Abstract:
Atherosclerotic renal artery disease (ARAD) is a major cause of secondary hypertension and ischemic nephropathy. Angiotensinogen
(AGT), as the precursor of angiotensin peptides in the renin-angiotensin-aldosterone system (RAAS), is central to many of the pathophysiologic
mechanisms in ARAD. In this review, we examine clinical studies on AGT gene polymorphisms, outcomes of RAAS blockade, and the impact of AGT-fo cused therapies in ARAD. The aim is to clarify what is known, what remains controversial, and which areas merit further investigation
