Abstract: SA-PO0564
Calcitriol-Mediated Hypercalcemia in Pneumocystis jirovecii Pneumonia
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Ohonba, Nosagie, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Sedlacek, Martin, Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction
Hypercalcemia in chronic kidney disease is often attributed to hyperparathyroidism, medications, malignancy, or granulomatous disease. However, elevated 1,25-dihydroxyvitamin D–mediated hypercalcemia can rarely occur with opportunistic infections. Here, we present a case of hypercalcemia from Pneumocystis Jirovecii pneumonia (PJP) as a result of extrarenal calcitriol production.
Case Description
A 37-year-old woman with systemic lupus erythematosus complicated by lupus nephritis, CKD stage IV, presented with acute hypoxia shortly after hospitalization for acute pancreatitis and recent AKI. Her baseline creatinine was 1.7–2.0 mg/dL and had recently risen to the low 3 mg/dL range before improving. Evaluation did not suggest active lupus nephritis, with stable complements, non-elevated anti-dsDNA, and urinalysis without hematuria or significant proteinuria. She remained on mycophenolate mofetil, tacrolimus, and low dose corticosteroids.
She developed respiratory failure requiring intubation and was diagnosed with severe PJP pneumonia. Subsequent laboratory results showed corrected calcium maintained around11.5 mg/dL, and ionized calcium 1.65 mmol/L. Intact PTH was 21 pg/mL, inappropriately low-normal for hypercalcemia, while 1,25-dihydroxyvitamin D was markedly elevated at 300 pg/mL. In the absence of lupus flare, malignancy, or another granulomatous process, her hypercalcemia was attributed to PJP-associated calcitriol excess. She received intravenous dexamethasone with improvement.
Discussion
Calcitriol-mediated hypercalcemia is classically associated with lymphoma, sarcoidosis, tuberculosis, and other granulomatous diseases, but PJP is an important rare cause in immunocompromised patients. Prior case series have reported hypercalcemia in approximately one-third of PJP cases, usually with low or suppressed PTH and elevated 1,25-dihydroxyvitamin D, supporting macrophage-mediated extrarenal calcitriol production. This unregulated calcitriol excess increases intestinal calcium absorption and may be clinically significant in patients with CKD.
This case highlights the need to include opportunistic infections in the differential for non-PTH-mediated hypercalcemia. Treatment focuses on PJP therapy, supportive hypercalcemia management, and glucocorticoids when appropriate, as steroids may suppress macrophage-mediated calcitriol production while also treating hypoxic PJP.