TESTING Corticosteroids in IgA Nephropathy

Tam, Frederick W.K.; Pusey, Charles D.

doi:10.2215/cjn.10560917

Cited by 16 publications

(11 citation statements)

References 10 publications

(7 reference statements)

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“…There were some patients that showed benefit, however, the trial ended prematurely, which prevents us from extrapolating a definitive treatment benefit. Another recent trial studied the role of rituximab, showing that peripheral B cell counts decreased, however, there was no effect on under-glycosylated IgA1, immune complexes, nor severity of disease [12]. Although IgAN is less commonly seen in the Hispanic population, we must consider this diagnosis in a Hispanic patient presenting with acute renal failure, hematuria, and proteinuria.…”

Section: Discussionmentioning

confidence: 99%

Uremic Pancolitis in an Adult Patient with Newly Diagnosed, Rapidly Progressive Crescentic Immunoglobulin A Nephropathy

González

McMahon

Sanchez

et al. 2019

Cureus

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Uremic gastroenteropathy is a well-accepted but less often described sequelae of an underlying renal disease. With the advent of modern dialysis treatments, rarer manifestations, such as pancolitis, may go overlooked in the evaluation, pursuing more common diagnoses. The underlying pathophysiology of uremic gastroenteropathy is not completely understood; however, several underlying mechanisms have been identified to play a role. Here, we present an exceptionally rare case of uremic pancolitis in a Hispanic male who presented with clinical, imaging, and pathological findings consistent with newly diagnosed, rapidly progressive crescentic IgA nephropathy (IgAN).

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Section: Discussionmentioning

confidence: 99%

Uremic Pancolitis in an Adult Patient with Newly Diagnosed, Rapidly Progressive Crescentic Immunoglobulin A Nephropathy

González

McMahon

Sanchez

et al. 2019

Cureus

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“…The TESTING trial, which recruited the majority of patients from China, compared methylprednisolone (0.8 mg/kg/day; maximum 48 mg/day) against placebo, and demonstrated that a relatively high corticosteroid dose had potential renal benefit, with a reduction of patients in the methylprednisolone group reaching the primary composite renal outcome (40% decrease in eGFR, ESRD or death due to kidney failure; 5.9% vs 15.9% in the placebo group), and a reduced mean annual eGFR decline in this group (− 1.79 in the methylprednisolone group vs − 6.95 ml/min/1.73 m 2 in the placebo group). However, this came at a cost with a significantly increased rate of adverse events, and the study was terminated early by the data safety monitoring committee due to the increased number of life-threatening infections in the treatment arm [ 65 ]. Of interest, the rate of annual eGFR decline in the placebo arm of the TESTING study was much higher compared to the supportive care arm of the STOP-IgAN study (− 6.95 vs − 1.6 ml/min/1.73 m 2 ), supporting findings from a previous observational study that patients of East Asian origin may have more rapid rates of renal decline in IgAN [ 66 ], and therefore could conceivably respond differently to immunosuppressive therapy.…”

Section: Current Approachesmentioning

confidence: 99%

New strategies and perspectives on managing IgA nephropathy

et al. 2019

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IgA nephropathy is an inflammatory renal disease characterised by the deposition of IgA in the glomerular mesangium and is the most commonly reported primary glomerulonephritis worldwide. Thirty to forty percent of patients with the disease develop progressive renal function decline, requiring renal replacement therapy within two decades of diagnosis. Despite this, accurate individual risk stratification at diagnosis and predicting treatment response remains a challenge. Furthermore, there are currently no disease specific treatments currently licensed to treat the condition due to long standing challenges in the nature and prevalence of the disease. Despite this, there have been exciting recent advances in the field that may represent paradigm shifts in the way IgA nephropathy is managed in the near future. In this review, we explore the evidence base informing current approaches to management and explore new strategies and future directions in the diagnosis and management of IgA nephropathy.

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“…According to current guidelines, patients with GFR > 50 ml/min/1.73 m 2 who fail to achieve levels of proteinuria below 1 g/day despite 3–6 months of optimized supportive care (including RAS blockers) are candidates for a 6-month course of systemic corticosteroid therapy [2]. The majority of recently published randomized controlled trials (RCTs) support the claim that corticosteroids reduce proteinuria and the probable progression of kidney function decline, but at the same time are associated with a number of adverse effects [87].…”

Section: T Cells As a Therapeutic Target Of Traditional And Biologicamentioning

confidence: 99%

T cells in IgA nephropathy: role in pathogenesis, clinical significance and potential therapeutic target

et al. 2018

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Background Immunoglobulin A nephropathy (IgAN), the most frequent cause of primary glomerulonephritis worldwide, is an autoimmune disease with complex pathogenesis. In this review, we focus on T cells and summarize knowledge about their involvement in pathophysiology and treatment of IgAN Methods We reviewed the literature for (1) alterations of T cell subpopulations in IgAN, (2) experimental and clinical proofs for T cells’ participation in IgAN pathogenesis, (3) clinical correlations with T cell-associated alterations, and (4) influence of drugs used in IgAN therapy on T cell subpopulations. Results We found that IgAN is characterized by higher proportions of circulatory Th2, Tfh, Th17, Th22 and γδ T cells, but lower Th1 and Treg cells. We discuss genetic and epigenetic makeup that may contribute to this immunological phenotype. We found that Th2, Th17 and Tfh-type interleukins contribute to elevated synthesis of galactose-deficient IgA1 (Gd-IgA1) and that the production of anti-Gd-IgA1 autoantibodies may be stimulated by Tfh cells. We described the roles of Th2, Th17, Th22 and Treg cells in the renal injury and summarized correlations between T cell-associated alterations and clinical features of IgAN (proteinuria, reduced GFR, hematuria). We detailed the impact of immunosuppressive drugs on T cell subpopulations and found that the majority of drugs have nonoptimal influence on T cells in IgAN patients. Conclusions T cells play an important role in IgAN pathogenesis and are correlated with its clinical severity. Clinical trials with the drugs targeting the reported alterations of the T-cell compartment are highly desirable.

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TESTING Corticosteroids in IgA Nephropathy

Cited by 16 publications

References 10 publications

Uremic Pancolitis in an Adult Patient with Newly Diagnosed, Rapidly Progressive Crescentic Immunoglobulin A Nephropathy

Uremic Pancolitis in an Adult Patient with Newly Diagnosed, Rapidly Progressive Crescentic Immunoglobulin A Nephropathy

New strategies and perspectives on managing IgA nephropathy

T cells in IgA nephropathy: role in pathogenesis, clinical significance and potential therapeutic target

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