Hypercalcaemia and metastatic calcification following chronic calcium loading: a novel role for calcimimetic therapy — ASN Events
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Hypercalcaemia and metastatic calcification following chronic calcium loading: a novel role for calcimimetic therapy (#176)

Patrice M Forner 1 2 , Ian D Caterson 1 2 , Arthur D Conigrave 1 3
  1. Endocrinology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
  2. Boden Initiative, Charles Perkins Centre, The University of Sydney , Camperdown, New South Wales, Australia
  3. SoLES, Charles Perkins Centre (D17), The University of Sydney , Camperdown, New South Wales, Australia

We describe two patients with severe hypercalcaemia following prolonged ingestion of calcium-containing laxatives, complicated by metastatic calcification and chronic kidney disease (CKD). Both had inappropriately normal serum parathyroid hormone (PTH) levels and elevated serum parathyroid hormone-related peptide (PTHrP) levels. We hypothesise that chronic calcium loading and CKD may lead to impaired global calcium-sensing receptor (CaSR) signalling. 

Two women with longstanding anorexia nervosa and ingestion of calcium phosphate-containing laxatives developed recurrent hypercalcaemia (peak corrected calcium 3.34 mmol/L (13.36 mg/dL) and 3.30 mmol/L(13.2 mg/dL)), progressive CKD, and metastatic calcification. Other causes of hypercalcaemia were excluded. Both patients had inappropriately normal serum PTH.

Case 1:  Hypercalcaemia (serum total calcium concentrations > 3.0 mM; 12 mg/dL) was persistent despite cessation of laxatives and treatment with pamidronate(1). Cinacalcet was commenced at 15 mg daily and uptitrated, with subsequent biochemical improvement and sustained normocalcaemia; it was later successfully withdrawn. Case 2: Cinacalcet was uptitrated to 60 mg twice daily, with only partial improvement. Denosumab and calcitonin were subsequently required. 

These cases suggest a previously undescribed mechanism of persistent hypercalcaemia after chronic calcium loading. CKD alters parathyroid and renal CaSR signalling, and impairs the intrarenal response to hypercalcaemia(2). Cinacalcet restores calcium homeostasis by boosting renal calcium excretion while maintaining suppression of PTH release (3). The reduced therapeutic response in Case 2 may reflect more advanced renal injury and reduced capacity for cinacalcet-stimulated urinary calcium excretion. Elevated PTHrP may represent a secondary response to tissue injury rather than the primary driver of hypercalcaemia. 

The successful response to cinacalcet described herein supports the use of calcimimetics in selected cases of laxative induced calcium overload and warrants further investigation.

  1. 1. Lah S, Caterson I, Forner P. JCEM Case Reports. 2026;4(2):luag022.
  2. 2. Hannan FM, Kallay E, Chang W, Brandi ML, Thakker RV. Nature Reviews Endocrinology. 2019;15(1):33-51.
  3. 3. Valle C, Rodriguez M, Santamaria R, Almaden Y, Rodriguez ME, Martin-Malo A, et al. Journal of the American Society of Nephrology. 2008;19(12):2430-6.