Cholecalciferol Supplementation in Hemodialysis Patients

Matias, Patrícia; Jorge, Cristina; Ferreira, Carina; Borges, Marília; Aires, Inês; Amaral, Tiago; Gil, Célia; Cortez, José; Ferreira, Aníbal

doi:10.2215/cjn.06510909

Cited by 206 publications

(181 citation statements)

References 44 publications

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“…Calciferol therapy has been reported to improve parameters of mineral metabolism in observational studies, with associations to decreased parathyroid hormone (PTH) and b-ALP levels (2,24,25). However, treatment allocation did not influence values of iPTH, ALP, or b-ALP in this study.…”

Section: Mineral Metabolism and Bone Turnovercontrasting

confidence: 65%

Effects of Cholecalciferol on Functional, Biochemical, Vascular, and Quality of Life Outcomes in Hemodialysis Patients

Hewitt

O'Connor

O’Shaughnessy

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Observational studies suggest that calciferol supplementation may improve laboratory and patient-level outcomes of hemodialysis patients with reduced 25-hydroxyvitamin D [25(OH)D] levels. This randomized controlled trial examined effects of cholecalciferol supplementation in patients on hemodialysis.Design, setting, participants, & measurements Sixty patients with 25(OH)D levels #24 ng/ml (#60 nmol/L) were randomized to receive 50,000 IU oral cholecalciferol or placebo, once weekly for 8 weeks and then monthly for 4 months. At baseline (autumn 2011) and 6 months, testing evaluated muscle strength, functional capacity, laboratory parameters, pulse wave velocity (PWV), and health-related quality of life (HRQOL) using the Kidney Disease Quality of Life-36 survey.Results Patients were well matched by treatment allocation. Median age was 62 years (range, 20-86), 52% were women, 55% had a history of diabetes, and mean serum 25(OH)D was 1765 ng/ml (43613 nmol/L). Patients were assessed over 6 months by repeated-measures ANOVA. Patients allocated to cholecalciferol had significantly higher values of 25(OH)D (P,0.001), 1,25-dihydroxyvitamin D (P=0.04), and tartrate-resistant acid phosphatase-5b) (P=0.04) and a greater reduction in phosphorus values (P=0.03) than placebo-treated patients Values of serum calcium, intact parathyroid hormone, and episodes of hypercalcemia and hyperphosphatemia did not differ significantly between the groups. No significant differences were detected in muscle strength, functional capacity, PWV, or HRQOL.Conclusions In this randomized controlled trial, patients supplemented with cholecalciferol had higher 25(OH)D, 1,25-dihydroxyvitamin D, and tartrate-resistant acid phosphatase-5b levels, without increased calcium or phosphorus values. However, no effects were detected in muscle strength, functional capacity, PWV, or HRQOL.

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Section: Mineral Metabolism and Bone Turnovercontrasting

confidence: 65%

Effects of Cholecalciferol on Functional, Biochemical, Vascular, and Quality of Life Outcomes in Hemodialysis Patients

Hewitt

O'Connor

O’Shaughnessy

et al. 2013

Clinical Journal of the American Society of Nephrology

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“…The potential interest of cholecalciferol administration was recently documented in patients with ESRD in whom a significant effect on hyperparathyroidism and left ventricular hypertrophy was recorded. 58 In contrast, a recent randomized controlled trial showed no effect of the active vitamin D compound paricalcitol on cardiac structure or function in patients with CKD. 59 Whether these discrepancies reflect a stronger effect of cholecalciferol supplementation on cardiac dysfunction in CKD remains to be tested.…”

Section: Discussionmentioning

confidence: 95%

Vitamin D Status and Outcomes After Renal Transplantation

Bienaimé

Girard

Anglicheau

et al. 2013

Journal of the American Society of Nephrology

100

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Kidney transplant recipients usually have low vitamin D levels, especially in the early posttransplantation period, but the association between vitamin D status with renal outcomes is not well described in this population. Here, we studied a prospective cohort of 634 kidney recipients who underwent transplantation at a single institution between January 2005 and June 2010. In this cohort, low 25-hydroxyvitamin D concentrations 3 months after transplantation did not predict early death or graft loss but were independently associated with lower measured GFR at 12 months (P=0.001) and higher risk for interstitial fibrosis and tubular atrophy (P=0.01). In contrast, levels of calcium, phosphorus, calcitriol, parathyroid hormone, or fibroblast growth factor-23 were not consistently associated with any of the studied outcomes. In conclusion, low 25-hydroxyvitamin D concentration measured 3 months after transplantation is an independent risk factor for interstitial fibrosis progression and is associated with a lower GFR 1 year after transplantation. 24: 831-841, 201324: 831-841, . doi: 10.1681 Kidney transplantation is the preferred treatment for the increasing number of patients with ESRD. Transplantation allows patients to avoid the heavy constraints associated with dialysis therapy and is associated with a lower mortality and morbidity than is hemodialysis. 1 Evolution of GFR in transplant recipients appears to be imprinted at an early stage after the surgery. Indeed, the estimated GFR (eGFR) reached 1 year after transplantation is critically associated with allograft outcome. 2,3 This observation prompts research on modifiable factors affecting GFR in the first year after transplantation. J Am Soc NephrolVitamin D is a critical hormone controlling mineral homeostasis. It promotes phosphate and calcium absorption by the gut and increases calcium reabsorption by the renal distal tubule, thereby providing the positive calcium and phosphorus flux required for bone mineralization.

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“…Extensive published evidence [22,23,26,27,[32][33][34][35] demonstrates a modest decrease in PTH levels after calcidiol supplementation that does not, however, correct the PTH levels to normal. VitD supplementation is not accompanied by an increased risk of hypercalcemia and hyperphosphatemia.…”

Section: Chronic Kidney Diseasementioning

confidence: 99%

“…PTH reduction could be attributed to either increased downstream calcitriol production, due to renal or extrarenal 1a hydroxylation of 25(OH)D, or/and to 25(OH)D actions independent of calcitriol generation [33,34]. Indeed, in vitro models [41] have shown that 25(OH)D can directly activate the VitD receptor in the parathyroid gland without calcitriol involvement.…”

Section: Mechanism Of Pth Decrease With Vitd Supplementationsmentioning

confidence: 99%