C3 glomerulopathy in a patient with a history of post-infectious glomerulonephritis

• Published in: Pediatric nephrology (Berlin, West) Vol. 39; no. 3; pp. 745 - 748
• Main Authors: Nnadi, Nicole, Hendricks, Allen R., Torrealba, Jose, Drake, Keri A., Gattineni, Jyothsna
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.03.2024; Springer Nature B.V
• Subjects: Apheresis; Biopsy; Child; Clinical Insights; Complement C3; Complement component C3; Creatinine; Disease; Glomerulonephritis; Glomerulonephritis - diagnosis; Glomerulonephritis - etiology; Glomerulonephritis, Membranoproliferative; Hematuria; Hemodialysis; Humans; Hypocomplementemia; Infections; Kidney diseases; Kidney Diseases - pathology; Kidney Glomerulus - pathology; Medicine; Medicine & Public Health; Microscopy; Nephrology; Patients; Pediatrics; Remission; Remission (Medicine); Stains & staining; Urinalysis; Urine; Urology; Gross hematuria; Dense deposit disease; C3 glomerulopathy; Post-infectious glomerulonephritis; Proteinuria
• ISSN: 0931-041X; 1432-198X
• DOI: 10.1007/s00467-023-06177-5

Post-infectious glomerulonephritis (PIGN) is an immune complex mediated glomerular injury occurring because of an infection, most commonly with group A beta-hemolytic streptococcus in children. C3 glomerulopathy (C3G) is a distinct clinicopathological entity occurring secondary to dysregulation of alternate complement pathway encompassing both C3 glomerulonephritis (C3GN) and dense deposit disease (DDD). While most patients with PIGN attain complete remission with normalized complement levels by 6–8 weeks after presentation, patients with C3G continue to have hypocomplementemia with high rates of progressive kidney disease. Here, we report a patient diagnosed with dense deposit disease after his initial presentation with PIGN three years prior. While current literature continues to explore the overlapping and distinguishing features of PIGN and C3G, including how underlying defects in the alternate complement pathway may commonly contribute to both diseases, this case further exemplifies the importance of recognizing the clinico-pathogenic features of PIGN and C3G in pediatric patients with glomerulonephritis.