Increased recognition of IgA nephropathy in African-American children

Based upon the percentage of cases of IgA nephropathy (IgAN) in biopsy series, a lower prevalence has been assumed for African-Americans compared with Americans of European descent. This may be due to a racial difference in the basic underlying pathology of IgAN or to racial differences in patterns of referral and biopsy selection practices. Over the past decade (1985 – 1994), we have found similar incidences of IgAN in Caucasian and African-American children from Shelby County, Tennessee. The incidence was 3.0 cases per million per year for Caucasian and 5.7 cases per million per year for African-American children. IgAN may be more common in African-American children than previously appreciated. Population-based incidence studies will be necessary to determine whether or not our experience has become a more widespread phenomenon. Received August 21, 1996; received in revised form and accepted December 18, 1996     

Terminal complement complexes in acute poststreptococcal glomerulonephritis

Activation of the complement cascade occurs in most cases of acute poststreptococcal glomerulonephritis (APSGN) and results in the formation of the terminal complement complexes (TCC). To examine the possible role of TCC in the pathogenesis of glomerular injury in APSGN, we studied 30 patients with the clinical diagnosis of APSGN. All patients had an elevated plasma SC5b-9 concentration at the onset of clinical nephritis. Serial plasma concentrations showed an inverse linear relationship with time after onset of clinical disease (r=–0.59,P=0.0008), while plasma C3 concentrations showed a positive linear relationship (r=0.78,P=0.0001). Renal biopsies of 5 patients demonstrated co-localization of C5b-9, S-protein, and C3 deposition in a glomerular capillary loop and mesangial distribution. Urinary excretion of TCC in the acute phase of APSGN was not elevated and was not a useful marker of disease activity. These data suggest that in APSGN with terminal complement pathway activation the local generation of TCC may contribute to the pathogenesis of the disease.