IGA SEROLOGY IN RECURRENT AND NONRECURRENT IGA NEPHROPATHY AFTER RENAL-TRANSPLANTATION

Background. This study investigated whether abnormal circulation of ma cromolecular IgA and IgA with altered glycosylation or electrical char ge plays a role in the recurrence of IgA nephropathy (IgAN) after tran splantation. Study design. A total of 92 renal transplant patients wer e enrolled; 52 IgAN patients and 40 with other non-IgAN. The IgAN grou p included 10 patients showing IgA mesangial deposits in the grafted k idneys (recurrent group) and 10 who did not (immunohistochemically pro ven non-recurrent group). In addition another 22 IgAN transplant patie nts were clinically free of recurrent disease. Methods. The analyses i ncluded macromolecular IgA (IgAIC) detected by the conglutinin assay ( K), heavy IgA precipitated in 2.5% polyethylene glycol (PEG), IgA-fibr onectin aggregates (IgA/F Aggr), mixed IgA/IgGIC, IgA binding to mesan gial matrix components (fibronectin, laminin, type IV collagen) or pol ycations (poly-L-lysine) and ISA with altered glycosylation (Jacalin-b inding assay). Results. After transplantation, IgAN patients displayed significantly higher mean levels for each variable measured than non- IgAN (ANOVA, P < 0.05). By stepwise regression analysis, the binding o f IgA to fibronectin had the highest coefficient. By comparing data in recurrent and clinically non-recurrent IgAN, we observed that two gro ups could be distinguished by the results of the two assays for macrom olecular IgA (conglutinin IgAIC and IgA-fibronectin aggregates) and Ig A with increased affinity for type IV collagen (P < 0.05). When the se lected group of immunohistochemically proven non-recurrent IgAN was co mpared to the recurrent one, a statistically significant difference wa s found only for the binding of IgA to type IV collagen (P < 0.05). Da ta from this test were significantly related with proteinuria (P < 0.0 5) and microscopic haematuria (P < 0.04). Conclusions. Even though the IgA serology of renal transplant IgAN patients shows peculiar feature s and recurrent and non-recurrent IgAN differ in many aspects, the pre valence of positive data in the two groups had no predictive value. Th is suggests that the recurrence of IgAN is modulated by factors affect ing the interaction between circulating abnormal IgA and mesangial cel ls and/or matrix.