Hypertension, Living Kidney Donors, and Transplantation: Where Are We Today?

Hypertension is a prevalent problem in kidney transplant recipients that is known to be a “traditional” risk factor for atherosclerotic cardiovascular disease leading to premature allograft failure and death. Donor, peritransplant, and recipient factors affect hypertension risk. Blood pressure control after transplantation is inversely associated with glomerular filtration rate (GFR). Calcineurin inhibitors, the most commonly used class of immunosuppressives, cause endothelial dysfunction, increase vascular tone, and sodium retention via the renin-angiotensin-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 estimated GFR. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are not recommended in the first 3 to 6 months given their effects on reduced estimated GFR, anemia, and hyperkalemia. The use of ß-blockers may be associated with improved patient survival, even for patients without cardiovascular disease. Living donation may increase blood pressure by 5 mm Hg or more. Some transplant centers accept Caucasian living donors with well-controlled hypertension on a single agent if they agree to close follow-up.