Nierziekte

Aldosteronsynthase-remmers bij ongecontroleerde en resistente hypertensie bij CKD

Hypertensie komt veel voor bij CKD en is bij tot 40% van de patiënten resistent. Aldosterondysregulatie speelt hierin een centrale rol. Dit overzicht bespreekt de nieuwe klasse aldosteronsynthase-remmers (ASI's) als veelbelovende aanvulling op de bestaande behandelopties, van preklinisch bewijs tot klinische toepassingen.

Abstract (original)

Hypertension is highly prevalent in CKD and frequently remains uncontrolled despite high treatment rates; resistant hypertension occurrs in up to 40% of CKD patients and markedly increases renal and cardiovascular risk. Aldosterone dysregulation plays a central role in this setting, contributing not only to sodium retention and volume expansion but also to inflammation, fibrosis, and target-organ damage in the kidney, heart, and vasculature. While spironolactone is recommended as the preferable 4th agent in resistant hypertension, its use in advanced CKD is limited by scarce data, and high rates of hyperkalemia and declining kidney function. Aldosterone synthase inhibitors (ASIs) are an emerging therapeutic class that directly suppress aldosterone production. Recent phase-2 and phase-3 randomized controlled trials demonstrate that next-generation, selective ASIs produce clinically meaningful reductions in office and ambulatory BP in patients with uncontrolled and resistant hypertension, with an acceptable safety profile. Early, phase-2, trials have also showed that ASIs are effective in lowering office BP levels in CKD with accompanying substantial reductions in albuminuria. This review examines the potential clinical benefits of aldosterone synthesis targeted therapy in the management of uncontrolled and resistant hypertension in CKD.

Dit artikel is een samenvatting van een publicatie in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Voor het volledige artikel, alle details en referenties verwijzen wij u naar de oorspronkelijke bron.

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DOI: 10.1093/ndt/gfag013