protein positivity and urinary level of N-acetyl--D-glucosaminidase was increased to 52.2 U/L, suggesting renal tubular injury.A second kidney biopsy was performed for diagnostic clarification.Results: In the second kidney biopsy, most glomeruli demonstrated mesangial matrix expansion and glomerular hypertrophy.Immunofluorescence staining, kappa light chain depositions were predominantly observed in tubular epithelial cells.Electron microscopy demonstrated irregular granular material within proximal tubular epithelial cells.Therefore, he was diagnosed with CN coexisting with LCPT.Proteinuria decreased to 2 g/gCr with bed rest and dietary restriction and stabilized around 3 g/gCr after initiation of a sodium glucose cotransporter 2 (SGLT2) inhibitor, without immunosuppressive therapy.In CN, a nephrotic level of proteinuria has been reportedly caused by secondary FSGS due to glomerular hyperfiltration.However, the current patient was diagnosed with membranous nephropathy in the first biopsy and LCPT in the second biopsy, respectively, suggesting that various renal diseases can coexist with CN.Therefore, when urinary abnormal findings are detected in CN, kidney biopsy should be considered for making an accurate diagnosis. Conclusion:We report a case emphasizing that patients with CN can coexist with multiple etiologies of renal diseases such as FSGS, MN and LCPT.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.
kudaka et al. (Wed,) studied this question.