Is IgA nephropathy the same disease in different parts of the world?

Zhang, Hong; Barratt, Jonathan

doi:10.1007/s00281-021-00884-7

Cited by 46 publications

(41 citation statements)

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“…In clinical practice, IgAN is diagnosed as dominant IgA deposition in the mesangial area by kidney biopsy. However, the clinical and pathological manifestations of IgAN are diverse ( Zhang and Barratt, 2021 ). The clinical course of the disease ranges from isolated hematuria, subnephrotic proteinuria, nephrotic proteinuria to rapidly progressive renal failure, and kidney biopsy findings vary from mild mesangial proliferation to diffuse crescent formation, suggesting those might not be the same disease ( Lai et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Immune Characteristics of IgA Nephropathy With Minimal Change Disease

et al. 2021

Front. Pharmacol.

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Background: IgA nephropathy (IgAN) has a high degree of heterogeneity in clinical and pathological features. Among all subsets of IgAN, the pathogenesis of IgAN with minimal change disease (MCD-IgAN) remained controversial.Methods: We analyzed the clinical and pathological characteristics of MCD-IgAN patients in a retrospective cohort. Patients diagnosed with IgAN, excluding MCD-IgAN, were randomly selected as controls. Levels of plasma galactose-deficient IgA1 (GdIgA1), IgG autoantibodies against GdIgA1, GdIgA1 deposition in the glomerulus, and inflammatory reactivity of circulating poly-IgA1 complexes to cultured mesangial cells were evaluated.Results: Patients with MCD-IgAN had significantly higher levels of proteinuria and estimated glomerular filtration rate (eGFR), lower levels of albumin and urine blood cells, and milder histological lesions by a light microscope compared to IgAN patients, which bears a resemblance to MCD. Lower levels of GdIgA1 (3.41 ± 1.68 vs. 4.92 ± 2.30 μg/ml, p = 0.009) and IgG antiglycan autoantibodies (23.25 ± 22.59 vs. 76.58 ± 71.22 IU/ml, p < 0.001) were found in MCD-IgAN patients than those in IgAN controls. Meanwhile, weaker fluorescence intensities of both IgA and GdIgA1 were observed in the glomerulus of MCD-IgAN patients compared to those in IgAN patients. Furthermore, poly-IgA1 complexes from MCD-IgAN patients induced weaker inflammatory effects on cultured mesangial cells than those from IgAN patients in vitro.Conclusion: The results demonstrated that MCD-IgAN cases represent a dual glomerulopathy, namely, mild IgAN with superimposed MCD, which furthermore provides substantial evidence for the corticosteroids therapy in MCD-IgAN patients as the guidelines recommended.

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Section: Introductionmentioning

confidence: 99%

Immune Characteristics of IgA Nephropathy With Minimal Change Disease

et al. 2021

Front. Pharmacol.

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“…IgAN is the most common form of glomerulonephritis in many countries in Europe, North America, and Australia, and east Asia (1,(28)(29)(30). In contrast, the disease is rare in Africa, many Asian and South American countries, in indigenous Australian Aborigines, and is uncommon in African Americans (28, 29,[31][32][33][34][35][36][37][38][39][40]188).…”

Section: Potential Role Of Ebv Infection In the Geographic Distributi...mentioning

confidence: 99%

IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease

Městecký

Julian²,

Raška³

2023

Front. Immunol.

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IgA nephropathy (IgAN) is an autoimmune disease in which poorly galactosylated IgA1 is the antigen recognized by naturally occurring anti-glycan antibodies, leading to formation of nephritogenic circulating immune complexes. Incidence of IgAN displays geographical and racial disparity: common in Europe, North America, Australia, and east Asia, uncommon in African Americans, many Asian and South American countries, Australian Aborigines, and rare in central Africa. In analyses of sera and cells from White IgAN patients, healthy controls, and African Americans, IgAN patients exhibited substantial enrichment for IgA-expressing B cells infected with Epstein-Barr virus (EBV), leading to enhanced production of poorly galactosylated IgA1. Disparities in incidence of IgAN may reflect a previously disregarded difference in the maturation of the IgA system as related to the timing of EBV infection. Compared with populations with higher incidences of IgAN, African Americans, African Blacks, and Australian Aborigines are more frequently infected with EBV during the first 1-2 years of life at the time of naturally occurring IgA deficiency when IgA cells are less numerous than in late childhood or adolescence. Therefore, in very young children EBV enters “non-IgA” cells. Ensuing immune responses prevent infection of IgA B cells during later exposure to EBV at older ages. Our data implicate EBV-infected cells as the source of poorly galactosylated IgA1 in circulating immune complexes and glomerular deposits in patients with IgAN. Thus, temporal differences in EBV primo-infection as related to naturally delayed maturation of the IgA system may contribute to geographic and racial variations in incidence of IgAN.

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“…Two key unanswered questions in IgAN are whether IgAN is a single disease and whether it is the same disease in different parts of the world. Hong Zhang and Jonathan Barratt discuss the available literature, comparing observations across populations, and in particular how reported differences in disease behaviour might necessitate differential therapeutic approaches in different patient populations [8].…”

Section: Iga Nephropathy: a Perspective For 2021mentioning

confidence: 99%