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- Eriko Takehara, Shintaro Mandai, Satomi Shikuma, Wataru Akita, Motoko Chiga, Takayasu Mori, Takashi Oda, Michio Kuwahara, and Shinichi Uchida.
- Department of Nephrology, Shuuwa General Hospital, Japan.
- Intern. Med. 2017 Jan 1; 56 (7): 811-817.
AbstractA 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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