Low Calcidiol Levels and Coronary Artery Calcification

Melamed, Michal L.; Thadhani, Ravi

doi:10.1681/asn.2009060610

Cited by 2 publications

(5 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Determining the 25(OH)D target level for optimal health is especially important in CKD population, where overuse of VD leads to hypercalcemia, hypercalciuria and hyperphosphatemia, which could predispose to vascular calcification, nephro lithiasis and reduced glomerular filtration rate [28][29][30] . All these data suggest an optimal level of VD exists that is neither too high nor too low [31] . Aware of the lack of evidence behind guidelines recommendations, and our concerns about VD oversupplementation, encouraged us to investigate the optimal VD status in non-dialysis CKD patients.…”

Section: Hydroxyvitamin D [25(oh)d]mentioning

confidence: 92%

“…In this context, it is noteworthy that the lack of association between 25(OH)D levels and vascular calcification observed in our study, is in agreement with some [12] , but not all [9,10] , previously published data. These findings indicate that 25(OH)D may impact on CKD outcomes by additional mechanisms including the suppression of the renin-angiotensin system, albuminuria reduction or amelioration of left ventricular hypertrophy [6,9,16,31,39] . Of note, we have detected ABPI as an independent predictor of VD deficiency, which could contribute to vascular stiffness and high cardiovascular risk for this population.…”

mentioning

confidence: 89%

See 1 more Smart Citation

What is the optimal level of vitamin D in non-dialysis chronic kidney disease population?

Molina¹,

Górriz²,

Molina³

et al. 2016

WJN

View full text Add to dashboard Cite

AIMTo evaluate thresholds for serum 25(OH)D concentrations in relation to death, kidney progression and hospitalization in non-dialysis chronic kidney disease (CKD) population. METHODSFour hundred and seventy non-dialysis 3-5 stage CKD patients participating in OSERCE-2 study, a prospective, multicenter, cohort study, were prospectively evaluated and categorized into 3 groups according to 25(OH)D levels at enrollment (less than 20 ng/mL, between 20 and 29 ng/mL, and at or above 30 ng/mL), considering 25(OH)D between 20 and 29 ng/mL as reference group. Association between 25(OH)D levels and death (primary outcome), and time to first hospitalization and renal progression (secondary outcomes) over a 3-year followup, were assessed by Kaplan-Meier survival curves and Cox-proportional hazard models. To identify 25(OH)D levels at highest risk for outcomes, receiver operating characteristic (ROC) curves were performed. RESULTSOver 29 ± 12 mo of follow-up, 46 (10%) patients dead, 156 (33%) showed kidney progression, and 126 (27%) were hospitalized. After multivariate adjustment, 25(OH)D < 20 ng/mL was an independent predictor of all-cause mortality (HR = 2.33; 95%CI: 1.10-4.91; P = 0.027) and kidney progression (HR = 2.46; 95%CI: 1.63-3.71; P < 0.001), whereas the group with 25(OH)D at or above 30 ng/mL did not have a different hazard for outcomes from the reference group. Hospitalization outcomes were predicted by 25(OH) levels (HR = 0.98; 95%CI: 0.96-1.00; P = 0.027) in the unadjusted Cox proportional hazards model, but not after multivariate adjusting. ROC curves identified 25(OH)D levels at highest risk for death, kidney progression, and hospitalization, at 17.4 ng/mL [area under the curve (AUC) = 0.60; 95%CI: 0.52-0.69; P = 0.027], 18.6 ng/mL (AUC = 0.65; 95%CI: 0.60-0.71; P < 0.001), and 19.0 ng/mL (AUC = 0.56; 95%CI: 0.50-0.62; P = 0.048), respectively. CONCLUSION 25(OH)D < 20 ng/mL was an independent predictor of death and progression in patients with stage 3-5 CKD, with no additional benefits when patients reached the levels at or above 30 ng/mL suggested as optimal by CKD guidelines. Core tip: This study examines the prognosis value of 25(OH)D levels on death, chronic kidney disease (CKD) progression, and hospitalization in a cohort of 3-5 stage CKD subjects not on dialysis. The main findings were the predictor value of vitamin D deficiency (< 20 ng/ mL), but not insufficiency (< 30 ng/mL), for the 3-year incidence of death and CKD progression, which remained significant after multivariate adjustments. These results could highlight the need for a revision of the current guidelines, which have defined optimal vitamin D status at ≥ 30 ng/mL based on levels required to suppress parathyroid hormone, as opposed to our study, which evaluates thresholds for serum 25(OH)D concentrations in relation to "hard" endpoints.

show abstract

Section: Hydroxyvitamin D [25(oh)d]mentioning

confidence: 92%

mentioning

confidence: 89%

What is the optimal level of vitamin D in non-dialysis chronic kidney disease population?

Molina¹,

Górriz²,

Molina³

et al. 2016

WJN

View full text Add to dashboard Cite

show abstract

“…Some of the body of evidence has been reviewed in the editorial by Melamed and Thadhani that accompanies the paper by de Boer et al 4 However, does the totality of evidence beg starting patients on vitamin D vitamin supplementation in the absence of further evidence from RCTs? If physicians collectively decide to routinely treat high risk patients-such as those with CKD and ESRD with vitamin D vitamin (cholecalciferol, ergocalciferol, etc.…”

Section: Epidemiologic Data: the Association Between Vitamin D Levelsmentioning

confidence: 99%

“…In the absence of data from rigorously conducted randomized clinical trials (RTCs), such studies, as part of a larger body of evidence fulfi lling the traditional BradfordHill considerations for causation, can serve to identify risk factors or at times, even harmful exposures that warrant corrective action. 4 It is in this context, that one should consider how a recent study by de Boer and colleagues informs the question of the potential role of vitamin D vitamin defi ciency in causing cardiovascular disease, and whether the totality of evidence necessitates specifi c therapeutic decisions. The current study by de Boer et al, as part of a larger body of evidence on the diverse potential effects of vitamin D and the diverse adverse medical consequences associated with vitamin D vitamin defi ciency, further supports the urgency of conducting robust clinical trials to examine the assertions that therapy can prevent disease.…”

mentioning

confidence: 99%