Study of 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 has become a common etiology of renovascular hypertension and chronic kidney disease that will eventually develop into end-stage renal disease (ESRD). However, the outcomes after renal revascularization are disappointing compared to RAS alone, as nearly half fails to achieve renal function improvement. This has urged the need for the study of mechanisms of nephropathy caused by ARAS and the exploit of the optimal treatment, including:

  • Exploring the pathophysiologic mechanism of kidney injuries due to renal artery stenosis and atherosclerotic detrimental factors (e.g., hypercholesterolemia)
  • Seeking predictive factors associated with renal recovery after percutaneous transluminal renal angioplasty (PTRA)
  • Discovering novel strategies to enhance the renal vascular repair and improve renal outcome after PTRA

One research interest is in the renal effect of angiotensin receptor blocker-valsartan in renal artery stenosis. This ongoing project is based on the controversy and uncertainty of whether angiotensin-converting enzyme inhibitor and angiotensin receptor blocker would protect or aggravate renal ischemia under the condition of renal hypoperfusion induced by renal artery stenosis. By adopting unique imaging techniques, intrarenal physiological and structural changes are accessed and evaluated in a RAS swine model.

Another project is on the effect of humanin on kidney insults caused by atherosclerosis. Humanin is an anti-apoptotic factor rescuing neuronal cells from apoptosis in Alzheimer's disease. In this project, by using a murine model, the potential role of humanin in the mechanisms of kidney damage induced by atherosclerosis including apoptosis, inflammation and angiogenesis is examined through kidney morphology, histology and biochemical analysis.

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