Dr Evelyn Perry1, Dr Gary Tjipto1, Dr Shi Choo1
1Barwon Health, , Australia
Biography:
Evelyn Perry is a renal advanced trainee at Barwon Health. She has an interest in general nephrology and renal genetics.
Background:
Pneumocystis jirovecii pneumonia (PJP) is a life-threatening opportunistic infection in immunocompromised hosts, including renal transplant recipients. Hypercalcaemia secondary to calcitriol overproduction by activated macrophages is a rare but recognized manifestation of granulomatous or atypical infections such as PJP.
Case Report:
A 57-year-old woman with a renal transplant presented with fever, chills, and mild cough. She had a history of Gitelman syndrome, bowel cancer with prior resections, a subtotal parathyroidectomy and was on long-term immunosuppression. Initial investigations showed acute kidney injury, lymphopenia, and radiologic evidence of bilateral interstitial and alveolar infiltrates. Despite empiric antibiotics, her condition deteriorated with worsening hypoxia and hypercalcaemia (peak corrected calcium 3.89 mmol/L). A positron emission tomography (PET) scan revealed widespread pulmonary uptake consistent with atypical infection. Given worsening respiratory failure, she was empirically treated for PJP with trimethoprim-sulfamethoxazole and corticosteroids, resulting in clinical improvement. Refractory hypercalcaemia was managed with fluids and frusemide, bisphosphonates, calcitonin, corticosteroids, and denosumab. Investigations revealed markedly elevated 1,25-dihydroxyvitamin D (>480 pmol/L) with suppressed PTH (2 pmol/L), supporting a calcitriol-driven, macrophage-mediated mechanism. She was discharged on day 15 of PJP therapy with plans for 28 days of treatment and lifelong prophylaxis.
Conclusions:
This case highlights PJP as an important differential in transplant recipients with pulmonary infiltrates and unexplained hypercalcaemia. The degree of hypercalcaemia was severe and refractory, requiring multimodal therapy. The presence of high calcitriol levels and suppressed PTH suggests macrophage-driven vitamin D activation.