Details

Autor(en) / Beteiligte

• van der Boog, Paul J.M.
• de Fijter, Johan W.
• van Kooten, Cees
• van der Holst, Rutger
• van Seggelen, Anneke
• van Es, Leendert A.
• Daha, Mohamed R.

Titel

Complexes of IgA with FcαRI/CD89 are not specific for primary IgA nephropathy

Ist Teil von

• Kidney international, 2003-02, Vol.63 (2), p.514-521

Ort / Verlag

New York, NY: Elsevier Inc

Erscheinungsjahr

2003

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Complexes of IgA with FcαRI/CD89 are not specific for primary IgA nephropathy. The presence of IgA together with the myeloid IgA-receptor FcαRI/CD89 in the circulation of patients with IgA nephropathy (IgAN) has been suggested as a specific pathogenic factor for mesangial deposition. However, in a recent study we found these complexes also in serum samples from healthy subjects. To investigate whether these circulating complexes are specific for IgAN, the levels and characteristics of IgA-CD89 complexes were analyzed in patients with IgAN and healthy controls. Specific ELISAs with different poly- and monoclonal antibodies and a sensitive dot-blot method were used to measure IgA-CD89 levels in serum and purified IgA samples obtained from healthy volunteers (N = 30) and patients with IgAN (N = 35). Fractionated samples of purified IgA were used to compare the size characteristics of the IgA-CD89 complexes. Almost all CD89 in serum of patients with IgAN and controls was associated with high molecular weight IgA. Quantitative analysis of IgA-CD89 complexes in purified IgA revealed no significant difference between patients with IgAN and controls. No correlation was found between levels of IgA-CD89 complexes and clinical parameters associated with progressive IgAN. CD89 in the circulation is found mainly linked to high molecular weight IgA. The presence of these complexes is not specific for IgAN. Therefore, if IgA-CD89 complexes are involved in the pathogenesis of primary IgA nephropathy, additional factors are required to explain the IgA-CD89 complex-mediated renal inflammation.