Hypercalcemia from Pneumocystis Jirovecii Pneumonia in a Renal Transplant Recipient

Learning Objective #1: Recognize clinical and laboratory features of Pneumocystis jirovecii pneumonia (PJP) in immunocompromised patients Learning Objective #2: Treat hypercalcemia in the setting of acute kidney injury CASE: A 63-year-old male with a past medical history of a living unrelated donor renal transplant secondary to autosomal dominant poly-cystic kidney disease presented with 3 weeks of fatigue, persistent nonproductive cough, subjective chills, and worsening exertional dyspnea. Chest computed tomography showed ground-glass opacities and increased interstitial markings involving the left lung and right perihilar region without pleural effusion, pneumothorax, or cardiomegaly. He was empirically started on daily intravenous (IV) azithromycin and ceftriax-one due to suspected multifocal pneumonia. Acute kidney injury (AKI) with a creatinine of 3.4 mg/dL and BUN of 67 mg/dL was noted. He was admitted to the intensive care unit with hypoxic respiratory failure and escalation to broader spectrum antibiotics: vancomycin and piperacillin/tazobactam. He was noted to have coarse breath sounds with wheezing on lung exam. Initial labs revealed a serum calcium (Ca+2) of 12.0 mg/dL. Vancomycin was subsequently changed to IV Linezolid. IV Clindamycin and Primaquine daily were added due to suspected PJP. Bronchoscopy with bronchoalveolar lavage revealed a white blood cell count of 103/μ L with no organisms. PJP on polymerase chain reaction and elevated-D-glucan were noted. Antibiotics were then tailored to 3 weeks of Clindamycin and Primaquine to treat PJP. His Ca+2 increased to 13.5 mg/dL likely due to PJP and AKI. Additional laboratory data revealed suppressed parathyroid hormone (PTH) levels at 15 pg/mL and elevated 1,25-dihydroxy-vitamin D (1,25-(OH)2 D3) at 156 pg/mL. His hypercal-cemia proved resistant to IV fluids followed by IV diuresis, ketoconazole, and calcitonin. However, his Ca+2 corrected to 10.0 mg/dL after administration of a denosumab injection. IMPACT/DISCUSSION: This case demonstrates the intricate care and teamwork needed to care for a patient with a complicated clinical course. Approaching the treatment of hypercalcemia in a stepwise manner with attention to AKI resulted in improvement. Previously, hypercalcemia has been reported with PJP in many case reports. Ling et al. presented cases of PJP-induced hypercalcemia. It has been suggested that in PJP, interferon-induced alveolar macrophage activation of 1-hydroxylase converts 25-(OH) vitamin D to active 1,25-(OH)2 D3. In turn, activated vitamin D3 increases Ca+2 absorption from the intestine and bone. PTH is suppressed as the normal inhibitory feedback mechanism is not affected. Conclusion: We present a particularly resistant case of PJP-induced hypercalcemia, which resolved with a single denosumab injection