Immune Characteristics of IgA Nephropathy With Minimal Change Disease

Li, Huixian; Lu, Wei; Li, Haiyun; Liu, Xiaoling; Zhang, Xue; Xie, Liyi; Lan, Ping; Yu, Xiaoyang; Dai, Yinjuan; Xie, Xinfang; Lv, Jicheng

doi:10.3389/fphar.2021.793511

Cited by 7 publications

(6 citation statements)

References 32 publications

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“…However, the levels of Gd-IgA1 were much higher in patients with MCD-IgAN than in healthy control participants. Furthermore, unlike previous studies ( 6 , 22 ), we found that Gd-IgA1 was rarely deposited in the glomerulus of patients with MCD-IgAN. Gd-IgA1 was deposited in the glomerulus in only 13.7% of patients with MCD-IgAN, compared with 82.4% of patients with non-MCD-IgAN.…”

Section: Discussioncontrasting

confidence: 99%

“…Gd-IgA1 is the key component in the pathogenesis of IgAN ( 10 ). In this study, we found that, compared with non-MCD-IgAN patients, MCD-IgAN patients presented with lower levels of serum Gd-IgA1, which was consistent with previous research ( 6 ). However, the levels of Gd-IgA1 were much higher in patients with MCD-IgAN than in healthy control participants.…”

Section: Discussionsupporting

confidence: 93%

“…These patients are defined as MCD-IgAN. Some studies have reported these patients to have a special clinical subtype of IgAN ( 5 , 6 ), whereas others have considered this to be MCD accompanied by IgA deposition ( 7 , 8 ).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of patients with IgA nephropathy with and without associated minimal change disease

Guo

Sun²,

Dong³

et al. 2023

Front. Nephrol.

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IntroductionImmunoglobulin A nephropathy (IgAN) presents various clinical manifestations and pathological phenotypes. Approximately 5% of patients with IgAN present with early onset nephrotic syndrome, mild mesangial lesions, and diffuse foot process effacement of podocytes, which resemble minimal change disease (MCD). These patients are defined as MCD-IgAN. Whether MCD-IgAN is a special type of IgAN or simply MCD accompanied by IgA deposition remains controversial.MethodsA total of 51 patients diagnosed with MCD-IgAN at Beijing Anzhen Hospital from January 2010 to September 2022 were recruited. The clinical and pathological characteristics of IgA-MCD were analyzed. Patients with IgAN but without MCD (non-MCD-IgAN) and healthy participants were enrolled as controls. Galactose-deficient immunoglobulin A1 (Gd-IgA1) and complement C3 were detected both in the circulation and in renal tissues.ResultsWe found that the levels of serum Gd-IgA1 were lower in participants with MCD-IgAN than in those with non-MCD-IgAN, but higher than in healthy participants. Gd-IgA1 was rarely deposited in the glomeruli of participants with MCD-IgAN, with a positive rate of only 13.7% (7/51); in contrast, the positive rate in participants with non-MCD-IgAN was 82.4% (42/51). Among renal Gd-IgA1-positive patients, Gd-IgA1 and immunoglobulin A (IgA) colocalized along the glomerular mesangial and capillary areas. Interestingly, we found that the circulating levels of complement C3 were significantly higher in participants with MCD-IgAN than in participants with non-MCD-IgAN. In addition, the intensity of C3c in glomeruli in participants with MCD-IgAN was significantly weaker than in participants with non-MCD-IgAN.ConclusionsOur study suggests that, in MCD-IgAN, most of the IgA that is deposited on glomeruli is not the same pathogenic Gd-IgA1 as found in general IgAN. Complement activation both in the circulation and in the renal locality was much weaker in MCD-IgAN than in non-MCD-IgAN. Our study suggests that IgAN with MCD might be MCD with coincidental IgA deposition.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 93%

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Characterization of patients with IgA nephropathy with and without associated minimal change disease

Guo

Sun²,

Dong³

et al. 2023

Front. Nephrol.

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“…The decrease of ALB in IgAN may be due to the renal injury, in accordance with a previous clinical study. 18 The findings suggest that there may not be a remarkable change in the expression level of these genes during the progression of IgAN. Analogously, these hub genes targeted by artemisinin may not have a remarkable expression change against IgAN.…”

Section: Resultsmentioning

confidence: 92%

Exploration of Artemisinin Against IgA Nephropathy via AKT/Nrf2 Pathway by Bioinformatics and Experimental Validation

Yang¹,

Sun²,

Zhu³

et al. 2023

DDDT

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Background Artemisinin (ART) is a safe and effective antimalarial drug. In recent years, antimalarial drugs have demonstrated a good therapeutic efficacy in IgA nephropathy, suggesting that this may become a new treatment option. Purpose We aimed to evaluate the effect and mechanism of artemisinin in IgA nephropathy. Methods In this study, CMap database was used to predict the artemisinin therapeutic effect for IgA nephropathy. A network pharmacology approach was applied to explore the unknown mechanism of artemisinin in IgA nephropathy. We used molecular docking to predict the binding affinity of artemisinin with the targets. A mouse model of IgA nephropathy was established to investigate the therapeutic effect of artemisinin on IgA nephropathy. In vitro, the cell counting Kit-8 assay was used to evaluate the cytotoxicity of artemisinin. Flow cytometry and PCR assays were used to detect the effects of artemisinin on oxidative stress and fibrosis in lipopolysaccharide (LPS)-stimulated mesangial cells. Western blot and immunofluorescence were used to detect the expression of pathway proteins. Results CMap analysis showed artemisinin may reverse the expression levels of differentially expressed genes in IgA nephropathy. Eighty-seven potential targets of artemisinin in the treatment of IgA nephropathy were screened. Among them, 15 hub targets were identified. Enrichment analysis and GSEA analysis indicated that response to reactive oxygen species is the core biological process. AKT1 and EGFR had the highest docking affinity with artemisinin. In vivo, artemisinin could improve renal injury and fibrosis in mice. In vitro, artemisinin attenuated LPS-induced oxidative stress and fibrosis promoted AKT phosphorylation and Nrf2 nuclear translocation. Conclusion Artemisinin reduced the level of fibrosis and oxidative stress with IgA nephropathy through the AKT/Nrf2 pathway, which provided an alternative treatment for IgAN.

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“…It appears that various environmental factors can stimulate aberrant immunoglobulin-A (IgA) production in areas such as the mucosal-related lymphoid tissue of the alimentary tract, resulting in immune complex deposition in the glomerular structures of the Kidneys (1)(2)(3). Renal biopsy, which is necessary for the definitive diagnosis of IgAN, can result in a range of observations including mild proliferation to significant extra-capillary proliferation of mesangial cells (4). The disease is caused by the dominant mesangial IgA1-immune complex deposits in the mesangial area of the glomeruli (5).…”

Section: Introductionmentioning

confidence: 99%

Administration of sodium-glucose cotransporter-2 inhibitors in IgA nephropathy; a new strategy in the management?

2023

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Some of the several effects of sodium-glucose cotransporter-2 inhibitors (SGLT-2i), including their metabolic, anti-inflammatory and hemodynamic properties, along with other kidney protective values, have directed clinicians to give these drugs in IgA-nephropathy (IgAN). According to recent studies regarding the beneficial effects of SGLT-2i on IgAN, it is clear that clinicians are changing their approach towards kidney transplantation when it comes to aggressive immunosuppression. This mini-review aims towards the evaluation of the protective efficacy of SGLT-2i in IgA-nephropathy.

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Immune Characteristics of IgA Nephropathy With Minimal Change Disease

Cited by 7 publications

References 32 publications

Characterization of patients with IgA nephropathy with and without associated minimal change disease

Characterization of patients with IgA nephropathy with and without associated minimal change disease

Exploration of Artemisinin Against IgA Nephropathy via AKT/Nrf2 Pathway by Bioinformatics and Experimental Validation

Administration of sodium-glucose cotransporter-2 inhibitors in IgA nephropathy; a new strategy in the management?

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