A 71-year-old male presented in 2012 with symptoms of alveolar hemorrhage, abnormal urine analysis, and renal dysfunction (serum creatinine level：4 mg/dL). The patient was positive for MPO-ANCA. Renal biopsy revealed crescentic glomerulonephritis, and he was diagnosed with ANCA-associated vasculitis. Treatment with prednisolone and various immunosuppressive drugs resolved the alveolar hemorrhage and improved the creatinine level to around 2 mg/dL. In March 2017, the patient was treated for alveolar hemorrhage with methylprednisolone pulse therapy. His renal function gradually worsened, and in October 2017, hemodialysis was initiated. At the time of initiation, alveolar hemorrhage was present, and the patient received methylprednisolone pulse therapy. Within a few days, the bloody sputum disappeared, and there were no respiratory symptoms. He had been taking trimethoprim-sulfamethoxazole to prevent pneumocystis pneumonia for a prolonged period and continued to take the drug after admission (80 mg of trimethoprim twice a week). However, on the 19th day, a nodule shadow appeared in the right middle lung field on plain chest X-ray and it was enlarging. No respiratory symptoms were present, but Nocardia was identified via sputum culture, ultimately leading to a diagnosis of pulmonary nocardiosis. The background of steroid therapy and induction of dialysis were considered to be the trigger for pulmonary nocardiosis in this case. Treatment with trimethoprim-sulfamethoxazole was initiated, and the nodule shadow reduced. In the early stages of dialysis initiation, there is a well-known higher incidence of tuberculosis due to cellular immunosuppression. In dialysis-initiated patients undergoing immunosuppressive therapy, Nocardia infection should also be considered.
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