Diagnostic pitfalls and therapeutic challenges of hypercalcaemia in chronic kidney disease: a case report and a narrative review

Abstract

Abstract Background Evaluation of hypercalcaemia in a patient with chronic kidney disease (CKD) is challenging, especially in low-resource settings. Hormone assays should be interpreted with caution as CKD affects both parathyroid hormone (PTH) and vitamin D. Therapies such as bisphosphonates are contraindicated in CKD, while fluid resuscitation can lead to volume overload. We report the diagnostic workup of a patient with stage V CKD who presented with symptomatic hypercalcaemia and discuss the diagnostic pitfalls and therapeutic challenges. Case presentation A 72-year-old Sri Lankan woman with stage V, non-oliguric CKD presented with a 2-week history of worsening lassitude, increased thirst and constipation. She was clinically euvolemic and did not have signs of uraemia. Bilateral lung fields had occasional coarse crepitations. The rest of the physical examination was normal. Her serum creatinine level was similar to her baseline (4.7 mg/dl, eGFR 9 ml/min). She was found to have a high serum calcium (14.3 mg/dl) and phosphate (5.0 mg/dl) levels. Her PTH level was 24.1 pg/ml (15–68), and she was deficient in 25-hydroxycholecalciferol (9 mg/ml (30–100)). She was not on calcium or vitamin D supplementation. Disseminated tuberculosis was diagnosed after detecting granulomata in the lungs and abdomen in the contrast-enhanced computed tomography (CECT) and mycobacterial DNA in sputum. She was hydrated with 0.9% NaCl with meticulous use of frusemide. The effect of frusemide waned off by the 10th day, requiring haemodialysis to control the hypercalcaemia. Vitamin D was replaced intramuscularly with 200,000 IU, after which the calcium levels increased. She was treated with IV pamidronate 30 mg, and the calcium levels started reducing drastically. Antituberculous therapy (ATT) was initiated 7 days after pamidronate treatment. The calcium levels normalised 2 days after ATT and sustained beyond 2 months. Conclusion Interpretation of PTH and phosphate levels should be done with caution when evaluating hypercalcaemia in patients with advanced chronic kidney disease. First- and second-generation assays detect PTH fragments which accumulate in CKD, leading to false positives. Hypophosphataemic effects of PTH/PTHrP can be masked by accumulation of phosphate in CKD. Bisphosphonates might have a role in treating calcitriol-induced hypercalcaemia, although this needs further evaluation.