title: [Role of vitamin D in the pathogenesis of chronic kidney disease].
abstract: Chronic kidney disease (CKD) is a relevant health problem due to its worldwide increasing prevalence and the morbidity and mortality linked to its complications. Since the early stages of CKD, although patients are completely asymptomatic, important mineral homeostasis disorders occur. These disorders, involving serum levels of calcium, phosphorus, parathyroid hormone, and vitamin D, have a striking impact on patient prognosis as they affect the cardiovascular system. The new term of Chronic Kidney Disease-Mineral Bone Disease (CKD-MBD) was introduced to label bone disease during CKD as a systemic disorder tightly linked to cardiovascular calcifications and disabilities. Vitamin D deficiency has a main role in the pathogenesis of CKD-MBD, throughout the pleiotropic actions of this hormone. Vitamin D receptors (VDRs) are ubiquitous and their activation has shown protective effects against secondary hyperparathyroidism development and anti-hypertensive, anti-inflammatory, anti-fibrotic, immunomodulating, anti-proliferative, anti-diabetic and anti-proteinuric properties. These mechanisms explain, at least in part, vitamin D status influence in avoiding and delaying cardiovascular disease and CKD progression. These findings strongly support the importance of an early diagnosis of mineral homeostasis disorders in CKD and the need for correction of vitamin D deficiency to prevent related disabilities and major events.
authors: Divisione Renale, Dipartimento di Scienze della Salute, Ospedale San Paolo, Università di Milano. mario.cozzolino@unimi.it
authors: Mario
authors: M
authors: Cozzolino
authors: Francesca
authors: F
authors: Brunini
authors: Valentina
authors: V
authors: Capone
authors: Flavia
authors: F
authors: Ricca
authors: Younes
authors: Y
authors: Kwaidri
authors: Emanuele
authors: E
authors: Montanari
authors: Daniele
authors: D
authors: Cusi
mesh_terms: D002118:Calcium / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D002908:Chronic Disease; D048909:Diabetes Complications / Q000503:physiopathology; D018450:Disease Progression; D042241:Early Diagnosis; D005355:Fibrosis; D006706:Homeostasis; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D007108:Immune Tolerance / Q000502:physiology; D007249:Inflammation / Q000150:complications / Q000503:physiopathology; D007674:Kidney Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D011507:Proteinuria / Q000209:etiology; D018167:Receptors, Calcitriol / Q000502:physiology; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood / Q000502:physiology* / Q000627:therapeutic use; D014808:Vitamin D Deficiency / Q000097:blood / Q000150:complications* / Q000503:physiopathology
chemical_list: D010281:Parathyroid Hormone; D018167:Receptors, Calcitriol; D014807:Vitamin D; D010758:Phosphorus; C104450:25-hydroxyvitamin D; D002118:Calcium