Please use this identifier to cite or link to this item: http://hdl.handle.net/10668/11369
Title: Correction of 25-OH-vitamin D deficiency improves control of secondary hyperparathyroidism and reduces the inflammation in stable haemodialysis patients.
Other Titles: La corrección del déficit de 25-OH-vitamina D mejora el control del hiperparatiroidismo secundario y el estado inflamatorio de pacientes estables en hemodiálisis.
Authors: Ojeda López, Raquel
Esquivias de Motta, Elvira
Carmona, Andrés
García Montemayor, Victoria
Berdud, Isabel
Martín Malo, Alejandro
Aljama García, Pedro
Keywords: Haemodialysis;Hemodiálisis;Hiperparatiroidismo secundario;Hipovitaminosis D;Hypovitaminosis D;Inflamación;Inflammation;Secondary hyperparathyroidism
metadata.dc.subject.mesh: Adult
Aged
Aged, 80 and over
C-Reactive Protein
Calcifediol
Calcium
Female
Fibroblast Growth Factor-23
Fibroblast Growth Factors
Homeostasis
Humans
Hyperparathyroidism, Secondary
Inflammation
Kidney Failure, Chronic
Male
Middle Aged
Parathyroid Hormone
Prospective Studies
Renal Dialysis
Vitamin D
Vitamin D Deficiency
Issue Date: 1-Jul-2017
Abstract: Patients on haemodialysis (HD) have a high prevalence of 25-OH-vitamin D (25-OH-D)deficiency. Secondary hyperparathyroidismis a common condition in these patients, which is very important to control. 25-OH-D is involved in regulating calcium homeostasis. As such, appropriate levels of this vitamin could help to control bone mineral metabolism. To evaluate the effect 25-OH-D repletion in HD patients with 25-OH-D deficiency ( Prospective observational study in which stable patients on HD with 25-OH-D deficiency ( Forty-five stable HD patients with a mean age of 74.08±12.49 years completed treatment. Twenty-seven patients (60%) achieved 25-OH-D levels above 20ng/ml (23 with levels>30ng/ml and 4 between 20-30ng/ml). Parathyroid hormone levels decreased in 32 of the 45 patients, 23 of which (51%) achieved a>30% decrease from baseline. In terms of concomitant treatment, we observed a significant reduction in the selective vitamin D receptor activator dose, but no changes in calcimimetic or phosphate binders administration. In terms of malnutrition-inflammation status, a decrease in C-reactive protein was noted, although other microinflammation parameters, such as activated monocytes (CD14+/CD16+ and CD 14++/CD16+) were unchanged. No changes were observed in the levels of FGF-23. Correcting 25-OH-D deficiency in HD patients is associated with better secondary hyperparathyroidism control with lower doses of vitamin D analogues, as well as an improvement in inflammatory status. Our results support the recommendation to determine 25-OH-D levels and correct its deficiency in these patients.
URI: http://hdl.handle.net/10668/11369
metadata.dc.identifier.doi: 10.1016/j.nefro.2017.05.008
Appears in Collections:Producción 2020

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