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      A prolonged course of Group A streptococcus-associated nephritis: a mild case of dense deposit disease (DDD)?

      Clinical Nephrology
      Antigens, Bacterial, ultrastructure, Child, Glomerulonephritis, Membranoproliferative, diagnosis, drug therapy, immunology, microbiology, Glucocorticoids, administration & dosage, Hematuria, Humans, Kidney, pathology, Male, Methylprednisolone, Proteinuria, Pulse Therapy, Drug, Receptors, Cell Surface, Severity of Illness Index, Streptococcal Infections, complications, Streptococcus pyogenes

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          Abstract

          We herein report the case of a 12-year-old boy with dense deposit disease (DDD) evoked by streptococcal infection. He had been diagnosed to have asymptomatic hematuria syndrome at the age of 6 during school screening. At 12 years of age, he was found to have macrohematuria and overt proteinuria with hypocomplementemia 2 months after streptococcal pharyngitis. Renal biopsy showed endocapillary proliferative glomerulonephritis with double contours of the glomerular basement membrane. Hypocomplementemia and proteinuria were sustained for over 8 weeks. He was suspected to have dense deposit disease due to intramembranous deposits in the first and the second biopsies. 1 month after treatment with methylprednisolone pulse therapy, proteinuria decreased to a normal level. Microscopic hematuria disappeared 2 years later, but mild hypocomplementemia persisted for more than 7 years. Nephritis-associated plasmin receptor (NAPlr), a nephritic antigen for acute poststreptococcal glomerulonephritis, was found to be positive in the glomeruli for more than 8 weeks. DDD is suggested to be caused by dysgeneration of the alternative pathway due to C3NeF and impaired Factor H activity. A persistent deposition of NAPlr might be one of the factors which lead to complement dysgeneration. A close relationship was suggested to exist between the streptococcal infection and dense deposit disease in this case.

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