Answers are grounded in this paper and cite their sources.
Case presentation reveals ANLN mutation causing C3 glomerulonephritis, suggesting new implications for management.
Background:C3 glomerulonephritis (C3GN) is a rare glomerular disease caused by alternative complement pathway dysregulation.ANLN gene mutations have been previously associated with podocytopathies but not linked to C3GN. Case Presentation:We describe two unrelated patients presenting with nephrotic-range proteinuria, low serum C3, and renal biopsy findings consistent with C3GN.Comprehensive workup excluded autoimmune and infectious causes; anti-factor H antibody and serum protein electrophoresis were negative.Genetic testing using whole exome sequencing and MLPA revealed a heterozygous missense variant (p.Asp556Asn) in exon 10 of the ANLN gene (chr7:g.36419276G>A,depth 79x).Treatment with angiotensin converting enzyme inhibitors, mycophenolate mofetil (1 g/day), and corticosteroids (0.5 mg/kg/day tapered over 6 months) resulted in marked proteinuria reduction (Case 1: from 5 g/day to 1.2 g/day in 3 months; Case 2: from 7.5 g/day to 900 mg/day in 6 months) with stable kidney function. Conclusions:These cases represent the first report linking ANLN mutation to C3GN, expanding the phenotypic spectrum of ANLN-associated nephropathies into complement-mediated glomerular disease.The findings highlight the importance of genetic testing in atypical C3GN and underscore implications for diagnosis, management, and counselling.
No takes yet. Share an insight, caveat, or question.
Shankar et al. (2026) studied this question.
Synapse has enriched 8 closely related papers on similar clinical questions. Consider them for comparative context: