Published online Mar 18, 2026. doi: 10.5500/wjt.v16.i1.113117
Revised: September 10, 2025
Accepted: November 21, 2025
Published online: March 18, 2026
Processing time: 152 Days and 13.8 Hours
Complement-mediated thrombotic microangiopathy (TMA) is a rare endothelial injury syndrome caused by dysregulated activation of the alternative complement pathway, often linked to genetic abnormalities in complement factor H (CFH), complement factor I, or complement factor H-related (CFHR) proteins. Both renal transplantation and pregnancy are independent triggers for recurrence. This case highlights a genetically high-risk patient who achieved a successful term preg
A 32-year-old woman with end-stage renal disease secondary to genetically confirmed complement-mediated TMA—homozygous CFH exon 17 deletion and CFHR3-CFHR1 duplication—was maintained on dialysis for 2.5 years before undergoing a successful live-donor kidney transplant from her mother. Post-transplant immu
High-risk complement-mediated TMA patients can achieve successful pregnancy post-transplant through indi
Core Tip: This case highlights a rare instance of successful term pregnancy in a renal transplant recipient with genetically confirmed complement-mediated thrombotic microangiopathy—homozygous complement factor H exon 17 deletion and complement factor H-related (CFHR3-CFHR1) duplication—managed without complement blockade. Despite the dual risk posed by transplantation and pregnancy, careful preconception counseling, immunosuppressive modification, and vigilant multidisciplinary surveillance ensured stable graft function and favorable maternal-fetal outcomes. This report emphasizes individualized, genotype-informed management and adds valuable evidence to guide pregnancy counseling in women with complement dysregulation post-transplant.
