Immunosuppressive agents for treating IgA nephropathy

Vecchio, Mariacristina; Bonerba, B; Palmer, Suetonia C.; Craig, Jonathan C.; Ruospo, Marinella; Samuels, Joshua; Molony, Donald A.; Schena, Francesco Paolo; Strippoli, Giovanni F.M.

doi:10.1002/14651858.cd003965.pub2

Cited by 67 publications

(36 citation statements)

References 69 publications

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“…It had previously been believed to be a benign illness, but is currently considered to be a progressive disease characterized by a gradually decreasing glomerular filtration rate (GFR), which results in end-stage renal disease (ESRD) in 15% to 20% of patients within 10 years and in 30% to 40% of patients within 20 years of disease onset[1,2]. …”

Section: Introductionmentioning

confidence: 99%

Aberrant IgA1 Glycosylation in IgA Nephropathy: A Systematic Review

Sun

Zhang

et al. 2016

PLoS ONE

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ObjectiveGalactose-deficient IgA1 was evaluated in patients with IgA nephropathy(IgAN) and controls in order to determine the predictive value of galactose-deficient IgA1 in cases of IgA nephropathy.MethodsPubMed, EMBASE, Cochrane central register of controlled trials, CNKI, CBM disc, and VIP database were searched to identify eligible studies that evaluated a difference in aberrant IgA1 glycosylation in IgAN patients compared with controls. A meta-analysis was conducted to evaluate the impact of galactose-deficient IgA1(Gd-IgA1) levels in different groups.ResultsA total of 22 studies (n = 1657) met inclusion criteria. The mean Newcastle-Ottawa Scale (NOS) score was 7.2 and ranged from 6 to 8. The standard mean difference(SMD) in the meta-analysis of 20 studies of the level of Gd-IgA1 in the serum and/or supernatant of cultured cells was higher in the IgAN group compared with healthy controls as well as in those with other renal diseases (SMD = 1.76, 95% CI = 1.18–2.34, P<0.00001; SMD = 1.05, 95% CI = 0.05–2.04, P = 0.04). The data synthesis suggested that IgAN patients had similar levels of serum Gd-IgA1, with no significant differences, compared with first-degree relatives and Henoch-Schonlein purpura nephritis (HSPN) patients (MD = 0.04, 95% CI = 0.00–0.08, P = 0.05; MD = -46.03, 95% CI = -217.70–125.64, P = 0.60). In addition, the combined MD of 5 studies indicated that there were no significant differences in Gd-IgA1 levels among patients with varying severities of IgAN (MD = 0.02, 95% CI = -0.02–0.05, P = 0.28).ConclusionsThe pooled evidence suggests that the level of Gd-IgA1 in the serum or supernatant of cultured cells from peripheral blood or tonsils may be a useful biomarker for predicting IgA nephropathy, though the level of Gd-IgA1 was not significantly associated with disease severity.

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Section: Introductionmentioning

confidence: 99%

Aberrant IgA1 Glycosylation in IgA Nephropathy: A Systematic Review

Sun

Zhang

et al. 2016

PLoS ONE

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“…Most glomerular disease are treated with drugs which affect immune response or the renin angiotensin pathway [49,50]. However, different strategies are undergoing in randomized controlled trials targeting fibrosis, inflammation, and intracellular signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

The chemokine (C-C motif) ligand protein synthesis inhibitor bindarit prevents cytoskeletal rearrangement and contraction of human mesangial cells

et al. 2016

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“…In summary, most studies indicate that glucocorticoids may lower the risk of kidney disease progression for IgA nephropathy. Meta-analyses have supported this conclusion (30,31). The main limiting issues are side effects of glucocorticoids.…”

Section: Lupus Nephritismentioning

confidence: 91%

Glucocorticoids in the Treatment of Glomerular Diseases

Ponticelli

Locatelli

2018

CJASN

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Glucocorticoids exert anti-inflammatory and immunosuppressive activities by genomic and nongenomic effects. The classic genomic effects are mediated by cytosolic glucocorticoid receptors that can upregulate the expression of anti-inflammatory proteins in the nucleus (transactivation) or repress the translocation of proinflammatory transcription factors from the cytosol into the nucleus (transrepression). The nongenomic effects are probably mediated by membrane glucocorticoid receptors. Glucocorticoid receptors are expressed also in podocytes and experimental data suggest that glucocorticoids may protect from podocyte injury. Glucocorticoids have a low therapeutic index and may exert a number of time-dependent and dose-dependent side effects. Measures to prevent or attenuate side effects include single-morning administration of short-acting glucocorticoids, dietetic counseling, increasing physical activity, frequent monitoring, and adapting the doses to the clinical conditions of the patient. Synthetic glucocorticoids, either given alone or in combination with other immunosuppressive drugs, are still the cornerstone therapy in multiple glomerular disorders. However, glucocorticoids are of little benefit in C3 glomerulopathy and may be potentially deleterious in patients with maladaptive focal glomerulosclerosis. Their efficacy depends not only on the type and severity of glomerular disease, but also on the timeliness of administration, the dosage, and the duration of treatment. Whereas an excessive use of glucocorticoids can be responsible for severe toxicity, too low a dosage and too short duration of glucocorticoid treatment can result in false steroid resistance.

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Immunosuppressive agents for treating IgA nephropathy

Cited by 67 publications

References 69 publications

Aberrant IgA1 Glycosylation in IgA Nephropathy: A Systematic Review

Aberrant IgA1 Glycosylation in IgA Nephropathy: A Systematic Review

The chemokine (C-C motif) ligand protein synthesis inhibitor bindarit prevents cytoskeletal rearrangement and contraction of human mesangial cells

Glucocorticoids in the Treatment of Glomerular Diseases

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