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<p>A 73-year-old woman had been treated with nintedanib for 40&#xa0;months for idiopathic pulmonary fibrosis. She presented to our hospital with lower extremity edema since a month and nephrotic syndrome (serum albumin 2.0&#xa0;mg/dL, urine protein 7.97&#xa0;g/g Cr). We performed a renal biopsy and diagnosed membranoproliferative glomerulonephritis (MPGN)-type IgA nephropathy (IgAN). We hypothesized that nintedanib-induced microangiopathy modified subclinical IgAN and caused the appearance of MPGN-type IgAN and nephrotic syndrome. After the discontinuation of nintedanib, the urinary protein level improved to 0.5&#xa0;g/g Cr, and hematuria disappeared.</p>

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A case of membranoproliferative glomerulonephritis-type IgA nephropathy modified by nintedanib

  • 期刊论文

  • 发表日期：

    2026年2月5日

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  • Yasushi Kunisho,
  • Tadashi Sofue,
  • Hirona Nagano,
  • Masato Higashitani,
  • Takafumi Shiga,
  • Aiko Shiraishi,
  • Yuhei Aoki,
  • Keisuke Onishi,
  • Emi Ibuki,
  • Tetsuo Minamino

摘要

A 73-year-old woman had been treated with nintedanib for 40 months for idiopathic pulmonary fibrosis. She presented to our hospital with lower extremity edema since a month and nephrotic syndrome (serum albumin 2.0 mg/dL, urine protein 7.97 g/g Cr). We performed a renal biopsy and diagnosed membranoproliferative glomerulonephritis (MPGN)-type IgA nephropathy (IgAN). We hypothesized that nintedanib-induced microangiopathy modified subclinical IgAN and caused the appearance of MPGN-type IgAN and nephrotic syndrome. After the discontinuation of nintedanib, the urinary protein level improved to 0.5 g/g Cr, and hematuria disappeared.