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<p>A young woman presented with a 17-year history of proteinuria, hematuria with persistent hypocomplementemia. She has been followed up for 2 years. The patient underwent comprehensive diagnostic evaluation, including two renal biopsies. The initial biopsy indicated membranoproliferative glomerulonephritis (MPGN), while the subsequent biopsy revealed concurrent thrombotic microangiopathy (TMA) kidney injury, suggesting a complement-mediated disorder. Genetic testing identified two heterozygous missense variants, c.848A &gt; G (p.Asp283Gly) and c.1339C &gt; T (p.Pro447Ser), in the Complement factor I (<i>CFI</i>) gene. Both are classified as variants of uncertain significance, suggestive of potential susceptibility to complement dysregulation. The clinical diagnosis was MPGN with overlapping TMA. Treatment with mycophenolate mofetil and losartan potassium resulted in reduced urinary protein, improved complement levels, and stabilized renal function; traditional Chinese herbal medicine was administered as supportive therapy. This case highlights the diagnostic challenges, when renal pathology indicates membranoproliferative-like lesions that cannot be explained by Ig-mediated or C3 glomerulopathy, especially accompanied by TMA lesions or persistent hypocomplementemia, complement system-related tests including complement regulatory gene mutation may helpful to establish the etiological diagnosis and guide management.</p>

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A young woman with membranoproliferative glomerulonephritis and persistent hypocomplementemia: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月28日

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  • Huimei Li,
  • Li Jinpu,
  • Lin Lan,
  • Zhou Shiqiang,
  • Li Shen,
  • Rao Xiangrong

摘要

A young woman presented with a 17-year history of proteinuria, hematuria with persistent hypocomplementemia. She has been followed up for 2 years. The patient underwent comprehensive diagnostic evaluation, including two renal biopsies. The initial biopsy indicated membranoproliferative glomerulonephritis (MPGN), while the subsequent biopsy revealed concurrent thrombotic microangiopathy (TMA) kidney injury, suggesting a complement-mediated disorder. Genetic testing identified two heterozygous missense variants, c.848A > G (p.Asp283Gly) and c.1339C > T (p.Pro447Ser), in the Complement factor I (CFI) gene. Both are classified as variants of uncertain significance, suggestive of potential susceptibility to complement dysregulation. The clinical diagnosis was MPGN with overlapping TMA. Treatment with mycophenolate mofetil and losartan potassium resulted in reduced urinary protein, improved complement levels, and stabilized renal function; traditional Chinese herbal medicine was administered as supportive therapy. This case highlights the diagnostic challenges, when renal pathology indicates membranoproliferative-like lesions that cannot be explained by Ig-mediated or C3 glomerulopathy, especially accompanied by TMA lesions or persistent hypocomplementemia, complement system-related tests including complement regulatory gene mutation may helpful to establish the etiological diagnosis and guide management.