Published online Aug 26, 2014. doi: 10.4330/wjc.v6.i8.855
Revised: March 4, 2014
Accepted: June 10, 2014
Published online: August 26, 2014
Processing time: 260 Days and 13 Hours
Optimal management of patients with renal artery stenosis (RAS) is a subject of considerable controversy. There is incontrovertible evidence that renal artery stenosis has profound effects on the heart and cardiovascular system in addition to the kidney. Recent evidence indicates that restoration of blood flow alone does not improve renal or cardiovascular outcomes in patients with renal artery stenosis. A number of human and experimental studies have documented the clinical, hemodynamic, and histopathologic features in renal artery stenosis. New approaches to the treatment of renovascular hypertension due to RAS depend on better understanding of basic mechanisms underlying the development of chronic renal disease in these patients. Several groups have employed the two kidney one clip model of renovascular hypertension to define basic signaling mechanisms responsible for the development of chronic renal disease. Recent studies have underscored the importance of inflammation in the development and progression of renal damage in renal artery stenosis. In particular, interactions between the renin-angiotensin system, oxidative stress, and inflammation appear to play a critical role in this process. In this overview, results of recent studies to define basic pathways responsible for renal disease progression will be highlighted. These studies may provide the rationale for novel therapeutic approaches to treat patients with renovascular hypertension.
Core tip: Renovascular hypertension is a common public health problem, particularly in older patients with underlying atherosclerotic vascular disease. Recent studies have shown that restoration of blood flow in these patients fails to improve renal function or survival. Recent studies to define basic mechanisms underlying the development of chronic renal disease in renin angiotensin system (RAS) have shown that pro-inflammatory pathways may play a critical role in this process. Therapeutic approaches that target inflammatory pathways may provide the basis for novel and more effective treatments for patients with RAS.