Long-term outcome of acute tubulointerstitial nephritis: report of a case

Abstract

microscopy revealed numerous discrete granular subepithelial deposits (“humps”), but no mesangial or subendothelial deposits were present (Figure 1b). Complement level returned to normal 1 month after initial presentation. Convalescence was uneventful and there were no recurrences. Eight months later, the patient has been entirely asymptomatic except for persistent microscopic hematuria. Both APSGN and HSP are thought to be the result of aberrant reactions to infectious agents, the former leading predominantly to complement activation and the latter to the formation of immune complexes containing IgA, which do not tend to activate complement [Krause et al. 1999]. It is not surprising that there are variations to this response as previously described [Cadnapaphornchai et al. 2000, Krause et al. 1999, Maruyama et al. 1995, Onisawa et al. 1989]. The final conclusion that this patient had both APSGN and HSP is not necessary and the findings are more likely to be one pathology which does not precisely fit the classical form of either disease.