Secondary IgA Nephropathy Shares the Same Immune Features With Primary IgA Nephropathy

Wang, Manliu; Lv, Jicheng; Xue, Zhang; Chen, Pei; Zhao, Ming‐Hui; Zhang, Hong

doi:10.1016/j.ekir.2019.10.012

Cited by 34 publications

(37 citation statements)

References 35 publications

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“…[ 13 ] Furthermore, Wang et al recently reported that secondary IgAN shared similar Gd-IgA1 with primary IgAN. [ 14 ] We believe the Gd-IgA1 was triggered by infection, since the secondary IgAN observed (IgA of lupus nephritis, hepatic IgAN, and Gd-IgA1) did not merge. [ 9 ] Additionally, as observed in our case, the Gd-IgA1 of staphylococcus associated glomerulonephritis showed weak to strong positive results.…”

Section: Discussionmentioning

confidence: 99%

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

et al. 2021

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Rational: Immunoglobulin A (IgA) nephropathy is a common heterogeneous kidney disease. One of the causes of secondary immunoglobulin A nephropathy is infection-related glomerulonephritis (IRGN), however, its accurate diagnosis is difficult. Patient concerns: We report a rare case of an 82-year-old male presenting rapidly progressive glomerulonephritis. Assessment of a kidney biopsy by light microscopy revealed endocapillary glomerulonephritis with subendothelial deposits, such as wire loop lesions and cellular crescents. Immunofluorescence demonstrated strong staining for IgA and C3 along the glomerular capillary. Additional tests included positive staining for nephritis-associated plasmin receptor and positive plasmin activity in the glomeruli. Moreover, IgA and galactose-deficient IgA1 (Gd-IgA1) staining merged using immunofluorescence, followed by confirmation of high serum levels of Gd-IgA1 (9.3 μg/mL) by ELISA was observed. Diagnosis: The diagnosis of IgA-dominant IRGN was made. Interventions and outcomes: We have initiated treatment with intravenous methylprednisolone 500 mg/day for 3 days, followed by oral prednisolone 25 mg/d as rapidly progressive glomerulonephritis. However immunosuppressive therapy was halted because of a poor response, and hemodialysis was initiated. Lessons: This is a case of IgA-dominant IRGN patient exhibiting positive glomerular staining for nephritis-associated plasmin receptor accompanied with high titers of serum Gd-IgA1. Our observations suggest that serum and kidney tissue of Gd-IgA1 may be useful for the diagnosis of IgA-dominant IRGN.

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Section: Discussionmentioning

confidence: 99%

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

et al. 2021

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“…Gd-IgA1 is reported to increase in blood circulation and/or be deposited in renal mesangium in patients with primary IgAN and/or HSPN [ 25 – 28 ]. The data are sparse and controversial on whether immunostaining of KM-55, a Gd-IgA1-specific monoclonal antibody, is specific for patients with primary IgAN and HSPN, but not secondary form [ 6 , 7 , 29 ]. Here, we demonstrate glomerular KM55 staining with a similar pattern and intensity to IgA in this malignancy-associated HSPN, a secondary form of IgA deposition.…”

Section: Discussionmentioning

confidence: 99%

Galactose-Deficient IgA1 Deposits in Clear Cell Renal Cell Carcinoma-Related Henoch–Schönlein Purpura Nephritis

Zhao

Kim

Junghare

et al. 2020

Case Reports in Nephrology

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Recent studies suggest that galactose-deficient IgA1 (Gd-IgA1) plays a role in the pathogenesis of primary IgA nephropathy (IgAN) and Henoch–Schönlein purpura nephritis (HSPN). Furthermore, immunostaining of KM55, an antibody that identifies Gd-IgA1, may be helpful to differentiate primary IgAN and HSPN from secondary causes of glomerular IgA deposition. We report sequential kidney biopsies of a malignancy-associated HSPN, showing intense glomerular mesangial IgA deposition at the initial kidney biopsy and dramatic decrease in disappearance of glomerular deposits after tumor removal. We demonstrate that the glomerular IgA deposition contains Gd-IgA1, detected by immunostaining of KM55, with similar distribution and intensity to IgA. This suggests that renal Gd-IgA1 deposition may play a role in the pathogenesis of malignancy-associated HSPN.

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“…Thus, in recent years, some experts have held the view that GALT might also be an important site for the production of Gd-IgA1, affecting the development of IgAN. Furthermore, it was evidenced that Gd-IgA1 was also present in patients with ulcerative colitis 59 . However, these findings were confined to sporadic cases and hence needed verification in large cohorts.…”

Section: The Mucosal Origin Of Gd-iga1mentioning

confidence: 99%

Perspectives on how mucosal immune responses, infections and gut microbiome shape IgA nephropathy and future therapies

He¹,

Zhou²,

Lv³

et al. 2020

Theranostics

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Infections have been considered to play a critical role in the pathogenesis of IgA nephropathy (IgAN) because synpharyngitic hematuria is a common feature in IgAN. However, how infections participate in this process is still debated. More recent studies have also revealed that the alteration of the gut microbiome exerts a profound effect on host immune responses, contributing to the etiology or progression of autoimmunity. Considering IgA as the first line of defense against bacterial and viral antigens, this review evaluates the relationships among intestinal infections, gut microbiome, and IgA for a better understanding of the pathogenesis of IgAN. Moreover, as a prototype of IgA immunity, we provide detailed clarification of IgAN pathogenesis to shed light on other diseases in which IgA plays a role. Finally, we discuss potential therapies focusing on microbes and mucosal immune responses in IgAN.

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Secondary IgA Nephropathy Shares the Same Immune Features With Primary IgA Nephropathy

Cited by 34 publications

References 35 publications

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

Galactose-Deficient IgA1 Deposits in Clear Cell Renal Cell Carcinoma-Related Henoch–Schönlein Purpura Nephritis

Perspectives on how mucosal immune responses, infections and gut microbiome shape IgA nephropathy and future therapies

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