The purpose of this review is to summarize current data on the role of
immunosuppressants in the pathogenesis of hypertension and the efficacy and
tolerability of major antihypertensive classes in kidney transplant recipients.
Arterial hypertension is a common complication after kidney transplantation
and a major risk factor for adverse outcome and graft rejection due to blood
pressure elevation by immunosuppressive medications.
Calcineurin inhibitors induce hypertension by a mechanism related to the imbalance
of vasoactive substances endothelin and nitric oxide, and probably by causing
overactivity of thiazide-sensitive sodium-chloride-cotransporter. Corticosteroids
are well known for their hypertensive effects. The interactions of calcineurin
inhibitors and mammalian target of rapamycin inhibitor sirolimus also promote hypertension.
Management of arterial hypertension is a complex problem in the care of kidney transplant recipients.
Target blood pressure values of <130/80 mm Hg are suggested by the National Kidney
Foundation/ Kidney Disease Outcomes Quality Initiative. Calcium channel blockers may be useful
in antagonizing the vasoconstrictive effects of calcineurin inhibitors. The renin-angiotensin
system inhibitors seem a good option, especially in patients with proteinuria, however their effects
on long-term graft and patient survival are controversial. β-Blockers could be beneficial in
patients with coronary heart disease, but caution is required due to metabolic adverse effects.
Thiazide diuretics could be the reasonable option for patients with glomerular filtration rate ≥30
mL/min/1.73 m2, also with caution regarding hypokalemia and glycemia.
Until more evidence is provided, the choice of optimal antihypertensive therapy in kidney transplant
recipients should be based on previous individual antihypertensive tolerability and efficacy,
comorbidities, concomitant medications and post-transplant kidney function.