Calcinosis and Metastatic Calcification due to Vitamin D Intoxication

Allen, Susan H.; Shah, Jayendra H.

doi:10.1159/000182285

Cited by 29 publications

(7 citation statements)

References 32 publications

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“…[5] Renal tübüler kalsiyum reabsorbsiyonunun artması-na bağlı olarak hiperkalsiüri ve tubuluslerde kalsiyum birikimi sonucu medüller tipte nefrokalsinozis gelişir. [1,2] Hastamızda Ca seviyesi ve total D vitamini dozu birlikte yüksek idi. Bununla beraber nefrokalsinozis olmaması ağır hiperkalsemi olmasına rağmen maruziyet süresinin kısa olmasına bağlandı.…”

Section: Discussionunclassified

“…[1][2][3] D vitaminin aşırı kullanımı bağırsaktan kalsiyum emilimini artırıp hiperkalsemi ve hiperkalsiüriye; bu ise nefrokalsinozis, ürolitiyazis ve yumuşak dokuda kalsifikasyonlara yol açabilir.[ …”

unclassified

“…[11] Vitamin D zehirlenmesinin tedavisinde maruziyetin kesilmesi, sıvı tedavisi, furosemid, steroid ve bifosfanat tedavileri uygulanmaktadır. [2,12,13] Bu yazıda, doktora danışılmadan kullanıldıktan sonra zehirlenmeye sebep olan vitamin D zehirlenmesi olgusu sunuldu. Sağlık çalışanlarının yanı sıra daha önemli olarak vitamin D kullanımı konusunda aile bilgilendirilmesi konusuna dikkat çekmek istedik.…”

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Treated with pamidronate infusions of vitamin D poisoning

Tutanç¹,

Yel²,

Gözü³

et al. 2012

J Kartal TR

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Section: Discussionunclassified

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Treated with pamidronate infusions of vitamin D poisoning

Tutanç¹,

Yel²,

Gözü³

et al. 2012

J Kartal TR

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“…By contrast, the Institute of Medicine advocates VD repletion as a level of 20 ng/mL [27] . 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] .…”

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

confidence: 99%

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

Molina¹,

Górriz²,

Molina³

et al. 2016

WJN

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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.

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“…In children, reliable oral intake of supplements can be difficult; inadequate intake can precipitate a hypocalcemic crisis. In addition, treated patients do not receive the full calcium retaining renal action of parathyroid hormone (PTH) [5][6][7][8][9][10][11][12][13][14]. Patients treated with vitamin D may exhibit hypercalciuria despite normal or even low serum calcium levels.…”

mentioning

confidence: 99%