Mechanisms of Nephropathy Caused by ARAS and Optimal Treatments

The prevalence of atherosclerotic renal artery stenosis (ARAS) is on the rise globally in the aging society, and it has become a common etiology of renovascular hypertension and chronic kidney disease, which eventually develop into end-stage renal disease.

However, outcomes after renal revascularization procedures are disappointing compared with those with renal artery stenosis alone, as nearly half fail to achieve renal function improvement. This has spurred the need for the study of mechanisms of nephropathy caused by ARAS and for the development of optimal treatment strategies.

In this research project on optimal treatments of atherosclerotic renal artery stenosis, our lab is:

  • Exploring the pathophysiological mechanism of kidney injury due to ARAS and detrimental atherosclerotic risk factors, such as hypercholesterolemia and hypertension
  • Seeking predictive factors associated with renal recovery after percutaneous transluminal renal angioplasty (PTRA)
  • Discovering novel strategies to enhance renal vascular repair and improve renal outcome after PTRA

One research interest is in the renal effect of low-energy shock wave therapy in renal artery stenosis. This ongoing project is based on the ability of shock wave therapy to increase microvascular density and decrease inflammation in the ischemic heart and kidney.

By using unique imaging techniques, adaptive intrarenal physiological and structural responses to shock wave therapy are accessed and evaluated in a RAS swine model.

Another project centers on the role of peristenotic and perirenal collateral circulation in preserving the structure and function of the post-stenotic kidneys in swine models and in patients. Our research team also is developing new methods to assess the collateral circulation using computerized tomography.