A case of bucillamine-induced membranous nephropathy presenting with acute kidney injury and requiring hemodialysis.

We present kidney biopsy findings in a 65-year-old male patient with rheumatoid arthritis who developed severe proteinuria 10 months after bucillamine administration and required hemodialysis 14 days later. Light microscopy revealed no spike formation but showed linear (partially granular) immunoglobulin (Ig)G-positive images (predominantly IgG1) along the capillary wall. Electron microscopy revealed widespread, large subepithelial electron-dense deposits (EDD). Foot process effacement was observed throughout the entire area, including areas with no apparent EDD. Neural epidermal growth factor-like 1 protein-positive images consistent with IgG were observed over a wide area. After administration of 60 mg of glucocorticoid, proteinuria subsided, and dialysis could be discontinued. Fifteen months after discharge, urinary protein was below 0.1 g/day. Even though bucillamine-induced membranous neuropathy may show few subepithelial EDDs, it has been reported cause severe proteinuria; however, no cases of acute kidney injury have been reported. The following mechanism is speculated as the cause of AKI. Although the arteriosclerotic lesions were mild in the kidney biopsy specimen, the severe hypoalbuminemia caused by severe proteinuria, combined with the drop in blood pressure due to losartan administration, led to an ischemic state, which is thought to have led to the onset of AKI.