title: Management of renal artery stenosis: What does the experimental evidence tell us?
abstract: 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.
authors.affiliation: Mohammed Al-Suraih, Joseph Peter Grande, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, United States.
authors.forename: Mohammed
authors.initials: M
authors.lastname: Al-Suraih
authors.affiliation: Mohammed Al-Suraih, Joseph Peter Grande, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, United States.
authors.forename: Joseph Peter
authors.initials: JP
authors.lastname: Grande
keywords: Atrophy; CCL2; CCR2; Inflammation; Kidney; Renovascular hypertension