Abnormal IgA glycosylation in Henoch-Schonlein purpura restricted to patients with clinical nephritis

Allen, Alice C.; Willis, Frank; Beattie, Tom F.; Feehally, John

doi:10.1093/ndt/13.4.930

Cited by 159 publications

(123 citation statements)

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“…It has been demonstrated that serum IgA1 display an abnormal O-glycosylation in patients with IgA-N (35-37) or HSP (38 -41) and that this abnormal glycosylation is also found in IgA deposits on mesangial cells (42). Moreover, it has been shown that abnormal IgA glycosylation is restricted to HSP patients with nephritis while it was not observed in HSP patients without nephritis (39). In addition, it has recently been shown that abnormally glycosylated IgA isolated from IgA-N patients significantly increased the apoptotic rate and nitric oxide synthesis activity of cultured mesangial cells, in comparison with IgA fractions isolated from controls (43).…”

Section: Discussionmentioning

confidence: 99%

Enhanced Expression of the CD71 Mesangial IgA1 Receptor in Berger Disease and Henoch-Schönlein Nephritis

Haddad¹,

Moura²,

Arcos-Fajardo³

et al. 2003

Journal of the American Society of Nephrology

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ABSTRACT. IgA nephropathy (IgA-N) that comprises Berger disease and Henoch-Schönlein Purpura (HSP) nephritis is defined by mesangial IgA deposits. Recently, this group has characterized a new receptor for IgA, the transferrin receptor (CD71), expressed on mesangial cells. To assess whether CD71 was involved in the pathogenesis of IgA-N, its expression was analyzed together with IgA deposits on 16 kidney biopsies from 16 patients with Berger disease (n = 4) or HSP (n = 12). These biopsies were compared with 17 kidney biopsies of a group of 15 patients (control group) with other glomerulonephritis, including systemic lupus erythematosus, poststreptococcal acute glomerulonephritis, membranoproliferative glomerulonephritis, steroid-sensitive minimal change nephrotic syndrome, steroid-resistant idiopathic nephrotic syndrome with focal and segmental glomerulosclerosis, and persistent and isolated proteinuria with minimal change on kidney biopsy. In this control group, IgA deposits could be observed in eight kidney biopsies of seven patients. These biopsies were also compared with normal kidney specimens (normal group). In normal kidney, it was found that CD71 was linearly expressed on tubular epithelium but was either not expressed or very dimly in glomeruli. In contrast, CD71 was strongly expressed in 105 of the 107 glomeruli of the kidney biopsies from the IgA-N group. For the control group, it was found that expression of CD71 in glomeruli was correlated to the presence of IgA deposits. Indeed, among the 87 glomeruli of nine kidney biopsies (eight patients) without IgA fixation, 78 exhibited no CD71 expression and nine exhibited a very dim one. On the other hand, all 49 glomeruli of the eight kidney biopsies (seven patients) in which IgA deposits were detected exhibited CD71 expression (P < 10−4). Performance of dual-labeling studies with confocal microscopy on kidney biopsies of IgA-N patients demonstrated that most of the IgA deposits co-localized with CD71. It was also demonstrated that the intensity of the expression of CD71 was not linked to the intensity of clinical or biologic findings but to the intensity of cellular proliferation in both IgA-N and control groups. These results show that mesangial CD71 expression is not specific to IgA-N. However, the association between IgA deposits and CD71 expression and their co-localization in the mesangium provide strong evidence that CD71 is a major IgA receptor on mesangial cells. Email: elie.haddad@rdb.ap-hop-paris.fr

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Section: Discussionmentioning

confidence: 99%

Enhanced Expression of the CD71 Mesangial IgA1 Receptor in Berger Disease and Henoch-Schönlein Nephritis

Haddad¹,

Moura²,

Arcos-Fajardo³

et al. 2003

Journal of the American Society of Nephrology

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“…A relationship between galactose deficiency and nephritis has been observed in other diseases. Galactose-deficient IgA1 (46) and IgA-IgG circulating complexes (47) are found in sera of patients with HenochSchöenlein purpura who develop nephritis but not in sera of patients who do not. Also, patients with IgA1 myeloma may have very high levels of circulatory IgA1, but only those with aberrantly glycosylated IgA1 develop an immune-complex glomerulonephritis (48,49).…”

Section: Igan -A Disease Of Aberrant Glycosylationmentioning

confidence: 96%

IgA Glycosylation and IgA Immune Complexes in the Pathogenesis of IgA Nephropathy

Novák

Julian

Tomana

et al. 2008

Seminars in Nephrology

185

134

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“…The lack of terminal ␤1-galactosyl residues in the hinge region of IgA1 observed in both diseases might be due to a reduced activity of the ␤1,3-galactosyltransferase in peripheral B cells (26 -28). This abnormality is present only in HSP complicated by nephritis, which suggests a pathophysiological role (26). N-Acetylgalactosamine (GalNac) residues exposed on IgA1 because of the lack of terminal ␤1 galactosylation constitute a novel antigen inducing a humoral auto-immune response (29).…”

Section: Iga Abnormalitiesmentioning

confidence: 99%

Henoch-Schönlein Purpura Nephritis

Davin¹

2011

Clinical Journal of the American Society of Nephrology

148

123

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SummaryHenoch-Schö nlein purpura nephritis is a rare kidney disease leading to chronic kidney disease in a non-negligible percentage of patients. Although retrospective studies suggest beneficial effects of some therapies, prospective randomized clinical trials proving treatment efficacy are still lacking. The dilemma of spontaneous recovery even in patients with severe clinical and histologic presentation and of late evolution to chronic kidney disease in patients with mild initial symptoms renders it difficult for clinicians to expose patients to treatment protocols that are not evidence-based. A better understanding of the pathophysiology of progression to chronic kidney disease in Henoch-Schö nlein purpura patients could be achieved by designing prospective international multicenter studies looking at determinants of clinical and histopathological evolution as well as possible circulating and urinary markers of progression. Such studies should be supported by a database available on the web and a new histologic classification of kidney lesions. This paper reports clinical, pathologic, and experimental data to be used for this strategy and to assist clinicians and clinical trial designers to reach therapeutic decisions.

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Abnormal IgA glycosylation in Henoch-Schonlein purpura restricted to patients with clinical nephritis

Cited by 159 publications

References 1 publication

Enhanced Expression of the CD71 Mesangial IgA1 Receptor in Berger Disease and Henoch-Schönlein Nephritis

Enhanced Expression of the CD71 Mesangial IgA1 Receptor in Berger Disease and Henoch-Schönlein Nephritis

IgA Glycosylation and IgA Immune Complexes in the Pathogenesis of IgA Nephropathy

Henoch-Schönlein Purpura Nephritis

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