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



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



Internal Medicine 56(7): 811-817



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.

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Accession: 060109251

Download citation: RISBibTeXText

PMID: 28381748

DOI: 10.2169/internalmedicine.56.7778


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