E-Poster Presentation ESA-SRB-ANZBMS 2021

PTH-independent hypercalcaemia due to Pneumocystis jiroveci pneumonia in a renal transplant recipient (#417)

Yeung-Ae Park 1 2 , Nicole Lafontaine 1 , Spiros Fourlanos 1 2
  1. Department of Diabetes and Endocrinology, Royal Melbourne Hospital, Parkville, Victoria, Australia
  2. Department of Medicine, Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia

A 68-year-old female presented to hospital with exertional dyspnoea five years post renal transplant for end-stage renal failure secondary to diabetic nephropathy. On admission, she was detected with hypercalcaemia (corrected calcium 3.39mmol/L), elevated phosphate (1.65mmol/L), non-suppressed PTH (7.9pmol/L; reference range 1.7-10.0pmol/L) and a mild acute kidney injury in the context of  known previous hyperparathyroidism (PTH of 48pmol/L, corrected calcium 2.64mmol/L and phosphate 1.05mmol/L one month prior). The significant reduction in PTH was suggestive of new PTH-independent hypercalcaemia.

CT chest demonstrated bilateral diffuse ground-glass opacities and pulmonary fibrosis, not suggestive of TB or lymphoma. Due to clinical improvement with empirical ceftriaxone and doxycycline, the patient was planned for discharge as per Respiratory colleagues. However further investigations were performed due to the concern of a systemic process causing PTH-independent hypercalcaemia.

Her serum 25-hydroxyvitamin D level (55nmol/L; reference range >50nmol/L), 1,25-dihyroxyvitamin D level (118pmol/L; reference range 50-190pmol/L) and Angiotensin-Converting Enzyme level were unremarkable and myeloma screen was negative. Sputum samples and later bronchoscopy confirmed Pneumocystis jiroveci pneumonia (PJP), which is known to cause PTH-independent hypercalcaemia. Intravenous pamidronate 30mg was administered to manage persistent hypercalcaemia while investigations were being performed. Corrected calcium improved to 2.66mmol/L. Five months post treatment of PJP, hypercalcaemia resolved (2.50mmol/L) and PTH increased (144.0pmol/L) consistent with longstanding secondary hyperparathyroidism. She remains normocalcaemic two years later.

Cases of hypercalcaemia due to PJP have been previously reported (1-12). A granuloma-mediated mechanism with extrarenal production of 1-alpha hydroxylase has been hypothesised (1). However in our case, macroscopic bronchoscopy was unremarkable, no granulomas were noted on imaging, and serum 1,25-dihyroxyvitamin D level was not elevated, which has been infrequently reported in previous cases (2). 

In patients with chronic hyperparathyroidism, hypercalcaemia with a reduction in PTH should prompt consideration of PTH-independent causes. In immunocompromised patients with PTH-independent hypercalcaemia and exertional dyspnoea, PJP should be considered.

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