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Nephrol Dial Transplant (1995) 10: 2310-2315
© 1995 European Renal Association-European Dialysis and Transplant Association

research-article

IgA serology in recurrent and non-recurrent IgA nephropathy after renal transplantation

R. Coppo1,, A. Amore1, P. Cirina1, M. Messina1, B. Basolo1, G. Segoloni1, F. Bertgoux2, R. Boulharouz2, J. Egido3, R. Alcazar3, A. R. Clarkson4 and A. Woodroffe4

1Multicentre Collaborative Study among the Nephrology and Dialysis Units of: Torino (Regina Margherita Children's Hospital, G. Bosco Hospital, S. Giovanni Hospital) Italy 2Multicentre Collaborative Study among the Nephrology and Dialysis Units of: St Etienne (CHU de Saint Etienne, Hôpital du Nord) France 3Multicentre Collaborative Study among the Nephrology and Dialysis Units of: Madrid (Fundacion J. Diaz) Spain 4Multicentre Collaborative Study among the Nephrology and Dialysis Units of: Adelaide (Royal Adelaide Hospital) Australia

Correspondence and offprint requests to: Correspondence and offprint requests to: Rosanna Coppo MD, Divisione di Nefrologia e Dialisi, Ospedale Regina Margherita, Piazza Polonia 94, 10126 Torino, Italy

BACKGROUND: This study investigated whether abnormal circulation of macromolecular IgA and IgA with altered glycosylation or electrical charge plays a role in the recurrence of IgA nephropathy (IgAN) after transplantation.

STUDY DESIGN: A total of 92 renal transplant patients were enrolled; 52 IgAN patients and 40 with other non-IgAN. The IgAN group included 10 patients showing IgA mesangial deposits in the grafted kidneys (recurrent group) and 10 who did not (immunohistochemically proven non-recurrent group). In addition another 22 IgAN transplant patients were clinically free of recurrent disease.

METHODS: The analyses included macromolecular IgA (IgAIC) detected by the conglutinin assay (K), heavy IgA precipitated in 2.5% polyethylene glycol (PEG), IgA-fibronectin aggregates (IgA/F Aggr), mixed IgA/IgGIC, IgA binding to mesangial matrix components (fibronectin, laminin, type IV collagen) or polycations (poly-L-lysine) and IgA with altered glycosylation (Jacalin-binding 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 of IgA to fibronectin had the highest coefficient. By comparing data in recurrent and clinically non-recurrent IgAN, we observed that two groups could be distinguished by the results of the two assays for macromolecular IgA (conglutinin IgAIC and IgA-fibronectin aggregates) and IgA with increased affinity for type IV collagen (P <0.05). When the selected group of immunohistochemically proven non-recurrent IgAN was compared to the recurrent one, a statistically significant difference was found only for the binding of IgA to type IV collagen (P<0.05). Data from this test were significantly related with proteinuria (P<0.05) and microscopic haematuria (P <0.04).

CONCLUSION: Even though the IgA serology of renal transplant IgAN patients shows peculiar features and recurrent and non-recurrent IgAN differ in many aspects, the prevalence of positive data in the two groups had no predictive value. This suggests that the recurrence of IgAN is modulated by factors affecting the interaction between circulating abnormal IgA and mesangial cells and/or matrix.

Keywords: IgA immune complexes; IgA serology in IgA nephropathy; kidney transplantation; recurrence of glomerulonephritis; transplanted IgA nephropathy


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