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<p>Immune checkpoint inhibitors can trigger renal immune-related adverse events, including glomerular disease. We report an 84-year-old man with non–small cell lung cancer who developed nephrotic syndrome after starting durvalumab. Proteinuria rose to 4+ four weeks into durvalumab therapy, and by week 6 serum albumin had fallen to 2.7&#xa0;g/dL, prompting discontinuation. He was referred in January 2024 with serum albumin 2.0&#xa0;g/dL and a urine protein–creatinine ratio of 13.57&#xa0;g/gCr. Kidney biopsy demonstrated membranous nephropathy: capillary-wall thickening with spike formation on PAM, granular capillary-wall IgG on immunofluorescence, and scattered subepithelial deposits with widespread foot-process effacement on electron microscopy. IgG subclass staining showed a non-IgG4-dominant pattern (IgG1 &gt; IgG4 &gt; IgG2 &gt; IgG3), supporting secondary MN in the setting of ICI exposure. Prednisolone 0.7&#xa0;mg/kg/day (50&#xa0;mg/day) was initiated, inducing complete remission by day 13, with sustained remission during taper to 5&#xa0;mg/day. To our knowledge, this is the first report of de novo MN temporally associated with durvalumab; together with the available literature on ICI-associated MN, these findings support prednisolone (glucocorticoids) as a reasonable first-line therapy.</p>

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Durvalumab-associated membranous nephropathy: a case report and brief literature review

  • 期刊论文

  • 发表日期：

    2026年1月22日

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  • Ryotaro Mizoguchi,
  • Takeshi Tashiro,
  • Masanori Sakakima

摘要

Immune checkpoint inhibitors can trigger renal immune-related adverse events, including glomerular disease. We report an 84-year-old man with non–small cell lung cancer who developed nephrotic syndrome after starting durvalumab. Proteinuria rose to 4+ four weeks into durvalumab therapy, and by week 6 serum albumin had fallen to 2.7 g/dL, prompting discontinuation. He was referred in January 2024 with serum albumin 2.0 g/dL and a urine protein–creatinine ratio of 13.57 g/gCr. Kidney biopsy demonstrated membranous nephropathy: capillary-wall thickening with spike formation on PAM, granular capillary-wall IgG on immunofluorescence, and scattered subepithelial deposits with widespread foot-process effacement on electron microscopy. IgG subclass staining showed a non-IgG4-dominant pattern (IgG1 > IgG4 > IgG2 > IgG3), supporting secondary MN in the setting of ICI exposure. Prednisolone 0.7 mg/kg/day (50 mg/day) was initiated, inducing complete remission by day 13, with sustained remission during taper to 5 mg/day. To our knowledge, this is the first report of de novo MN temporally associated with durvalumab; together with the available literature on ICI-associated MN, these findings support prednisolone (glucocorticoids) as a reasonable first-line therapy.