RESUMEN
C3 glomerulopathy is a series of diseases of glomeruli mediated by abnormal activation of alternative complement pathway. A series of researches have revealed in recent years that there are diversity and multiplicity of pathogenic mechanism in the pathogenesis of C3 glomerulopathy. The pathogenic mechanism of C3 glomerulopathy may be different in different individuals and types of disease. Congenital genetic defects and/or acquired autoantibodies may be found in the same individual. Individualized therapy should be given to individual patient in order to target different pathogenic mechanisms. Chinese herbal medicine, Tripterygium wilfordii, shows promise as a potential therapeutic agent for C3 glomerulopathy. The pathogenic mechanism and countermeasures for C3 glomerulopathy have been reviewed in present paper.
RESUMEN
A 21-year-old male was presented with sudden headache, fever, petechiae and neck stiffness. The diagnosis of meningococcal meningitis was confirmed by examination of cerebrospinal fluid. The clinical symptoms of the illness were improved after treatment of antibiotics. However the patient developed generalized edema, oliguria, azotemia, and heavy proteinuria in the recovery phase of illness. Low serum C3 level was also noted. A kidney biopsy was performed and showed the features of postinfectious glomerulonephritis and typical subepithelial humps on electron-microscopic examination. His symptoms and laboratory findings were improved, and C3 level returned to normal range after conservative treatment. We suggest that a complement deficiency should be ruled out in patients of glomerulonephritis developed during the recovery phase of meningococcal meningitis. C3 nephritic factor detection and renal biopsy should be carefully considered in these patients.