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Modulation of Mesangial Cell Reactivity by Aberrantly Glycosylated IgA

The hallmark of primary IgA nephropathy with mesangial IgA deposits (IgAN) is the presence of detectable amounts of IgA in the mesangial area [1]. The pathogenesis of this glomerulonephritis was ascribed to the accumulation of IgA immune complexes (IgAIC) within glomeruli [2, 3]. This hypothesis offered a unifying explanation of the relationship between infection of the upper airways, mucosal immune responses associated with predominant IgA synthesis and mesangial deposition of IgA aggregates leading to gross hematuria. Although many studies revealed high levels of IgAIC during clinically active phases of IgAN [4–6], circulating IgAIC were detected in only 30–70% of the patients, even if serial samples were analyzed [7]. Moreover, attempts to identify the antigens inciting IgAN have failed to yield consistent results. In 20–30% of the patients, IgA specific for alimentary antigens has been detected, but often the levels of such antibodies did not correlate with IgAIC levels or disease activity [8]. Efforts to detect alimentary or viral antigens (CMV, HSV, EBV) in glomerular deposits produced inconsistent results as well [9, 10]. In summary, much of the data implicating true IgAIC as the unique mechanism in the pathogenesis of IgAN are inconclusive. Aberrant IgA Glycosylation