Improving Treatment in Atherosclerotic Renal Artery Stenosis (ARAS)
Renal artery stenosis (RAS), most commonly caused by atherosclerosis, has an incidence rate of almost 7 percent in the older adult population.
Patients with atherosclerotic renal artery stenosis (ARAS) have increased risk of development of cardiovascular diseases and progression to end-stage renal failure.
A common intervention in patients with atherosclerotic renal artery stenosis is the restoration of vessel patency by revascularization, but the procedure's ability to restore renal function and improve blood pressure control is still controversial.
Therefore, strategies to more effectively preserve kidney function distal to the stenosis are urgently needed.
Dr. Lerman's Renovascular Disease Lab has been engaged in elucidating mechanisms of renal injury in ARAS for the past two decades. The research team has recently focused on different strategies to improve the response to revascularization.
The Renovascular Disease Lab has also recently developed and characterized a novel swine model of ARAS and unique physiological imaging techniques that allow study of the single-kidney function and structure, both in vivo and in vitro. Even more recently, Dr. Lerman's research team has explored the effect of metabolic syndrome on renal injury in renal artery stenosis.
Studies in the lab related to improving treatment in atherosclerotic renal artery stenosis include:
- Stem cell therapy
- Mitochondria-targeted drugs
Stem cell therapy
Therapeutic utilization of progenitor cells and stem cells is becoming an attractive alternative to conventional treatments, especially for diseases that are refractory to other treatments.
Recent projects involved delivery of adipose tissue-derived mesenchymal stem cells (MSC) into the stenotic kidney with or without concurrent revascularization to restore cellular integrity and to decrease the progression to renal failure in swine ARAS.
Current projects in the Renovascular Disease Lab involve delivery of MSC in metabolic syndrome and characterization and delivery of MSC-derived membrane microparticles (microvesicles and exosomes) using RNAseq and proteomics approaches.
One of the potential underlying causes for the failure of revascularization to restore renal function is mitochondrial damage. MTP-131 (bendavia) is a novel compound that targets the mitochondria to stabilize cardiolipin, improve energy utilization and attenuate apoptosis associated with cardiovascular insults.
Research in the Renovascular Disease Lab evaluates the potential effects of intrarenal infusion or subcutaneous injections of bendavia for improving renal function, reducing apoptosis and the progression to fibrosis in the swine ARAS kidney and heart, as well as in the metabolic syndrome.
For more information about the Renovascular Disease Lab's research project on improving treatment in atherosclerotic renal artery stenosis, email Alfonso Eirin Massat, M.D.