The effects of vitamin D therapy on left ventricular structure and function - are these the underlying explanations for improved CKD patient survival?
Cardiovascular disease is a major cause of death among patients with chronic kidney disease and vitamin D deficiency is a common problem also among these patients. Abnormalities in left ventricular size and function are frequent, as they are encountered in 70-80% of incident dialysis patients. These alterations develop early in the course of renal disease and their prevalence progresses in parallel with the decline in renal function. This process of left ventricular dilatation with compensatory hypertrophy continues after the institution of dialysis therapy, especially in the first year. The main factors responsible for the progression of left ventricular hypertrophy (LVH) are considered to be blood pressure and anemia, and in patients receiving hemodialysis, the arteriovenous fistula, volume overload and abnormalities in mineral metabolism. This additional potential set of factors related to LVH - mineral and bone metabolism - is intriguing and begs an immediate question: by what possible mechanism can these factors be linked to cardiac morphology? Recent observational studies have indeed indicated that vitamin D treatment was associated with a significant reduction of cardiovascular death among dialysis patients, and a reduction in LVH; in contrast, other studies suggested that excess vitamin D contributes to risk of hypercalcemia and vascular calcification, which is associated with reduced survival and morbidity. This review examines the evidence linking vitamin D with cardiac structure and function.
Covic
Adrian
A
Nephrology Clinic, Parhon University Hospital, Gr. T. Popa University of Medicine and Pharmacy, Iasi, Romania. lumivoro@yahoo.com
Voroneanu
Luminita
L
Goldsmith
David
D
D000740:Anemia / Q000209:etiology; D001161:Arteriosclerosis / Q000188:drug therapy; D001842:Bone and Bones / Q000378:metabolism; D002117:Calcitriol / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000401:mortality; D002908:Chronic Disease; D006352:Heart Ventricles / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006934:Hypercalcemia / Q000139:chemically induced; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D007249:Inflammation / Q000188:drug therapy; D007674:Kidney Diseases / Q000150:complications* / Q000401:mortality; D010281:Parathyroid Hormone / Q000502:physiology; D018167:Receptors, Calcitriol / Q000502:physiology; D006435:Renal Dialysis / Q000009:adverse effects; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D015996:Survival Rate; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D014807:Vitamin D / Q000009:adverse effects / Q000031:analogs & derivatives / Q000494:pharmacology / Q000502:physiology / Q000627:therapeutic use*; D014808:Vitamin D Deficiency / Q000188:drug therapy / Q000517:prevention & control
D010281:Parathyroid Hormone; D018167:Receptors, Calcitriol; D014807:Vitamin D; D002117:Calcitriol