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1 etiologic agent of a large 1998 outbreak of poststreptococcal acute glomerulonephritis (PSGN) in Nov
2 ology was also significantly elevated in the poststreptococcal ADEM group compared with neurological
3 ntense basal ganglia in 80% of patients with poststreptococcal ADEM, compared to 18% of patients with
5 coccal reactive arthritis (PSRA) refers to a poststreptococcal arthritic condition that does not fulf
6 ortant role in the expression of tics, and a poststreptococcal autoimmune cause has been proposed but
10 is no effective disease-specific therapy for poststreptococcal glomerulonephritis or IgA nephropathy.
11 ve been found at a higher frequency in acute poststreptococcal glomerulonephritis patients than in he
12 roup A streptococcal disease including acute poststreptococcal glomerulonephritis remains a cause of
13 by a nephritogenic streptococcal protein in poststreptococcal glomerulonephritis, and by mesangial d
14 rulonephritis that occur in childhood: acute poststreptococcal glomerulonephritis, IgA nephropathy, A
15 onephritis without systemic disease includes poststreptococcal glomerulonephritis, IgA nephropathy, r
20 requency of the DRB1*01 allele was higher in poststreptococcal ReA patients (odds ratio [OR] 2.7, P=0
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