Post-infectious Proliferative Glomerulonephritis with Monoclonal Immunoglobulin G Deposits Associated with Complement Factor H Mutation

Intern Med. 2017;56(7):811-817. doi: 10.2169/internalmedicine.56.7778. Epub 2017 Apr 1.


A 55-year-old man developed rapidly progressive glomerulonephritis and nephrotic syndrome. A kidney biopsy specimen showed diffuse proliferative and crescentic glomerulonephritis with monoclonal IgG1κ, humps, and nephritis-associated plasmin receptor, indicating infection-associated proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID). Despite dialysis-dependent renal failure, symptomatic therapy resulted in spontaneous recovery of the renal function, mimicking post-infectious glomerulonephritis (PIGN). A heterozygous complement factor H mutation was detected by comprehensive genetic testing of alternative pathway regulatory genes, which might lead to persistent infection-triggered alternative pathway activation and account for severe glomerulonephritis. Post-infectious PGNMID and PIGN might share common clinical presentations and pathogenesis related to the complement pathway.

Publication types

  • Case Reports

MeSH terms

  • Complement Factor H / genetics
  • Glomerulonephritis, Membranoproliferative / drug therapy
  • Glomerulonephritis, Membranoproliferative / physiopathology*
  • Humans
  • Immunoglobulin G / metabolism*
  • Male
  • Middle Aged
  • Mutation
  • Receptors, Peptide / metabolism
  • Renal Dialysis
  • Renal Insufficiency / physiopathology


  • CFH protein, human
  • Immunoglobulin G
  • Receptors, Peptide
  • plasmin receptor
  • Complement Factor H