Complement gene mutations in children with C3 glomerulopathy: do they affect the response to mycophenolate mofetil?

Neslihan Günay1, İsmail Dursun2, İbrahim Gökçe3

  • 1Department of Pediatric Nephrology, Kayseri City Training and Research Hospital, Kayseri, Turkey.

Insights

Genetic mutations in pediatric C3 glomerulopathy (C3G) patients are linked to later diagnosis and asymptomatic urinary issues. Mycophenolate mofetil treatment did not impact kidney survival in either group.

Area of Science:

  • Nephrology
  • Genetics
  • Complement System

Background:

  • C3 glomerulopathy (C3G) is a complement-mediated kidney disease.
  • Genetic testing aids in treatment planning and prognosis for C3G.
  • Understanding genotype-phenotype correlations is crucial for pediatric C3G management.

Purpose of the Study:

  • To investigate clinical phenotypes in pediatric C3G patients with and without complement-related gene mutations.
  • To assess kidney survival rates in these pediatric C3G patient groups.
  • To evaluate the response to mycophenolate mofetil (MMF) treatment based on genetic status.

Main Methods:

  • Retrospective analysis of 60 pediatric C3G patients.
  • Stratification into groups based on the presence or absence of complement-related gene mutations.
  • Comparison of demographic, clinical-pathological, treatment, and outcome data; Kaplan-Meier analysis for kidney survival.

Main Results:

  • 17 out of 60 patients had mutations, most commonly in the CFH gene.
  • Mutation group had a higher mean age at diagnosis and more asymptomatic urinary abnormalities.
  • No significant difference in MMF treatment response or kidney survival between groups; MMF showed no effect on progression.

Conclusions:

  • The mutation group in pediatric C3G often presents with asymptomatic urinary abnormalities and later diagnosis.
  • Despite genetic differences, MMF treatment response and kidney survival were similar between mutated and non-mutated C3G groups.
  • This study highlights the importance of genotype in understanding C3G phenotypes but not treatment outcomes.
Abstract