Aliskiren in the treatment of renal disease; a narrative review

Abstract

The renin–angiotensin–aldosterone system (RAAS) cascade has a significant effect on several systems. Angiotensin II (AngII) has appeared as not only a vasoactive peptide but also as a multifunctional cytokine that displays several non-hemodynamic properties beyond renal hemodynamic properties. The kidney includes total components of the RAAS such as aldosterone and AngII not only adjust renal hemodynamics and reabsorption of sodium but also activating various inflammatory and fibrotic responses. Inhibition of the RAAS is one of the most potent methods to impede the development of renal diseases such as chronic kidney disease (CKD) and its related problems such as high blood pressure and heart disorders. Aliskiren, an octanamide, nonpeptide piperidine, orally, active, first commercially available, and direct renin inhibitor (DRI), impedes RAAS and operates by attaching to the active sites of renin and may be effective for the management of renal disease because of blocking the RAAS at its point of start and most sensitive step. Based on numerous studies, aliskiren is the greatest powerful inhibitor of AngII extents among RAAS inhibitors, even though it is unable to prevent the (pro) renin receptor-mediated extracellular signal-regulated kinase 1 and 2 (ERK1/2) activations. In this review, it is described renoprotective effects of aliskiren against different types of nephropathy such as acute kidney injury, diabetic nephropathy, and hypertensive nephropathy.

Keywords: Renin–angiotensin–aldosterone system, Angiotensin II, Direct renin inhibitor, Chronic kidney disease, Acute kidney injury, Hypertensive nephropathy, Aliskiren