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Post-vaccine glomerulonephritis in an infant with hereditary C2 complement deficiency: case study
1Tanja Kersnik Levart, Department of Pediatric Nephrology, University Medical Centre, Bohoriceva 20, 1000 Ljubljana, Slovenia, tanja.kersnik@guest.arnes.si.
Insights
This study reports the first case of immune complex-mediated glomerulonephritis in an infant with C2 complement gene mutations following vaccination. Treatment with methylprednisolone was successful, suggesting a link between C2 deficiency and vaccine-induced kidney disease.
Area of Science:
- Pediatric Nephrology
- Immunology
- Genetics
Background:
- Immune complex-mediated glomerulonephritis (ICGN) is a kidney inflammation.
- Complement component 2 (C2) deficiency is a rare genetic disorder affecting immune response.
- Vaccination can sometimes trigger immune-related adverse events.
Observation:
- A 3.5-month-old infant presented with nephritic syndrome post-vaccination.
- The infant had compound heterozygous mutations in the C2 complement component gene.
- Clinical and laboratory findings indicated ICGN.
Findings:
- This is the first reported case of post-vaccine ICGN in an infant with C2 deficiency.
- The patient showed a positive response to methylprednisolone treatment.
- The findings suggest a potential interaction between C2 deficiency and vaccine-induced immune responses.
Implications:
- Highlights a potential risk in infants with C2 deficiency following vaccination.
- Suggests C2 deficiency as a possible predisposing factor for vaccine-related glomerulonephritis.
- Underscores the importance of considering genetic complement deficiencies in unexplained nephritic syndromes.
Abstract:
We describe a case of a post vaccine immune complex-mediated glomerulonephritis in an infant with compound heterozygous mutations of C2 complement component gene, which is the first such case in the literature. The three and a half months old boy presented with clinical and laboratory signs of nephritic syndrome and was successfully treated with methylprednisolone. An explanation of such a clinical picture may lie in the interaction between C2 deficiency and vaccination.
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