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Marina Lopez-Martinez and María José Soler

Endothelin-1 (ET-1) plays a role in chronic kidney disease (CKD) progression (1). In the kidney, ET-1 binding of the endothelin A (ETA) receptor drives afferent arteriole vasoconstriction, cell proliferation, podocyte and glycocalyx damage, matrix accumulation, and proinflammatory effects, whereas binding of the endothelin B (ETB) receptor produces vasodilation, antifibrotic effects, and decreased sodium reabsorption and natriuresis (1, 2). Although renin-angiotensin-aldosterone system (RAAS) inhibition has proven a reduction of albuminuria and a proportional effect on kidney protection (3, 4), residual albuminuria still implies a significant risk of CKD progression (5