Lack of Antireticulin and IgA Antiendomysium Antibodies in Sera of Patients with Primary IgA Nephropathy Associated with Circulating IgA Antibodies to Gliadin

Rostoker, Guy; André, C.; Branellec, A; Bourhala, S.; Laurent, J.; Lagrue, G

doi:10.1159/000184877

Cited by 13 publications

(7 citation statements)

References 3 publications

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“…This is consistent with data reported by Rostoker et al [24]. The finding in primary IgA NP of increased levels of IgA against food antigens and particularly gliadin prompted the hypothesis that a subgroup of these patients may have latent celiac disease.…”

Section: Discussionsupporting

confidence: 92%

“…The finding in primary IgA NP of increased levels of IgA against food antigens and particularly gliadin prompted the hypothesis that a subgroup of these patients may have latent celiac disease. We did not find, similarly to others [24,25], specific markers of this disease, e.g., EMA or ARA. Striking findings in our study were differences in clinical parameters in patients with positive and negative IgA-AGA results.…”

Section: Discussionsupporting

confidence: 87%

See 1 more Smart Citation

IgA-Antigliadin Antibodies in Patients with IgA Nephropathy: The Secondary Phenomenon?

Ots¹,

Uibo²,

Metsküla

et al. 1999

Am J Nephrol

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Circulating IgA-antigliadin antibodies (IgA-AGA) are often found in patients with IgA nephropathy (NP). IgA-AGA are sensitive markers of an abnormal immune system reaction to gluten, seen particularly in patients with celiac disease. However, a lack of IgA-antireticulin and IgA-antiendomysium antibodies and often jejunal mucosal atrophy of patients with IgA NP suggest that most patients do not have latent celiac disease. To examine the relationship between IgA-AGA and clinical data, enzyme-linked immunosorbent assays for IgA-AGA were performed in 28 patients with IgA NP and in 50 healthy persons. The results were calculated in arbitrary units (AU). The cutoff level for a negative or a positive test was found to be 60 AU, calculated according to the AGA test result (mean + 3 SD) in 50 healthy persons. The following clinical data were assessed: age, gender, disease duration, daily proteinuria, blood pressure, serum creatinine, and creatinine clearance. Control sera were negative for IgA-AGA. Positive IgA-AGA tests were observed in 14 of the 28 patients (p < 0.0001 vs. controls) and high levels of IgA-AGA (AU >90) in 6 of the 28 patients (p < 0.001 vs. controls). The mean duration of the disease of the patients with positive IgA-AGA was significantly longer as compared with the patients who had a negative antibody test. IgA-AGA correlated with age (p < 0.05, r = 0.56), disease duration (p < 0.05, r = 0.40), and blood pressure (p < 0.05, r = 0.48). Antireticulin and antiendomysium antibody tests were negative in all patient and control sera. We conclude that IgA-AGA are associated with the progression of IgA NP. Our findings support the current concept about the pathogenesis of IgA NP, where the defective IgA production itself may be the primary and intestinal lesions as well as the production of IgA-AGA the secondary phenomenon.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 87%

IgA-Antigliadin Antibodies in Patients with IgA Nephropathy: The Secondary Phenomenon?

Ots¹,

Uibo²,

Metsküla

et al. 1999

Am J Nephrol

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“…The etiology of human IgA nephropathies is not exactly known; viral or bacterial infections/inflammations of the upper respiratory tract [28, 57, 58, 59]have been discussed as well as dietary antigens, mainly gliadin, soy protein or lactalbumin [14, 15, 17, 60, 61, 62, 63, 64]or mycotoxins [65]. Antireticulin and antiendomyosin antibodies were not detected in parallel to antigliadin antibodies [66]. Other autoantibodies were demonstrated in some IgA nephropathy patients.…”

Section: Discussionmentioning

confidence: 99%

IgM/IgA Nephropathy in Callitrichids: Antigen Studies

Brack

Schroeder²,

Fooke³

et al. 1999

Nephron

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Renal tissues of callitrichids with IgM nephropathy were immunohistochemically examined for the participation of IgA in pathogenesis. In 58 histopathologically nephropathy-positive kidneys, IgM predominated in 20 cases and IgA in 7 cases, and in 31 cases both immunoglobulins were rated to be approximately equally involved. The disease, therefore, might be described as IgM/IgA nephropathy. The renal tissues and sera were also tested for nutritional antigens or antinutritional antigen antibodies, using immunohistochemistry and Western blots (tissues) and enzyme-linked immunosorbent assay (sera). Evidences of nutritional antigens in the renal tissues were inconclusive, although circulating IgG class antibodies against cereals, milk, and egg proteins were present in quite a number of sera. Particular consideration was paid to IgA-antigliadin antibodies, which were statistically significantly associated with nephropathy as were IgA rheumatoid factors. The findings are discussed in relation to human IgA and IgM nephropathies.

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“…However, anti reticulin and/or antiendomysial antibodies, which are characteristic of coeliac disease, were not detected in patient or control sera in most studies [76][77][78][79] . Only a single paper described the presence of IgG antiendomysial antibodies in ~40% of patients with IgAN 80 .…”

Section: Coeliac Diseasementioning

confidence: 99%

The mucosa–kidney axis in IgA nephropathy

2015

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Links between IgA nephropathy (IgAN) and the mucosa have been recognized since the 1970s. In particular, the observation of visible haematuria induced by respiratory infections in patients with IgAN and the association of IgAN with diseases in which the mucosa plays a part, especially coeliac disease, have been taken as evidence of a mucosa-kidney axis. Here, we review current evidence that links the mucosa, in particular the gastrointestinal mucosa, and IgA produced by the bone marrow with IgAN. Genome-wide association studies in patients with IgAN have identified risk loci in genes involved in the intestinal mucosal integrity and immune network. Furthermore, the systemic immune response to mucosal antigens in IgAN is increased. Moreover, patients with IgAN have an increased reactivity to dietary proteins associated with subclinical intestinal mucosal inflammation. Associations between IgAN and gastrointestinal diseases have also been reported in a small number of patients, but whether these diseases share a common pathogenesis or whether gastrointestinal inflammation exacerbates IgAN is uncertain. Indeed, mucosal alterations such as infections could activate the innate immune system, aggravate a pre-existing IgAN and promote disease manifestations such as macrohaematuria. Various clinical interventions and trials targeting the mucosa or presumed mucosa-associated mechanisms have so far not yielded consistent findings and the results of ongoing trials are eagerly awaited.

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Lack of Antireticulin and IgA Antiendomysium Antibodies in Sera of Patients with Primary IgA Nephropathy Associated with Circulating IgA Antibodies to Gliadin

Cited by 13 publications

References 3 publications

IgA-Antigliadin Antibodies in Patients with IgA Nephropathy: The Secondary Phenomenon?

IgA-Antigliadin Antibodies in Patients with IgA Nephropathy: The Secondary Phenomenon?

IgM/IgA Nephropathy in Callitrichids: Antigen Studies

The mucosa–kidney axis in IgA nephropathy

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