Pneumocystis carinii Pneumonia with Hypercalcemia and Suppressed Parathyroid Hormone Levels in a Renal Transplant Patient

Pneumocystis carinii pneumonia (PCP) is a rare complication of immunosuppressive therapy. It may cause significant morbidity and mortality after renal transplantation (1, 2) Its incidence after kidney transplantation is 2–11.5% and the clinical course varies from being virtually asymptomatic to lethal (2–4) The overall incidence of PCP in the population on cyclosporine(CsA) is relatively low (5). Hypercalcemia occurs frequently after kidney transplantation and is due to preexisting hyperparathyroidism. To the best of our knowledge, there has very few cases of hypercalcemia with normal intact parathyroid hormone (I-PTH) levels caused by PCP in a renal transplant recipient (6). We describe a renal transplant recipient with CsA based regimen infected with PCP who developed hypercalcemia, and suppressed I-PTH levels. A 53-year-old male with a history of end-stage renal failure due to chronic herbal use received renal transplant 3 months earlier in China. The posttransplant course was smooth without episode of acute rejection. The maintenance immunosuppressives were cyclosporine (CsA) 175 mg bid, mycophenolate 500 mg bid and prednisolone 20 mg qd. The patient presented with symptoms of dyspnea on exertion, dry cough and fever for 6 days before this admission. On physical examination, chest auscultation did not reveal any abnormal breath sound initially. On the second day of hospitalization, physical examination revealed basal rales over right lower lung. The chest X-ray revealed right lower lung fields nonspecific infiltration. The laboratory data showed mild leukocytosis with left shift. Serum free calcium level was 5.6 mg/dL (normal 4.5–5.1 mg/dl), phosphate 4.3 mg/dl, I-PTH: 12 pg/ml. (normal 12 to 72) Sputum smear showed some PMN without definite pathogen. The interval from the appearance of symptoms to the detection of pulmonary infiltration was 8 days. On the third day of hospitalization, sudden onset of severe dyspnea and cysnosis were noted. Endotracheal intubation was performed and the sputum smear showed negative for fungus, bacteria and acid-fast stain. Trimethoprim-sulfamethoxazole, and ganciclovir were given for empirical therapy. CXR featured diffuse ground-glass opacity over bilateral basal lung fields. The respiratory distress went worse even under the above medication. An open lung biopsy was performed and the pathological examination revealed finding indicative of pneumocystic carinii pneumonia that was further confirmed by Grocott's methenamine silver stain. Aggressive treatment by high dose steroid and ventilator were given for 2 more weeks and the general condition improved. Serum calcium return to normal and the patient was discharged in stable condition. Our case presented initially with fever and cough without pneumonia and then hypercalcemia with suppressed i-PTH levels. This may mimic the extrarenal production of 1,25-dihydroxyvitamin D by activated alveolar macrophages in granulomatous diseases with hypercalcemia (6). We were not able to measure serum 1,25-OH-vitamin D3 levels due to unavailable laboratory facility. However, serum calcium return to normal after complete treatment and open lung biopsy revealed pneumocystic carinii pneumonia. In conclusion, we described a renal transplant recipient with CsA based regimen infected with PCP who developed hypercalcemia and suppressed I-PTH. This entity should be included in the differential diagnosis for renal transplant recipients with hypercalcemia, especially in patients with pneumonia.