IgA nephropathy during treatment with TNF-alpha blockers: Could it be predicted?
Section snippets
Background
Tumor necrosis factor (TNF)-alpha is an extremely important regulatory cytokine in the immune system. The recognition of its central role in several immune‐mediated inflammatory diseases led to the introduction of a number of biologic drugs belonging of the group of TNF-alpha inhibitors [1], [2]. These drugs have been developed with the aim to produce a more targeted approach to immunomodulation [3]. TNF-alpha blockers have in fact changed the course of dermatologic, rheumatic and intestinal
Hypothesis
Patients developing IgAN after treatment with anti-TNF alpha agents may have a similar intrinsic defect in the structure of IgA1. Since aberrant glycosylation alone is insufficient to induce renal injury, the participation of antibodies directed against glycan structures of the heavy chains of TNF alpha blockers and cross-reacting with glycans on IgA1 molecules may occur. Alternatively, aberrantly glycosylated IgA1 might bind to antigenic epitopes of TNF-blockers. One way or another, large
Discussion
IgAN has been associated with several diseases, including dermatitis herpetiformis, celiac sprue and seronegative spondylarthropathies [17]. Patients with moderate-to-severe psoriasis have an increased risk of glomerular disease, particularly IgA nephropathy [18]. Psoriasis patients show elevated serum and salivary IgA levels compared with healthy individuals and with eczema. In addition patients with severe psoriasis, longer duration of disease and psoriatic arthritis have higher serum IgA
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