Immunoglobulin A nephropathy: a pathophysiology view

Fabiano, Rafaela Cabral Gonçalves; Pinheiro, Sérgio Veloso Brant; Silva, Ana Cristina Simões e

doi:10.1007/s00011-016-0962-x

Cited by 34 publications

(40 citation statements)

References 104 publications

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“…In the majority of patients, the presence of mesangial IgA deposits colocalizes with C3 but not with IgG or C1q deposits, suggesting that activation occurs through the alternative pathway. Between 25% and 30% of patients have mesangial mannose binding lectin (MBL) deposits that are colocalized with IgA, C3, and C4d deposits, indicating complement activation through the lectin pathway, which is a pathway associated with a higher degree of kidney damage, a lower eGFR, and proteinuria at diagnosis (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Mesangial C4d Deposits in Early IgA Nephropathy

Segarra

Romero

Agraz

et al. 2017

CJASN

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Section: Introductionmentioning

confidence: 99%

Mesangial C4d Deposits in Early IgA Nephropathy

Segarra

Romero

Agraz

et al. 2017

CJASN

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“…Immunoglobulin A (IgA) nephropathy (IgAN) is the most common type of primary glomerulonephritis and a principal cause of end-stage renal disease (ESRD) worldwide. IgAN is a heterogeneous disease with different clinical and pathological phenotypes (1,2); therefore, appropriate therapy for IgAN is debated among nephrologists. The recent Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for IgA nephropathy recommend long-term angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) as treatment when proteinuria is 0.5-1 g/day (3).…”

Section: Introductionmentioning

confidence: 99%

Corticosteroid therapy in IgA nephropathy with minimal proteinuria and high renal pathological score: A single‑center cohort study

Tang

Sun

et al. 2018

Mol Med Report

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Currently, there is no clear evidence that advocates the widespread use of corticosteroids for the treatment of immunoglobulin A nephropathy (IgAN) with minimal proteinuria (<1 g/day). The recent Kidney Disease: Improving Global Outcomes Clinical Practice Guideline recommends supportive corticosteroid treatment. In the present study, 45 IgAN patients with high renal pathological scores and minimal proteinuria were enrolled. The patients were randomly divided into two groups. The treatment group received methylprednisolone tablets in addition to angiotensin‑converting‑enzyme inhibitor (ACE‑I) and/or angiotensin‑receptor blocker (ARB) treatment. The control group only received ACE‑I and/or ARB treatment. In the treatment group, a single dose of 1 mg/kg (maximum 60 mg/day) methylprednisolone tablets was given daily followed by gradually decreasing dosage. The follow‑up time of the patients was 3 years. In addition, the underlying mechanisms were investigated. The results indicated that there was a significant reduction in the amount of urinary proteins in the treatment group compared with the control group. At the end of the follow‑up, the endpoint event rate of moderate or severe proteinuria and decrease in estimated glomerular filtration rate (eGFR) in the treatment group was significantly lower than the control group. Furthermore, higher levels of serum cytokines, interleukin (IL)‑4, IL‑17, transforming growth factor‑β1 and IL‑21, were detected in patients with IgAN compared with a group of healthy controls. There was no significant difference in IFN‑γ expression between the IgAN and healthy control groups. Furthermore, the expression of Janus kinase (Jak)1, Jak3, signal transducer and activator of transcription (STAT)3 and STAT6 was significantly upregulated in patients with IgAN compared with healthy controls. However, the expression levels of STAT5 and chaperone protein, C1GALT1 specific chaperone 1, in IgAN patients were significantly reduced compared with healthy controls. In addition, there was no significant difference in the expression of Jak2, tyrosine kinase 2, STAT1 and STAT4 between the two groups. In conclusion, for IgAN patients with minimal proteinuria and high renal pathological score corticosteroid therapy is likely to be effective. The dysregulation of serum cytokine levels in these patients with IgAN may have a role in the pathogenesis and progression of disease, which is associated with the activation of the JAK/STAT signaling pathway.

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“…Activation of this receptor after the binding of polymeric IgA1 lead to mesangial cell proliferation and pro-inflammatory cytokine production [22]. Emerging data indicate that mesangial-derived mediators that are released following mesangial deposition of IgA1 lead to podocyte and tubulointerstitial injury via humoral crosstalk [23,24].…”

Section: Journal Of Clinical and Cellular Immunologymentioning

confidence: 99%

Gluten, Transglutaminase, Celiac Disease and IgA Nephropathy

Lerner¹,

Berthelot²,

Jeremias³

et al. 2017

J Clin Cell Immunol

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Both, celiac disease and IgA nephropathy are autoimmune diseases that are IgA mediated and share multiple clinical, pathophysiological, genetic, nutritional and immunological aspects. In view of recent observations and wider understanding of the central role played by the intestinal ecosystem in celiac disease and IgA nephropathy development, the present review highlights those shared aspects, concentrating on potential nutritional therapeutic strategies in IgA nephropathy.

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Immunoglobulin A nephropathy: a pathophysiology view

Abstract: The knowledge of the whole pathophysiology of this disease could provide the rational bases for developing novel approaches for diagnosis, for monitoring disease activity, and for disease-specific treatment.

Cited by 34 publications

References 104 publications

Mesangial C4d Deposits in Early IgA Nephropathy

Mesangial C4d Deposits in Early IgA Nephropathy

Corticosteroid therapy in IgA nephropathy with minimal proteinuria and high renal pathological score: A single‑center cohort study

Gluten, Transglutaminase, Celiac Disease and IgA Nephropathy

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