2007 Volume 20 Issue 1 Pages 67-70
We report a 14-year-old-boy with recurrent poststreptococcal acute glomerulonephritis (PSAGN).
On 17 November 2003 (at the age of 11y10mo), he was brought to hospital because of facial edema, macrohematuria and dyspnea. His blood pressure was 170/130mmHg. Laboratory data showed depression of complement C3 44mg/dl (norma l86-160mg/dl) and mild renal insufficiency. He was diagnosed as PSAGN, and improved in a short time by intravenous administration of furosemide. Four weeks later, urinary abnormalities had subsided completely. In June 2006 (at the age of 14y5m), he had a sore throat, which subsided without any medication. On 10 June 2006, he was brought to hospital and diagnosed as PSAGN again. Therefore, he was referred to our hospital and renal biopsy was performed. Light microscopic examination showed diffuse and global endocapillary proliferation. Immunofluorescense showed diffuse and granular deposition of C3. Because of histological findings compatible with PSAGN, no specific therapy was perfomed. Four months later, his laboratory data were normal except for mild proteinuria (less than 0.5g/day).Recurrence of PSAGN is a rare phenomenon. While the mechanism leading to the recurrence of PSAGN has not yet been identified, Watanabe et al suggested that an absence of a natural immune response against a streptococcal cytoplasmic antigen (nephritis-associated plasmin receptor protein, NAPlr) caused recurrent PSAGN in some patients. We consider that present case is similar to their report.
