Improving Treatment in Atherosclerotic Renal Artery Stenosis (ARAS)

Improving Treatment in Atherosclerotic Renal Artery Stenosis (ARAS)

Renal artery stenosis (RAS), most commonly caused by atherosclerosis, has an incidence of almost 7 percent in the elderly population. Patients with atherosclerotic RAS (ARAS) have increased risk of development of cardiovascular diseases and progression to end-stage renal failure. Restoration of vessel patency by revascularization is a common intervention in patients with ARAS, but its capability to restore renal function and improve blood pressure control is still controversial. Therefore, more effective strategies to preserve kidney function distal to the stenosis are urgently needed.

The laboratory has been engaged over the past 15 years in elucidating mechanisms of renal injury in ARAS and has recently focused on different strategies to improve the response to revascularization. Furthermore, the team has developed and characterized a novel swine model of ARAS and unique physiological imaging techniques that allow studying the single-kidney function and structure, both in vivo and in vitro.

Research projects include:

Stem cell therapy

Therapeutic utilization of stem cells is becoming an attractive alternative to conventional treatments, especially for diseases that are refractory to other treatments. Current projects involve the delivery of mesenchymal stem cells into the stenotic kidney at the time of revascularization to restore cellular integrity and decrease the progression to renal failure in swine ARAS.

Anti-apoptotic drugs

One of the potential underlying causes for the failure of revascularization to restore renal function is ischemia reperfusion injury (IRI). MTP-131 (bendavia) is a novel compound that targets the mitochondria to attenuate apoptosis and IRI associated with cardiovascular insults. The research evaluates the potential effects of intrarenal infusion of bendavia during revascularization for improving renal function, reducing apoptosis and the progression to fibrosis in the swine ARAS kidney.

For more information contact: eirinmassat.alfonso@mayo.edu