We performed a genome-wide association study (GWAS) of IgA nephropathy (IgAN), the most common form of glomerulonephritis, with discovery and follow-up in 20,612 individuals of European and East Asian ancestry. We identified six new genome-wide significant associations, four in ITGAM-ITGAX, VAV3 and CARD9 and two new independent signals at HLA-DQB1 and DEFA. We replicated the nine previously reported signals, including known SNPs in the HLA-DQB1 and DEFA loci. The cumulative burden of risk alleles is strongly associated with age at disease onset. Most loci are either directly associated with risk of inflammatory bowel disease (IBD) or maintenance of the intestinal epithelial barrier and response to mucosal pathogens. The geospatial distribution of risk alleles is highly suggestive of multi-locus adaptation, and genetic risk correlates strongly with variation in local pathogens, particularly helminth diversity, suggesting a possible role for host-intestinal pathogen interactions in shaping the genetic landscape of IgAN.

] Department of Genetics Yale University School of Medicine New Haven Connecticut USA [2] Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea

] Department of Genetics Yale University School of Medicine New Haven Connecticut USA [2] Howard Hughes Medical Institute Yale University School of Medicine New Haven Connecticut USA

] Department of Medicine University of Calgary Calgary Alberta Canada [2] Department of Community Health Sciences University of Calgary Calgary Alberta Canada

] Department of Nephrology RWTH University of Aachen Aachen Germany [2] Kidney Diseases Research Bayer Pharma Wuppertal Germany

] Division of Nephrology Azienda Ospedaliera Spedali Civili of Brescia Montichiari Hospital University of Brescia Brescia Italy [2] Department of Medical and Surgical Specialties Radiological Sciences University of Brescia Brescia Italy

] Division of Nephrology Azienda Ospedaliera Spedali Civili of Brescia Montichiari Hospital University of Brescia Brescia Italy [2] Prenatal Diagnosis Unit Department of Obstetrics and Gynecology University of Brescia Brescia Italy

] Division of Nephrology Azienda Ospedaliero Universitaria Parma Italy [2] Chair of Nephrology University of Parma Parma Italy

] Division of Pediatric Nephrology University of Tennessee Health Sciences Center Memphis Tennessee USA [2] Children's Foundation Research Center Le Bonheur Children's Hospital Memphis Tennessee USA

] Immunogenetics and Biology of Transplantation Città della Salute e della Scienza University Hospital of Turin Turin Italy [2] Medical Genetics Department of Medical Sciences University of Torino Turin Italy

] INSERM Centre for Research in Epidemiology and Population Health Villejuif France [2] University Paris Sud Villejuif France

] John Walls Renal Unit University Hospitals of Leicester Leicester UK [2] Department of Infection Immunity and Inflammation University of Leicester Leicester UK

] Nephrology Center Medical Faculty University of Pécs Pécs Hungary [2] 2nd Department of Internal Medicine Medical Faculty University of Pécs Pécs Hungary

] Service de Néphrologie Transplantation Adultes Hôpital Necker Enfants Malades Paris France [2] INSERM Institut Necker Enfants Malades Université Paris Descartes Sorbonne Paris Cité Paris France

3 Medizinische Klinik Universitätsklinikum Hamburg Eppendorf Hamburg Germany

Centre National de Génotypage Commissariat à l'Energie Atomique Institut de Génomique Evry France

Chair of Nephrology Division of Nephology and Dialysis University of Messina Azienda Ospedaliero Universitaria Policlinico Messina Italy

Department of Immunology Transplantology and Internal Medicine Medical University of Warsaw Warsaw Poland

Department of Medical and Surgical Sciences University of Foggia Foggia Italy

Department of Medicine University of Alabama at Birmingham Birmingham Alabama USA

Department of Microbiology University of Alabama at Birmingham Birmingham Alabama USA

Department of Nephrology 1st Faculty of Medicine and General University Hospital Charles University Prague Czech Republic

Department of Nephrology 2nd University of Naples Naples Italy

Department of Nephrology and Dialysis G Brotzu Hospital Cagliari Italy

Department of Nephrology Dialysis and Renal Transplantation University North Hospital Saint Etienne France

Department of Nephrology Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China

Department of Nephrology RWTH University of Aachen Aachen Germany

Department of Nephrology Transplantology and Internal Medicine Poznan Medical University Poznan Poland

Department of Pediatrics and Nephrology Medical University of Warsaw Warsaw Poland

Division of Clinical Nephrology and Rheumatology Niigata University Niigata Japan

Division of Nephrology and Dialysis Gorizia Hospital Gorizia Italy

Division of Nephrology and Dialysis Infermi Hospital Rimini Italy

Division of Nephrology and Dialysis Sandro Pertini Hospital Rome Italy

Division of Nephrology and Renal Transplantation Carreggi Hospital Florence Italy

Division of Nephrology Azienda Ospedaliera Spedali Civili of Brescia Spedali Civili Hospital University of Brescia Brescia Italy

Division of Nephrology Azienda Ospedaliero Universitaria Ospedali Riuniti di Trieste Trieste Italy

Division of Nephrology Cannizzaro Hospital Catania Italy

Division of Nephrology Department of Internal Medicine Juntendo University Faculty of Medicine Tokyo Japan

Division of Nephrology Department of Medicine College of Physicians and Surgeons Columbia University New York New York USA

Division of Nephrology Dialysis and Renal Transplantation Riuniti Hospital Ancona Italy

Division of Nephrology Dialysis and Transplantation Azienda Ospedaliero Universitaria Policlinico di Modena Università di Modena e Reggio Emilia Modena Italy

Division of Nephrology Dialysis and Transplantation Giannina Gaslini Institute Genova Italy

Division of Nephrology Istanbul Faculty of Medicine Istanbul University Istanbul Turkey

Krysiewicza Children's Hospital Poznań Poland

Nephrology and Dialysis Hospital of Viterbo Viterbo Italy

Nephrology and Dialysis Unit Humanitas Clinical and Research Center Milan Italy

Nephrology and Dialysis Unit Ospedali di Cirié e Chivasso Cirié Turin Italy

Nephrology Dialysis and Transplantation Unit Regina Margheritra Hospital Turin Italy

Renal Division DMCO San Paolo Hospital School of Medicine University of Milan Milan Italy

Renal Division Peking University 1st Hospital Peking University Institute of Nephrology Beijing China

Section of Nephrology Department of Emergency and Organ Transplantation University of Bari Bari Italy

Unità Operativa di Nefrologia e Dialisi Ospedale di Acireale Acireale Italy

University College London Centre for Nephrology Royal Free Hospital Pond Street London UK

Zobrazit více v PubMed

Liu ZH. Nephrology in china. Nat Rev Nephrol. 2013;9:523–8. PubMed

Kiryluk K, et al. Geographic differences in genetic susceptibility to IgA nephropathy: GWAS replication study and geospatial risk analysis. PLoS Genet. 2012;8:e1002765. PubMed PMC

Gharavi AG, et al. Genome-wide association study identifies susceptibility loci for IgA nephropathy. Nat Genet. 2011;43:321–7. PubMed PMC

Yu XQ, et al. A genome-wide association study in Han Chinese identifies multiple susceptibility loci for IgA nephropathy. Nat Genet. 2012;44:178–82. PubMed

Feehally J, et al. HLA has strongest association with IgA nephropathy in genome-wide analysis. J Am Soc Nephrol. 2010;21:1791–7. PubMed PMC

Corbi AL, Larson RS, Kishimoto TK, Springer TA, Morton CC. Chromosomal location of the genes encoding the leukocyte adhesion receptors LFA-1, Mac-1 and p150,95. Identification of a gene cluster involved in cell adhesion. J Exp Med. 1988;167:1597–607. PubMed PMC

Hom G, et al. Association of systemic lupus erythematosus with C8orf13-BLK and ITGAM-ITGAX. N Engl J Med. 2008;358:900–9. PubMed

Westra HJ, et al. Systematic identification of trans eQTLs as putative drivers of known disease associations. Nat Genet. 2013;45:1238–43. PubMed PMC

Fairfax BP, et al. Genetics of gene expression in primary immune cells identifies cell type-specific master regulators and roles of HLA alleles. Nat Genet. 2012;44:502–10. PubMed PMC

Dixon AL, et al. A genome-wide association study of global gene expression. Nat Genet. 2007;39:1202–7. PubMed

Franke A, et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn’s disease susceptibility loci. Nat Genet. 2010;42:1118–25. PubMed PMC

Jostins L, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491:119–24. PubMed PMC

Fujikawa K, et al. Vav1/2/3-null mice define an essential role for Vav family proteins in lymphocyte development and activation but a differential requirement in MAPK signaling in T and B cells. J Exp Med. 2003;198:1595–608. PubMed PMC

Swat W, Fujikawa K. The Vav family: at the crossroads of signaling pathways. Immunol Res. 2005;32:259–65. PubMed

Eriksson N, et al. Novel associations for hypothyroidism include known autoimmune risk loci. PLoS One. 2012;7:e34442. PubMed PMC

Pickrell JK, et al. Signals of recent positive selection in a worldwide sample of human populations. Genome Res. 2009;19:826–37. PubMed PMC

Pritchard JK, Pickrell JK, Coop G. The genetics of human adaptation: hard sweeps, soft sweeps, and polygenic adaptation. Curr Biol. 2010;20:R208–15. PubMed PMC

Teshima KM, Coop G, Przeworski M. How reliable are empirical genomic scans for selective sweeps? Genome Res. 2006;16:702–12. PubMed PMC

Wellcome Trust Case Control C. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature. 2007;447:661–78. PubMed PMC

Radstake TR, et al. Genome-wide association study of systemic sclerosis identifies CD247 as a new susceptibility locus. Nat Genet. 2010;42:426–9. PubMed PMC

Petukhova L, et al. Genome-wide association study in alopecia areata implicates both innate and adaptive immunity. Nature. 2010;466:113–7. PubMed PMC

Chu X, et al. A genome-wide association study identifies two new risk loci for Graves’ disease. Nat Genet. 2011;43:897–901. PubMed

Smedby KE, et al. GWAS of follicular lymphoma reveals allelic heterogeneity at 6p21.32 and suggests shared genetic susceptibility with diffuse large B-cell lymphoma. PLoS Genet. 2011;7:e1001378. PubMed PMC

Ferreira RC, et al. Association of IFIH1 and other autoimmunity risk alleles with selective IgA deficiency. Nat Genet. 2010;42:777–80. PubMed

Yang W, et al. Meta-analysis followed by replication identifies loci in or near CDKN1B, TET3, CD80, DRAM1, and ARID5B as associated with systemic lupus erythematosus in Asians. Am J Hum Genet. 2013;92:41–51. PubMed PMC

International Multiple Sclerosis Genetics C et al. Risk alleles for multiple sclerosis identified by a genomewide study. N Engl J Med. 2007;357:851–62. PubMed

Okada Y, et al. HLA-Cw*1202-B*5201-DRB1*1502 haplotype increases risk for ulcerative colitis but reduces risk for Crohn’s disease. Gastroenterology. 2011;141:864–871. e1–5. PubMed

Kumar V, et al. Genome-wide association study identifies a susceptibility locus for HCV-induced hepatocellular carcinoma. Nat Genet. 2011;43:455–8. PubMed

Osman W, et al. Association of common variants in TNFRSF13B, TNFSF13, and ANXA3 with serum levels of non-albumin protein and immunoglobulin isotypes in Japanese. PLoS One. 2012;7:e32683. PubMed PMC

Chen W, et al. Genetic variants near TIMP3 and high-density lipoprotein-associated loci influence susceptibility to age-related macular degeneration. Proc Natl Acad Sci U S A. 2010;107:7401–6. PubMed PMC

Barrett JC, et al. Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes. Nat Genet. 2009;41:703–7. PubMed PMC

Zhao J, et al. Association of genetic variants in complement factor H and factor H-related genes with systemic lupus erythematosus susceptibility. PLoS Genet. 2011;7:e1002079. PubMed PMC

Imielinski M, et al. Common variants at five new loci associated with early-onset inflammatory bowel disease. Nat Genet. 2009;41:1335–40. PubMed PMC

McGovern DP, et al. Genome-wide association identifies multiple ulcerative colitis susceptibility loci. Nat Genet. 2010;42:332–7. PubMed PMC

Litinskiy MB, et al. DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL. Nat Immunol. 2002;3:822–9. PubMed PMC

Kunisawa J, et al. Microbe-dependent CD11b+ IgA+ plasma cells mediate robust early-phase intestinal IgA responses in mice. Nat Commun. 2013;4:1772. PubMed PMC

van Egmond M, et al. Human immunoglobulin A receptor (FcalphaRI, CD89) function in transgenic mice requires both FcR gamma chain and CR3 (CD11b/CD18) Blood. 1999;93:4387–94. PubMed

Van Spriel AB, Leusen JH, Vile H, Van De Winkel JG. Mac-1 (CD11b/CD18) as accessory molecule for Fc alpha R (CD89) binding of IgA. J Immunol. 2002;169:3831–6. PubMed

Bevins CL, Salzman NH. Paneth cells, antimicrobial peptides and maintenance of intestinal homeostasis. Nat Rev Microbiol. 2011;9:356–68. PubMed

Wehkamp J, et al. Reduced Paneth cell alpha-defensins in ileal Crohn’s disease. Proc Natl Acad Sci U S A. 2005;102:18129–34. PubMed PMC

Sokol H, et al. Card9 mediates intestinal epithelial cell restitution, T-helper 17 responses, and control of bacterial infection in mice. Gastroenterology. 2013;145:591–601. e3. PubMed PMC

Liu JY, et al. Vav proteins are necessary for correct differentiation of mouse cecal and colonic enterocytes. J Cell Sci. 2009;122:324–34. PubMed PMC

Vigorito E, Gambardella L, Colucci F, McAdam S, Turner M. Vav proteins regulate peripheral B-cell survival. Blood. 2005;106:2391–8. PubMed

Freudenberg J, et al. Genome-wide association study of rheumatoid arthritis in Koreans: population-specific loci as well as overlap with European susceptibility loci. Arthritis Rheum. 2011;63:884–93. PubMed

Fumagalli M, et al. Signatures of environmental genetic adaptation pinpoint pathogens as the main selective pressure through human evolution. PLoS Genet. 2011;7:e1002355. PubMed PMC

Pullan RL, Smith JL, Jasrasaria R, Brooker SJ. Global numbers of infection and disease burden of soil transmitted helminth infections in 2010. Parasit Vectors. 2014;7:37. PubMed PMC

Barry MA, Simon GG, Mistry N, Hotez PJ. Global trends in neglected tropical disease control and elimination: impact on child health. Arch Dis Child. 2013;98:635–41. PubMed

Barsoum RS. Schistosomal glomerulopathy: selection factors. Nephrol Dial Transplant. 1987;2:488–97. PubMed

Ferragine CE, Walls CD, Davies SJ. Modulation of innate antigen-presenting cell function by pre-patent schistosome infection. PLoS Negl Trop Dis. 2013;7:e2136. PubMed PMC

Ambruzs JM, Walker PD, Larsen CP. The histopathologic spectrum of kidney biopsies in patients with inflammatory bowel disease. Clin J Am Soc Nephrol. 2014;9:265–70. PubMed PMC

Wyatt RJ, Julian BA. IgA nephropathy. N Engl J Med. 2013;368:2402–14. PubMed

Fujimoto K, et al. A new subset of CD103+CD8alpha+ dendritic cells in the small intestine expresses TLR3, TLR7, and TLR9 and induces Th1 response and CTL activity. J Immunol. 2011;186:6287–95. PubMed

Uematsu S, et al. Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5. Nat Immunol. 2008;9:769–76. PubMed

Bertin J, et al. CARD9 is a novel caspase recruitment domain-containing protein that interacts with BCL10/CLAP and activates NF-kappa B. J Biol Chem. 2000;275:41082–6. PubMed

Prunotto M, et al. Autoimmunity in membranous nephropathy targets aldose reductase and SOD2. J Am Soc Nephrol. 2010;21:507–19. PubMed PMC

Rivas MA, et al. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease. Nat Genet. 2011;43:1066–73. PubMed PMC

Beaudoin M, et al. Deep resequencing of GWAS loci identifies rare variants in CARD9, IL23R and RNF186 that are associated with ulcerative colitis. PLoS Genet. 2013;9:e1003723. PubMed PMC

Lanternier F, et al. Deep dermatophytosis and inherited CARD9 deficiency. N Engl J Med. 2013;369:1704–14. PubMed PMC

Levison SE, et al. Genetic analysis of the Trichuris muris-induced model of colitis reveals QTL overlap and a novel gene cluster for establishing colonic inflammation. BMC Genomics. 2013;14:127. PubMed PMC

Chu H, et al. Human alpha-defensin 6 promotes mucosal innate immunity through self-assembled peptide nanonets. Science. 2012;337:477–81. PubMed PMC

McCarthy DD, et al. Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy. J Clin Invest. 2011;121:3991–4002. PubMed PMC

Castigli E, et al. TACI is mutant in common variable immunodeficiency and IgA deficiency. Nat Genet. 2005;37:829–34. PubMed

Imielinski M, et al. Common variants at five new loci associated with early-onset inflammatory bowel disease. Nat Genet. 2009;41:1335–40. PubMed PMC

Cella M, et al. A human natural killer cell subset provides an innate source of IL-22 for mucosal immunity. Nature. 2009;457:722–5. PubMed PMC

Fritz DK, et al. A mouse model of airway disease: oncostatin M-induced pulmonary eosinophilia, goblet cell hyperplasia, and airway hyperresponsiveness are STAT6 dependent, and interstitial pulmonary fibrosis is STAT6 independent. J Immunol. 2011;186:1107–18. PubMed

Ernst M, et al. Defective gp130-mediated signal transducer and activator of transcription (STAT) signaling results in degenerative joint disease, gastrointestinal ulceration, and failure of uterine implantation. J Exp Med. 2001;194:189–203. PubMed PMC

Rockman SP, et al. Expression of interleukin-6, leukemia inhibitory factor and their receptors by colonic epithelium and pericryptal fibroblasts. J Gastroenterol Hepatol. 2001;16:991–1000. PubMed

Kalabis J, et al. Stimulation of human colonic epithelial cells by leukemia inhibitory factor is dependent on collagen-embedded fibroblasts in organotypic culture. FASEB J. 2003;17:1115–7. PubMed

Visekruna A, et al. Proteasome-mediated degradation of IkappaBalpha and processing of p105 in Crohn disease and ulcerative colitis. J Clin Invest. 2006;116:3195–203. PubMed PMC

Wu F, et al. Genome-wide gene expression differences in Crohn’s disease and ulcerative colitis from endoscopic pinch biopsies: insights into distinctive pathogenesis. Inflamm Bowel Dis. 2007;13:807–21. PubMed

Schmidt N, et al. Targeting the proteasome: partial inhibition of the proteasome by bortezomib or deletion of the immunosubunit LMP7 attenuates experimental colitis. Gut. 2010;59:896–906. PubMed

van Heel DA, et al. A genome-wide association study for celiac disease identifies risk variants in the region harboring IL2 and IL21. Nat Genet. 2007;39:827–9. PubMed PMC

Dubois PC, et al. Multiple common variants for celiac disease influencing immune gene expression. Nat Genet. 2010;42:295–302. PubMed PMC

Yang SK, et al. Genome-wide association study of ulcerative colitis in Koreans suggests extensive overlapping of genetic susceptibility with Caucasians. Inflamm Bowel Dis. 2013;19:954–66. PubMed

Skol AD, Scott LJ, Abecasis GR, Boehnke M. Joint analysis is more efficient than replication-based analysis for two-stage genome-wide association studies. Nat Genet. 2006;38:209–13. PubMed

Purcell S, et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am J Hum Genet. 2007;81:559–75. PubMed PMC

Willer CJ, Li Y, Abecasis GR. METAL: fast and efficient meta-analysis of genomewide association scans. Bioinformatics. 2010;26:2190–1. PubMed PMC

Devlin B, Roeder K, Bacanu SA. Unbiased methods for population-based association studies. Genet Epidemiol. 2001;21:273–84. PubMed

Storey JD, Tibshirani R. Statistical significance for genomewide studies. Proc Natl Acad Sci U S A. 2003;100:9440–5. PubMed PMC

Huedo-Medina TB, Sanchez-Meca J, Marin-Martinez F, Botella J. Assessing heterogeneity in meta-analysis: Q statistic or I2 index? Psychol Methods. 2006;11:193–206. PubMed

Li Y, Willer CJ, Ding J, Scheet P, Abecasis GR. MaCH: using sequence and genotype data to estimate haplotypes and unobserved genotypes. Genet Epidemiol. 2010;34:816–34. PubMed PMC

Browning SR, Browning BL. Rapid and accurate haplotype phasing and missing-data inference for whole-genome association studies by use of localized haplotype clustering. Am J Hum Genet. 2007;81:1084–97. PubMed PMC

Rossin EJ, et al. Proteins encoded in genomic regions associated with immune-mediated disease physically interact and suggest underlying biology. PLoS Genet. 2011;7:e1001273. PubMed PMC

Lage K, et al. A human phenome-interactome network of protein complexes implicated in genetic disorders. Nat Biotechnol. 2007;25:309–16. PubMed

Wu J, et al. Integrated network analysis platform for protein-protein interactions. Nat Methods. 2009;6:75–7. PubMed

Jia P, Zheng S, Long J, Zheng W, Zhao Z. dmGWAS: dense module searching for genome-wide association studies in protein-protein interaction networks. Bioinformatics. 2011;27:95–102. PubMed PMC

Wang K, Li M, Hakonarson H. ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data. Nucleic Acids Res. 2010;38:e164. PubMed PMC

Ng SB, et al. Targeted capture and massively parallel sequencing of 12 human exomes. Nature. 2009;461:272–6. PubMed PMC

Ward LD, Kellis M. HaploReg: a resource for exploring chromatin states, conservation, and regulatory motif alterations within sets of genetically linked variants. Nucleic Acids Res. 2012;40:D930–4. PubMed PMC

Conrad DF, et al. Origins and functional impact of copy number variation in the human genome. Nature. 2010;464:704–12. PubMed PMC

Raychaudhuri S, et al. Identifying relationships among genomic disease regions: predicting genes at pathogenic SNP associations and rare deletions. PLoS Genet. 2009;5:e1000534. PubMed PMC

Haas M. Histologic subclassification of IgA nephropathy: a clinicopathologic study of 244 cases. Am J Kidney Dis. 1997;29:829–42. PubMed

Levey AS, et al. Using standardized serum creatinine values in the modification of diet in renal disease study equation for estimating glomerular filtration rate. Ann Intern Med. 2006;145:247–54. PubMed

Bisceglia L, et al. Genetic Heterogeneity in Italian Families with IgA Nephropathy: Suggestive Linkage for Two Novel IgA Nephropathy Loci. Am J Hum Genet. 2006;79:1130–1134. PubMed PMC

K/DOQI clinical practice guidelines for chronic kidney disease: evaluation classification stratification. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2002;39:S1–266. PubMed

Hindorff LA, et al. Potential etiologic and functional implications of genome-wide association loci for human diseases and traits. Proc Natl Acad Sci U S A. 2009;106:9362–7. PubMed PMC

Sun L, et al. Multiple apical plasma membrane constituents are associated with susceptibility to meconium ileus in individuals with cystic fibrosis. Nat Genet. 2012;44:562–9. PubMed PMC

Subramanian A, et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc Natl Acad Sci U S A. 2005;102:15545–50. PubMed PMC

Merico D, Isserlin R, Stueker O, Emili A, Bader GD. Enrichment map: a network-based method for gene-set enrichment visualization and interpretation. PLoS One. 2010;5:e13984. PubMed PMC

Targeting APRIL in the Treatment of IgA Nephropathy

IgA nephropathy

The role of complement in kidney disease

Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy

IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease

The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies

Emerging Modes of Treatment of IgA Nephropathy

Leukemia Inhibitory Factor Signaling Enhances Production of Galactose-Deficient IgA1 in IgA Nephropathy

Role of Epstein-Barr Virus in Pathogenesis and Racial Distribution of IgA Nephropathy

The Emerging Role of Complement Proteins as a Target for Therapy of IgA Nephropathy

Galactose-deficient IgA1 and the corresponding IgG autoantibodies predict IgA nephropathy progression

Inhibition of STAT3 Signaling Reduces IgA1 Autoantigen Production in IgA Nephropathy

Common variants at PVT1, ATG13-AMBRA1, AHI1 and CLEC16A are associated with selective IgA deficiency

IgA nephropathy enigma

Somatic Mutations Modulate Autoantibodies against Galactose-Deficient IgA1 in IgA Nephropathy

Markers for the progression of IgA nephropathy

The Origin and Activities of IgA1-Containing Immune Complexes in IgA Nephropathy

Zobrazit více v PubMed

dbGaP
PHS000431.V1.P1, PHS000431.V2.P1