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      Spondyloarthritis-Associated IgA Nephropathy

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          Abstract

          Introduction

          IgA nephropathy (IgAN) can be associated with spondyloarthritis (SpA). The course of SpA-associated IgAN remains largely unknown due to the absence of large cohorts.

          Methods

          This retrospective study included patients with biopsy-proven IgAN and definite SpA. Kidney biopsies were centrally examined and scored according to the IgAN Oxford Classification. Thirty-two patients fulfilled the inclusion criteria, with a male:female ratio of 9:1 and median age of 27 and 37 years at SpA and IgAN diagnosis, respectively. HLA-B27 was positive in 90% of cases, and most patients (60%) presented with ankylosing spondylitis. The mean baseline estimated glomerular filtration rate (eGFR) was 84 ± 26 ml/min per 1.73 m 2, and the urine protein-to-creatinine ratio was 0.19 g/mmol.

          Results

          Renal biopsy revealed frequent presence of crescents (33%) and interstitial inflammation (18%). Despite almost constant use of renin-angiotensin system inhibitors, combined with steroids in 13 of 32 patients, renal outcome was particularly poor. After a median follow-up of 5.9 years, 4 patients (12.5%) reached end-stage renal disease and 41% of patients experienced a >50% decrease of eGFR. The mean annual eGFR decline rate was −4.3 ± 6.7 ml/min per 1.73 m 2. The risk of reaching class IV or V chronic kidney disease (CKD) stage during follow-up was associated with the presence of hypertension, level of proteinuria, and baseline S- and T-scores of the Oxford.

          Conclusion

          SpA-associated IgAN is associated with a poor renal outcome, despite frequent use of steroids. Tumor necrosis factor (TNF)-α blockade did not appear to influence the rate of eGFR decline in this setting.

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          Most cited references 21

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          The commonest glomerulonephritis in the world: IgA nephropathy.

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            New developments in the genetics, pathogenesis, and therapy of IgA nephropathy

            Recent years have brought notable progress in the field of IgA nephropathy. Here, we highlight important new directions and latest developments, including successful discovery of several genetic susceptibility loci, formulation of the multi-hit pathogenesis model that integrates findings from studies of galactose-deficient IgA1, anti-glycan response and immune complex-induced kidney injury, introduction of the Oxford pathology scoring system, and formalization of the Kidney Disease Improving Global Outcomes (KDIGO) consensus treatment guidelines. We focus on the latest genetic findings that confirm a strong contribution of inherited factors and explain some of the geo-ethnic disparities in disease susceptibility. Most IgA nephropathy susceptibility loci discovered to date encode genes involved in the maintenance of the intestinal epithelial barrier and response to mucosal pathogens. The concerted pattern of inter-population allelic differentiation across all Genome Wide Association Studies (GWAS) loci parallels the disease prevalence and correlates with variation in local pathogens, suggesting that multi-locus adaptation might have shaped the present-day landscape of IgA nephropathy. Importantly, the “Intestinal Immune Network for IgA Production” emerged as one of the new targets for potential therapeutic intervention. We place these findings in the context of the multi-hit pathogenesis model and existing knowledge of IgA immunobiology. Lastly, we provide our perspective on the existing treatment options, discuss areas of clinical uncertainty, and outline ongoing clinical trials and translational studies.
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              Corticosteroid effectiveness in IgA nephropathy: long-term results of a randomized, controlled trial.

              Proteinuria plays a causal role in the progression of IgA nephropathy (IgAN). A previous controlled trial showed that steroids are effective in reducing proteinuria and preserving renal function in patients with IgAN. The objective of this study was to evaluate the long-term effectiveness of steroids in IgAN, examine the trend of proteinuria during follow-up (starting from the hypothesis that the degree of reduction in proteinuria may influence IgAN outcome), and evaluate how histologic scores can influence steroid response. A secondary analysis of a multicenter, randomized, controlled trial of 86 adult IgAN patients who were receiving supportive therapy or intravenous methylprednisolone plus oral prednisone for 6 mo was conducted. Ten-year renal survival was significantly better in the steroid than in the control group (97% versus 53%; log rank test P = 0.0003). In the 72 patients who did not reach the end point (doubling in baseline serum creatinine), median proteinuria significantly decreased (1.9 g/24 h at baseline, 1.1 g/24 h after 6 mo, and 0.6 g/24 h after a median of 7 yr). In the 14 progressive patients, proteinuria increased from a median of 1.7 g/24 h at baseline to 2.0 g/24 h after 6 mo and 3.3 g/24 h after a median of 5 yr. Steroids were effective in every histologic class. Cox multivariate regression analyses showed that, in addition to steroids, a low baseline histologic score, a reduction in proteinuria after 6 mo, and no increase in proteinuria during follow-up all were independent predictors of a beneficial outcome. Steroids significantly reduce proteinuria and protect against renal function deterioration in IgAN. The histologic picture and proteinuria during early and late follow-up improve the prediction of outcome, but considerable variability remains outside the model.
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                Author and article information

                Contributors
                Journal
                Kidney Int Rep
                Kidney Int Rep
                Kidney International Reports
                Elsevier
                2468-0249
                16 March 2020
                June 2020
                16 March 2020
                : 5
                : 6
                : 813-820
                Affiliations
                [1 ]Department of Internal Medicine, Hôpital de la Pitié-Salpétrière, Assistance Pulique-Hopitaux de Paris, Paris, France
                [2 ]Department of Nephrology, Hôpital Européen Georges-Pompidou, Assistance Publique-Hopitaux de Paris, Paris, France
                [3 ]Department of Rheumatology, Inserm UMR 1132, Centre Viggo Petersen, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, Paris, France
                [4 ]Paris Diderot University, Sorbonne Paris Cité, Paris, France
                [5 ]Department of Nephrology, Hôpital Necker, Assistance Pubique-Hopitaux de Paris, Paris, France
                [6 ]Department of Nephrology, CHU, Rennes, France
                [7 ]Department of Rheumatology, Hôpital Bicêtre, Assistance Publique-Hopitaux de Paris, Le Kremlin Bicêtre, France
                [8 ]Department of Nephrology, CHU, Brest, France
                [9 ]Department of Nephrology, Hôpital Henri Mondor, Assistance Publique-Hopitaux de Paris, Créteil, France
                [10 ]Department of Nephrology, Dialysis and Transplantation, CHU Amiens, Amiens, France
                [11 ]UMR 1088 INSERM, University of Picardie Jules Verne, Amiens, France
                [12 ]Department of Nephrology, CHU de Nantes, Nantes, France
                [13 ]Department of Nephrology, CHU de Clermont Ferrand, Clermont-Ferrand, France
                [14 ]Department of Nephrology, Hôpital Saint Louis, Assistance Publique-Hopitaux de Paris, Paris, France
                [15 ]Department of Nephrology, CHU de Caen, Caen, France
                [16 ]Department of Nephrology, CHU de Reims, Reims, France
                [17 ]Department of Nephrology, Centre Hospitalier de Roubaix, Roubaix, France
                [18 ]INSERM CIC-1431 Centre Investigation Clinique Biothérapie, Department of Rheumatology, CHRU de Besançon, Besançon, France
                [19 ]Université de Paris, Paris, France
                [20 ]Department of Pathology, Hôpital Necker, Assistance Pubique-Hopitaux de Paris, Paris, France
                Author notes
                [] Correspondence: Alexandre Karras, Department of Nephrology, Hôpital Européen Georges-Pompidou, 20, rue Leblanc, 75015 Paris, France. alexandre.karras@ 123456aphp.fr
                [21]

                FL, CM, LV, and ET are members of the Club Rhumatismes et Inflammation (CRI).

                Article
                S2468-0249(20)31120-7
                10.1016/j.ekir.2020.03.012
                7271945
                © 2020 International Society of Nephrology. Published by Elsevier Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                Categories
                Clinical Research

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