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• W1983181507 abstract "To the Editor: IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide. Nonspecific treatments such as steroids are unfortunately often not particularly efficacious in IgAN and, as the pathogenesis of the disease has remained obscure, specific treatment has been lacking. Recently, Xu and Zhao [1.Xu L.-X. Zhao M.-H. Aberrantly glycosylated serum IgA1 are closely associated with pathologic phenotypes of IgA nephropathy.Kidney Int. 2005; 68: 167-172Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar] have found aberrantly glycosylated serum IgA1 in IgAN. In particular, they find that the IgA1 in IgAN patients with the more severe histologic subtypes of focal proliferative and sclerosing disease has reduced O-linked sialic acid and galactosylation than samples from normal controls, and that all groups of IgAN patients have increased exposure of N-acetylgalactosamine residues in their IgA1 compared with normal controls. This work is consistent with previous work that also found decreased sialation in IgAN patients (see e.g., [2.Coppo R. Amore A. Aberrant glycosylation in IgA nephropathy (IgAN).Kidney Int. 2005; 65: 1544-1547Abstract Full Text Full Text PDF Scopus (146) Google Scholar] and others therein). The decreased sialation may be fundamental in the pathogenesis of IgAN as desialation may further expose IgA1 to degalactosylation. Such aberrantly glycosalted IgA1 may be important in the pathogenesis of IgAN because it may be deposited in the mesangium. Whether fundamental to the pathogenesis or not, we just want to note that desialation may be a useful point at which to intervene for therapy for IgAN. It may be possible to screen for and design medicinals that specifically block the desialation of IgA1 without unacceptable side effects. We further note that there is at least a small possibility that a useful sialation inhibitor not only already exists, but is also approved for use worldwide. Indeed, neuraminic acid is a synonym for sialic acid. Two neuraminidase inhibitors—oseltamivir and zanamivir—are currently licensed and in use worldwide for treatment and immediate prophylaxis for influenza virus infection [3.Nicholson K.G. Wood J.M. Zambon M. Influenza.Lancet. 2003; 362: 1733-1745Abstract Full Text Full Text PDF PubMed Scopus (695) Google Scholar]. While designed to work against the viral neuraminidase, there is at least some evidence that these medicines are also active against a mammalian neuraminidase [4.Crain S.M. Shen K.F. Neuraminidase inhibitor, oseltamivir blocks GM1 ganglioside-regulated excitatory opioid receptor-mediated hyperalgesia, enhances opioid analgesia and attenuates tolerance in mice.Brain Research. 2004; 995: 260-266Crossref PubMed Scopus (41) Google Scholar]. Neuraminidase inhibitors—oseltamivir and zanamivir or others—would be a much needed addition to the treatment armamentarium for IgAN and are worthy of further consideration and potential study." @default.
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• W1983181507 date "2005-12-01" @default.
• W1983181507 modified "2023-09-30" @default.
• W1983181507 title "Consideration of use of neuraminidase inhibitors such as oseltamivir and zanamivir in IgA nephropathy" @default.
• W1983181507 cites W1993857686 @default.
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• W1983181507 doi "https://doi.org/10.1111/j.1523-1755.2005.00583_7.x" @default.
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