title: Endothelial dysfunction in chronic renal failure.
abstract: Cardiovascular disease is a very early phenomenon in the course of chronic renal failure, and increases continuously with decrease of renal function. Endothelial dysfunction seems to be a starting point in vascular changes leading to atherosclerosis and artery calcification. Endothelium, considered the largest organ in the body, has many functions. It senses mechanical and hormonal stimuli and in response the endothelial cells secrete a range of compounds which modulate vascular tone, coagulation, cell proliferation, and inflammation. The central role of endothelium in the development of vascular disease has led to identification of new relevant biomarkers and methods to estimate endothelial function and injury. Arterial stiffness, which is not an early phenomenon in endothelial dysfunction but a common complication of chronic renal failure may be evaluated through Pulse Wave Velocity and Augmentation Index obtained by pulse-wave analysis. Aortic stiffness is an independent predictor of cardiovascular morbidity and mortality in patients with hypertension. A new fascinating aspect of research in endothelial function is rising through the studies on endothelial progenitor cells. These are primitive bone marrow cells that have the ability to mature into endothelial cells and have a physiologic role in the repair of endothelial lesions.
authors.affiliation: Unit of Nephrology, University of Messina, Faranda, Messina, Italy. santisi@hotmail.com
authors.forename: Domenico
authors.initials: D
authors.lastname: Santoro
authors.forename: Guido
authors.initials: G
authors.lastname: Bellinghieri
authors.forename: Giovanni
authors.initials: G
authors.lastname: Conti
authors.forename: Dario
authors.initials: D
authors.lastname: Pazzano
authors.forename: Ersilia
authors.initials: E
authors.lastname: Satta
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Costantino
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Savica
mesh_terms: D001158:Arteries / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology; D002114:Calcinosis / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D013234:Stem Cells; D014652:Vascular Diseases / Q000209:etiology