Direct renin inhibition and other strategies to more effectively block the intrarenal renin-angiotensin-aldosterone system may help reduce the progression of chronic kidney disease.
This review emphasizes the pathogenic role of the intrarenal RAAS in CKD and explores direct renin inhibition as a potential strategy to overcome the limitations of current ACEi/ARB therapies.
The existence of local or tissue-based renin-angiotensin-aldosterone systems (RAAS) is well documented and has been implicated as a key player in the pathogenesis of cardiovascular and renal diseases. The kidney contains all elements of the RAAS, and intrarenal formation of angiotensin II not only controls glomerular hemodynamics and tubule sodium transport, but also activates a number of inflammatory and fibrotic pathways. Experimental and clinical studies have shown that the intrarenal RAAS is activated early in diabetic nephropathy, the leading cause of chronic kidney disease (CKD). Although angiotensin-converting enzyme inhibitors and angiotensin receptor blockers decrease the rate of decline in kidney function in patients with diabetic and non-diabetic nephropathy, many patients still progress to end-stage renal disease or die from cardiovascular events. There is still a clear need for additional strategies to block the RAAS more effectively to reduce progression of CKD. The focus of this paper is to review the importance of the intrarenal RAAS in CKD and recent findings in renin-angiotensin biology pertinent to the kidney. We also discuss additional strategies to inhibit the RAAS more effectively and the potential impact of direct renin inhibition on the prevention and management of CKD.
Siragy et al. (Fri,) conducted a review in Chronic Kidney Disease. RAAS inhibition / direct renin inhibition was evaluated. Direct renin inhibition and other strategies to more effectively block the intrarenal renin-angiotensin-aldosterone system may help reduce the progression of chronic kidney disease.