A 26-year-old, nonsmoking man with history of Alport syndrome (ie, X-linked Alport syndrome [XLAS]), who was receiving hemodialysis consequent to a previously rejected living donor renal allograft, underwent retransplantation with a cadaveric renal allograft. His medical history was significant for the occurrence of DAH 2 years previously, which had been thought to be secondary to sirolimus therapy in the setting of chronic allograft nephropathy and uremia. Preoperative medications included lisinopril, multivitamins, and calcium acetate. Intraoperatively during the retransplantation procedure, the patient received a single dose of alemtuzumab, 30 mg IV, as a part of the immunosuppressive induction protocol. On the second postoperative day, mild hemoptysis and dyspnea developed in the patient, along with new-onset anemia (hemoglobin level, 7.3 g/dL) and thrombocytopenia (platelet count, 54,000 cells/μL) compared to hospital admission values of 9.1 g/dL and 127,000 cells/μL, respectively. Notably, tacrolimus therapy was started 4 days after surgery, and his symptoms thus occurred well before the initiation of tacrolimus therapy. Pulmonary consultation was sought after his symptoms failed to improve, and he continued to have worsening hemoptysis and a requirement for oxygen therapy. Arterial blood gas levels obtained with a 0.4 fraction of inspired oxygen showed a Pao2 of 74 mm Hg, with a Pao2/fraction of inspired oxygen ratio of 185. A physical examination of the chest revealed bilateral late, fine, inspiratory crackles in the mid-to-lower lung fields. The results of serial chest radiographs showed evolving bilaterally diffuse alveolar opacities, which were confirmed by a chest CT scan (Fig 1
). BAL fluid, which showed a characteristic increasingly bloody return in the sequential aliquots and an RBC count of 239,500 cells/μL, was obtained from the right middle lobe. There was no growth of pathogenic bacteria or evidence of opportunistic infection in the BAL fluid. A peripheral smear did not reveal any significant schistocytes, and the serum haptoglobin level was 70 mg/dL (range, 30 to 200 mg/dL). He required intubation and mechanical ventilation for 5 days secondary to acute respiratory failure. Acute renal failure developed, and thus he was placed on therapy with plasmapheresis (six plasma exchanges) for presumed anti-glomerular basement membrane (GBM) antibody disease of the allograft.3 Concomitantly, he required hemodialysis for 1 week for the treatment of his acute renal failure secondary to acute tubular necrosis, which was confirmed by renal biopsy. There was no evidence of acute rejection or anti-GBM disease (the immunofluorescence stain performed was negative for humorally mediated injury on the renal biopsy specimen). Testing results for serum antineutrophil cytoplasmic antibody, anti-GBM antibody, and antinuclear and antiphospholipid antibody levels were negative. The hospital course was complicated by the development of sigmoid perforation requiring end-colostomy. The patient was eventually discharged from the hospital on postoperative day 28.