title: Vascular calcification: When should we interfere in chronic kidney disease patients and how?
abstract: Chronic kidney disease (CKD) patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifications affect most of the CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 and klotho deficiency were incriminated in the pathogenesis of vascular calcification through different mechanisms including their effects on endothelium and arterial wall smooth muscle cells. In addition, deficient klotho gene expression, a constant feature of CKD, promotes vascular pathology and shares in progression of the CKD. The role of gut in the etio-pathogenesis of systemic inflammation and vascular calcification is a newly discovered mechanism. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, different tools used to diagnose, the ideal timing to prevent or to withhold the progression of vascular calcification and the different medications and medical procedures that can help to prolong the survival of CKD patients.
authors.affiliation: Usama Abdel Azim Sharaf El Din, Department of Nephrology, School of Medicine, Cairo University, Cairo 11759, Egypt.
authors.forename: Usama Abdel Azim
authors.initials: UA
authors.lastname: Sharaf El Din
authors.affiliation: Usama Abdel Azim Sharaf El Din, Department of Nephrology, School of Medicine, Cairo University, Cairo 11759, Egypt.
authors.forename: Mona Mansour
authors.initials: MM
authors.lastname: Salem
authors.affiliation: Usama Abdel Azim Sharaf El Din, Department of Nephrology, School of Medicine, Cairo University, Cairo 11759, Egypt.
authors.forename: Dina Ossama
authors.initials: DO
authors.lastname: Abdulazim
keywords: Calcific uremic arteriolopathy; Calcification; Chronic kidney disease; Fibroblast growth factor 23; Kidney transplantation; Klotho; Phosphate binders; Sevelamer; Uremia