Optimal BP medication for kidney transplant recipients

What is the optimal blood pressure medication for kidney transplant recipients?

Because there is no evidence that a particular class of antihypertensive agents is more effective than other classes, the choice of medications should be individualized and based on various comorbidities. Calcium channel blockers (CCBs) are an attractive first-line agent, mainly because they counteract the vasoconstrictive effects of CNIs. CCB use may cause untoward effects, particularly nondependent edema and worsening proteinuria. In addition, CNI doses may need reduction with the use of nondihydropyridine CCBs.

The use of angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs) in kidney transplant recipients is safe. However, the effectiveness has been questioned. Hiremath et al. performed a meta-analysis of eight trials involving a total of 1502 patients, with only two trials going beyond 5 years. The study did not show an improvement in kidney outcomes. Other studies have shown the use of ACE inhibitors/ARBs has been associated with prolonged allograft and patient survival. In summary, ACE inhibitors/ARBs should be used thoughtfully, weighing the pros and cons in the transplant patient.

Because the combination of afferent arteriolar vasoconstriction from CNI and efferent arteriolar vasodilation as a result of renin-angiotensin system (RAS) blockade can predispose to acute kidney injury, we routinely advise our patients to discontinue their ACE inhibitors/ARBs if they are acutely ill and at risk for volume depletion. In addition, we advise postponing the addition of RAS blockers until 3 months post transplantation to avoid superfluous kidney biopsies.

Beta blockers should be considered in all kidney transplant patients with CVD. Diuretics can be used to control volume-mediated HTN and to enhance the antihypertensive effects of ACE inhibitors/ARBs. These drugs help with volume control and augment urine output. Thiazide-type diuretics are particularly effective at countering CNI-induced hyperkalemia. Alpha-1 blockers and centrally acting agents may be necessary to achieve blood pressure goals.

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