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Absence of mesangial IgA in AIDS: a postmortem study.

Marie-Christine Béné, Laboratoire d’lmmunologie, Centre Hospitalier Régional Universitaire de Nancy-Brabois, F-54500 Vandœuvre (France) Sir, A recent paper published in Nephron [5] reports the discovery of IgA nephropathy (IgAN) upon renal biopsy in 2 patients with AIDS-related complex. The authors stress the similarities that may be observed between these two diseases, namely high levels of serum IgA, IgAl, and IgAcontaining immune complexes. Both patient populations also suffer from frequent respiratory or, at large, mucosal infections. These similarities have been noted for some time; therefore, the small number of reported AIDS patients with IgAN is quite surprising. It might be that the renal disease goes unnoticed in a population with major health impairment. AIDS patients also have an unfortunately short life expectancy, while renal failure often occurs in IgAN patients after several years of development [3]. Based on these assumptions, we undertook a systematic study of renal biopsies performed within 24 h post mortem in deceased AIDS patients, and snap-frozen in liquid nitrogen. IgA deposits have been shown to remain for up to 15 days in postmortem samples [7], and the protocol used was similar to that used in a previous study on liver cirrhosis patients [2]. Between January 1986 and May 1990, frozen-cut sections of 54 kidney samples, obtained from 48 men and 6 women (mean age 32 years) were thus examined in direct immunofluorescence using antisera to IgA and complement factor C3 (reagents from Behring, Marburg, FRG). There was no significant labelling in 53 of these biopsies. Granular endomembraneous deposits of both IgA and C3 were observed in 1 patient. This 40-year-old man was a hemophiliac with transfu-sional AIDS. He developed severe hepatitis associated with high levels of anti-HSV antibodies, and evidence of liver infection by HSV. The histologic examination of liver biopsies disclosed progressive cirrhosis. He had portal hypertension and large volumes of ascitic fluid were repeatedely removed from his abdomen. Several urine analyses were performed, never disclosing hematu-ria. Serum IgA levels were assessed in February and May 1988 and were 2.22 and 3.21 g/l, respectively. He died in December 1988 from pulmonary complications. The im-munofluorescent labelling observed in his kidney was very similar to the pattern previously reported in liver cirrhosis patients and differed from the strictly mesangial deposits of Berger’s disease [1, 2].