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Abstract: SA-PO696

Refractory Hypercalcemia: Unmasking Pneumocystis jirovecii Pneumonia in a Renal Transplant Recipient

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Ng, Wern Lynn, UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Sangha, Lillian, UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Ravichander, Benjamin, UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Calderon Martinez, Evelyn J., UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Ng, Lay She, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Calderon Barahona, Gabriela M., UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Tan, Jia Yi, New York Medical College, Newark, New Jersey, United States
  • Sharma Gautam, Seema, UPMC Harrisburg, Harrisburg, Pennsylvania, United States
  • Mishagina, Irina, UPMC Harrisburg, Harrisburg, Pennsylvania, United States

Refractory hypercalcemia in renal transplant recipients is a challenging consequence of Pneumocystis jirovecii pneumonia (PJP). Accurate diagnosis is crucial, as PJP can present subtly, leading to increased mortality rates. In renal transplant patients, hypercalcemia frequently accompanies PJP and serves as a vital diagnostic clue. In this report, we present a case of refractory hypercalcemia resulting from PJP in a renal transplant recipient, highlighting the need for effective recognition and management.

Case Description

A 57-year-old male with a history of renal transplant, currently on immunosuppressive therapy, who was admitted to the hospital with fevers and general malaise. Laboratory findings revealed marked hypercalcemia (15.6 mg/dL) with suppressed parathyroid hormone (PTH) levels. Extensive Infectious investigations, including urinalysis, chest x-ray, commuted tomography (CT) of the chest, abdomen, and pelvis, blood cultures, viral panel tests yielded no significant findings. Despite administration of isotonic saline, calcitonin, and bisphosphonates, the patient’s hypercalcemia remained unresponsive. Further laboratory studies revealed normal PTH-Related Protein (14 pg/mL), elevated 1,25 dihydroxy vitamin D (133 pg/dL), and normal 25-dihydroxy vitamin D (52 ng/dL). Due to persistent fever in an immunosuppressed individual, an extensive infectious investigation was conducted, including tests for various viruses and pathogens. A breakthrough was achieved when the qualitative PCR test for PJ returned positive. The patient was promptly initiated on systemic steroids and atovaquone therapy targeting PJP. Serum calcium returned to normal after completion of therapy.


Hypercalcemia in renal transplant patients with PJP results from a granulomatous-like mechanism. Macrophages and monocytes in granulomas play a vital role by producing 1-alpha hydroxylase, converting calcidiol to calcitriol, the active form of Vitamin D. Calcitriol stimulates increased calcium absorption in the intestines and kidneys and calcium mobilization from bone tissue, leading to hypercalcemia. Therefore, when evaluating a renal transplant patient presenting with hypercalcemia, it is crucial to consider PJP as a potential differential diagnosis.