosuppressives, cause endothelial dysfunction, increase vascular tone, and sodium retention via the reninangiotensin-aldosterone system resulting in systemic hypertension. Steroid withdrawal seems to have little impact on blood pressure control. Newer agents like belatacept appear to be associated with less hypertension. Transplant renal artery stenosis is an important, potentially treatable cause of hypertension. Dihydropyridine calcium channel blockers mitigate calcineurin inhibitor nephrotoxicity and may be associated with improved eGFR. ACE inhibitors and angiotensin receptor blockers are not recommended in the first 3-6 months given their effects on reduced eGFR, anemia and hyperkalemia. The use of ßblockers may be associated with improved patient survival, even for patients with no history of cardiovascular disease.

The cumulative number of kidney transplant recipients living with a functioning allograft continues to grow approximating 186,303 in 2012 within the USA, a 3.6 % increase from 2011. This population is at increased risk for cardiovascular disease and death compared to the general population. Hypertension is a prevalent, important, independent traditional risk factor for the development of atherosclerotic cardiovascular disease, premature allograft failure, and death with a functioning allograft. Hypertension risk factors include: donor, peri-transplant, and recipient variables. Some of the more prominent specific risk factors associated with post-transplant hypertension include: deceased compared with live donor source, use of immunotherapeutics that promote salt retention and vasoconstriction, development of allograft renal artery stenosis, rejection and chronic allograft nephropathy. It has been suggested that hypertension may trigger mechanical injury that amplifies an initial immunological process, leading to tissue fibrosis and atrophy which subsequently decreases glomerular filtration rate (GFR). Blood pressure control post-transplantation has been associated with an improved allograft survival and reduced risk of death.