Mechanisms of Nephropathy Caused by ARAS
The prevalence of atherosclerotic renal artery stenosis (ARAS) is on the rise globally in the aging society. It also has become a common cause 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 of these procedures fail to achieve renal function improvement. This has spurred the need to study mechanisms of nephropathy caused by ARAS and to develop optimal treatment strategies.
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 outcomes after PTRA.
Another project centers on the role of peristenotic and perirenal collateral circulation in preserving the structure and function of the post-stenotic kidneys in animal models and in people. Our research team also is developing new methods to assess the collateral circulation and post-stenotic dilation using computerized tomography.
We also study vascular and microvascular remodeling within the ischemic kidney and develop methods to quantify fibrosis as a function of disease severity. We also investigate the effects of renovascular disease on endogenous reparative systems, such as mesenchymal stem cells.