SUN-779 - Beyond Hyperparathyroidism: Pneumocystis Jirovecii as an Unexpected Cause of Hypercalcemia in A Kidney Transplant Recipient

Hypercalcemia is traditionally categorized as parathyroid- or non–parathyroid-mediated based on serum parathyroid hormone (PTH) levels. We present a case that challenges this binary approach.
A 51-year-old male with a history of FSGS s/p renal transplant (on immunosuppressives), Renal Cell Carcinoma (RCC), CKD; presented with fatigue, lightheadedness, anorexia, and dry cough x 2 weeks, and was admitted with Pneumocystis Jirovecii Pneumonia (PJP). Targeted antimicrobial treatment was initiated.
On admission serum calcium was 11.4 mg/dL. PTH was also elevated at 131.6 pg/mL (9.0-77 pg/mL), concerning for parathyroid-mediated hypercalcemia. Patient was started on IVFs and cinacalcet, but hypercalcemia worsened over the next few days regardless. On (hospital) day 6 Prednisone was started for hypoxia associated with PJP. On day 7 serum calcium reached its peak of 13.3 mg/dL. A subsequent in-depth Chart review revealed that previously his baseline PTH was 400–600 pg/mL in the setting of Secondary hyperparathyroidism. Current PTH being lower than his baseline was considered to be more consistent with a PTH-independent process. Patient denied taking calcium supplements. Two possible differential diagnoses at that time were PTHrp (in the setting of RCC) or calcitriol driven (in the setting of PJP) hypercalcemia. IM Calcitonin and IV Pamidronate were utilized to treat the surge in serum calcium, which led to a rapid resolution of hypercalcemia. PTHrp and 1,25-dihydroxyvitamin D labs were not collected until day 12; which was six days after Prednisone and eight days after anti-microbials were started. Patient was discharged on the same day on a prednisone taper. After discharge PTHrP resulted negative; while serum 1,25-dihydroxyvitamin D was 38 (20-79) pg/mL.
In granulomatous diseases the elevated levels of 1,25-dihydroxyvitamin D are due to extrarenal production by activated pulmonary macrophages. While PJP typically does not produce granulomas, approximately 5% of cases demonstrate granulomatous inflammation.
Glucocorticoids begin lowering 1,25-dihydroxyvitamin D levels within 2-5 days; while the half-life of calcitriol is 5-8 hours. In our case sufficient time had elapsed, by the time the lab was collected, for glucocorticoid-mediated suppression of calcitriol production and clearance of existing calcitriol.
This case highlights a critical diagnostic pitfall: a single elevated PTH value does not exclude PTH-independent hypercalcemia. Recognition of relative PTH suppression and the temporality in between hypercalcemia and the acute respiratory infection were key to identifying this rare presentation of PJP-associated hypercalcemia in an immunosuppressed host.

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