Abstract :
[en] Chronic kidney disease is frequent and usually responsible of mineral and bone disorder. These
abnormalities lead to increased morbidity and mortality. To become active, native vitamin D needs a first
hydroxylation in the liver, and a second one in the kidney. Next to its action on bone metabolism,
vitamin D also possesses pleiotropic actions on cardiovascular, immune and neurological systems as well
as antineoplastic activities. End-stage renal disease (ESRD) is also associated with a decrease in vitamin D
activity by mechanisms including the increase of plasma phosphate concentration, secretion of FGF-
23 and decrease in 1a-hydroxylase activity. The prevalence of 25 hydroxy-vitamin D deficiency depends
on the chosen cut-off value to define this lack. Currently it is well established that a patient has to be
substituted when 25 hydroxy-vitamin D level is under 30 ng/mL. The use and monitoring of
1.25 hydroxy-vitamin D is still not recommended in routine practice. The goals of vitamin D treatment in
case of ESRD are to substitute the deficiency and to prevent or treat hyperparathyroidism. Interest of
native vitamin D in first intention is now well demonstrated. This review article describes the vitamin D
metabolism and physiology and also the treatment for vitamin D deficiency in ESRD population.
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