From the Guidelines
Renal artery stenosis increases renin production in the affected kidney by activating the renin-angiotensin-aldosterone system (RAAS) in response to decreased renal perfusion pressure. When the renal artery narrows, blood flow to the kidney decreases, causing a drop in pressure within the afferent arterioles. This reduced pressure is detected by specialized cells called juxtaglomerular cells, which respond by increasing their secretion of renin into the bloodstream 1. The elevated renin production activates the RAAS, converting angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II causes vasoconstriction and stimulates aldosterone release, leading to sodium and water retention. The resulting increase in blood pressure is the body's attempt to restore adequate kidney perfusion.
Some key points to consider in the management of renal artery stenosis include:
- The use of ACE inhibitors or angiotensin receptor blockers may worsen kidney function in patients with bilateral renal artery stenosis or stenosis in a solitary functioning kidney 1.
- Endovascular therapy, such as angioplasty with stenting, may be considered in patients with symptomatic renal artery stenosis secondary to atherosclerosis 1.
- Surgical revascularization may be considered for patients undergoing surgical repair of the aorta, patients with complex anatomy of the renal arteries, or after a failed endovascular procedure 1.
- The presence of asymptomatic renal artery stenosis is a strong predictor of subsequent mortality, and the severity of renal artery stenosis is independently associated with mortality 1.
Overall, the management of renal artery stenosis should prioritize the reduction of morbidity, mortality, and improvement of quality of life, and should be guided by the most recent and highest quality evidence available 1.
From the Research
Renal Artery Stenosis and Renin
- Renal artery stenosis (RAS) is a condition that affects the renal artery, leading to a decrease in blood flow to the kidney 2.
- The renin-angiotensin-aldosterone system (RAAS) plays a central role in the pathogenesis of RAS, with angiotensin II being a key player 2.
- The activation of RAAS is the primary element in the pathophysiological cascade triggered in response to renal artery stenosis, leading to increased oxidative stress and the release of pro-inflammatory mediators 2.
- RAS can lead to renovascular hypertension, ischemic nephropathy, and chronic kidney disease, with the RAAS system contributing to the development of these conditions 2, 3, 4.
Impact on Renin
- The exact impact of RAS on renin levels is not explicitly stated in the provided studies, but it is known that RAS activates the RAAS system, which includes renin 2.
- The RAAS system is a complex pathway that involves the conversion of renin to angiotensin I, which is then converted to angiotensin II, leading to vasoconstriction and increased blood pressure 5.
- Blockers of the RAAS system, such as renin inhibitors and angiotensin-converting enzyme (ACE) inhibitors, are used to treat hypertension and can affect renin levels 5.
- The relationship between RAS and renin is complex and involves multiple pathophysiological mechanisms, including disturbances in the endothelin, kinin-kallikrein, and sympathetic nervous systems 2.