When more is not better in a case of hypercalcaemia secondary to vitamin D toxicity — ASN Events
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When more is not better in a case of hypercalcaemia secondary to vitamin D toxicity (#458)

Huien Tham 1 , Lai-Ming Kathleen Pak 1 , Shananthan Balachandran 1
  1. Endocrinology, Eastern Health, Box Hill, Victoria, Australia

Case  

A 70-year-old man with pre-existing stage 4 chronic kidney disease was admitted with symptomatic hypercalcaemia and acute kidney injury (AKI), presenting with a two-month history of fatigue, polydipsia, polyuria, and constipation. 

Initial biochemistry revealed elevated corrected calcium (cCa) 2.99 mmol/L, phosphate 1.67 mmol/L, suppressed parathyroid hormone (PTH) 1.0 pmol/L, and creatinine rise from baseline 253 μmol/L to 627 μmol/L (eGFR 7 mL/min/1.73 m²). Non-contrast CT of the chest, abdomen, and pelvis was unremarkable. Serum protein electrophoresis identified a small IgM lambda monoclonal band (<1 g/L) of uncertain significance. Further history revealed eight months of daily supplementation with cholecalciferol 30,000 IU, sourced online. Dilutional testing confirmed markedly elevated 25-hydroxyvitamin D (720 nmol/L), establishing vitamin D toxicity as the aetiology of PTH-independent hypercalcaemia. 

Initial treatment involved intravenous fluids and short-term use of calcitonin. Prednisolone 25 mg daily was commenced and a single dose of denosumab 60 mg administered, achieving cCa 2.61 at discharge. Prednisolone was tapered as an outpatient over 3 weeks, without recurrence of hypercalcaemia. 

Discussion 

Vitamin D toxicity is a rare cause of PTH-independent hypercalcaemia but may occur with prolonged ingestion of high-dose preparations exceeding the tolerable upper intake level of 4000 IU/day for healthy adults (1). It is associated with serum 25-hydroxyvitamin D concentrations above 375nmol/L. (2,3). Hypervitaminosis D increases intestinal calcium absorption and bone resorption, causing hypercalcaemia, which can result in nephrogenic diabetes insipidus and pre-renal AKI (4). Treatment approaches are typically multimodal. Prednisolone reduces vitamin D-mediated intestinal calcium absorption, bone resorption, and favours hepatic vitamin D metabolism to inactive metabolites (3). Anti-resorptive agents may also be used as adjunct therapy. Denosumab was selected in this case due to severe renal impairment precluding bisphosphonate use. This case highlights the importance of patient and clinician awareness regarding the potential harms of unsupervised high-dose vitamin D supplementation.

  1. Scientific Advisory Committee on Nutrition. Vitamin D and Health. London: Public Health England; 2016. Available from: SACN vitamin D and health report - GOV.UK
  2. Taylor, PN, and Davies, JS. A review of the growing risk of vitamin D toxicity from inappropriate practice. Br J Clin Pharmacol. 2018; 84(6): 1121–1127. doi: 10.1111/bcp.13573.
  3. Marcinowska-Suchowierska E, Kupisz-Urbańska M, Łukaszkiewicz J, Płudowski P, Jones G. Vitamin D Toxicity–A Clinical Perspective. Front Endocrinol (Lausanne). 2018;9:550. doi:10.3389/fendo.2018.00550.
  4. Makras, P, Papapoulos, SE. Medical treatment of hypercalcaemia. Hormones (Athens). 2009; 8(2):83–95. doi:10.14310/horm.2002.1225