AB0096 IGA VASCULITIS AND IGA NEPHROPATHY SHARE A SIMILAR IL17A ASSOCIATION PATTERN
Authors: D. Prieto-Peña, F. Genre, S. Remuzgo Martinez, V. Pulito-Cueto, B. Atienza-Mateo, B. Sevilla, J. Llorca, N. Ortego, L. Lera-Gómez, M. Leonardo, A. Peñalba, L. Martín-Penagos, J. A. Miranda-Filloy, J. Narváez, L. Caminal Montero, P. Collado, A. Fernandez-Nebro, G. Díaz-Cordoves, S. Cigarrán, J. Calviño, C. Cobelo, J. Sanchez Perez, D. De Argila, E. Rubio-Romero, M. Leon Luque, J. M. Blanco-Madrigal, E. Galindez, J. Martin Ibanez, S. Castañeda, R. Blanco, M. A. González-Gay, R. López-Mejías
Journal: Annals of the Rheumatic Diseases (2021)

Background: IgA vasculitis (IgAV) and IgA nephropathy (IgAN) are inflammatory conditions that share pathogenic and molecular mechanisms [1] and may represent different outcomes of a continuous spectrum of disease [2]. Interleukin (IL)17A has been identified as a common genetic risk locus for several immune-mediated diseases [3, 4]. Objectives: To determine whether IgAV and IgAN exhibit a different IL17A association pattern. Methods: Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were genotyped in 388 Caucasian patients with IgAV, 99 patients with IgAN and 1,003 sex and ethnically matched healthy controls. Results: No statistically significant differences between patients with IgAV and healthy controls and between patients with IgAN and healthy controls were observed when each IL17A genetic variant was analyzed independently (Table 1). Similarly, IgAV patients exhibited similar genotype and allele IL17A frequencies than those with IgAN (Table 1). Moreover, no genotype or allele differences between IgAV patients who developed nephritis and patients with IgAN were detected. Furthermore, haplotype frequencies were similar in patients with IgAV, IgAV and nephritis and those with IgAN. Table 1. Genotype and allele frequencies of IL17A gene in patients with IgA vasculitis, patients with IgA nephropathy and healthy controls. Polymorphism Change Data set 1/1 1/2 2/2 1 2 rs4711998 G/A IgAV 53.4 (207) 38.9 (151) 7.7 (30) 72.8 (565) 27.2 (211) IgAN 49.0 (48) 42.9 (42) 8.2 (8) 70.4 (138) 29.6 (58) Controls 52.7 (529) 41.2 (413) 6.1 (61) 73.3 (1471) 26.7 (535) rs8193036 T/C IgAV 57.0 (221) 38.4 (149) 4.6 (18) 76.2 (591) 23.8 (185) IgAN 64.3 (63) 31.6 (31) 4.1 (4) 80.1 (157) 19.9 (39) Controls 60.3 (605) 35.2 (353) 4.5 (45) 77.9 (1563) 22.1 (443) rs3819024 A/G IgAV 44.1 (171) 43.3 (168) 12.6 (49) 65.7 (510) 34.3 (266) IgAN 39.4 (39) 54.5 (54) 6.1 (6) 66.7 (132) 33.3 (66) Controls 45.6 (457) 44.6 (447) 9.9 (99) 67.8 (1361) 32.2 (645) rs2275913 G/A IgAV 44.6 (172) 43.3 (167) 12.2 (47) 66.2 (511) 33.8 (261) IgAN 39.8 (39) 53.1 (52) 7.1 (7) 66.3 (130) 33.7 (66) Controls 44.8 (449) 44.2 (443) 11.1 (111) 66.8 (1341) 33.2 (665) rs7747909 G/A IgAV 53.9 (209) 39.4 (153) 6.7 (26) 73.6 (571) 26.4 (205) IgAN 41.1 (39) 54.7 (52) 4.2 (4) 68.4 (130) 31.6 (60) Controls 53.0 (532) 39.4 (395) 7.6 (76) 72.7 (1459) 27.3 (547) Conclusion: Our results revealed that IgAV and IgAN share a similar IL17A association pattern. References: [1]N Engl J Med 2013;368:2402-14. [2]Am J Kidney Dis 1988;12:373-7. [3]Ann Rheum Dis 2014;73:1742-5. [4]Mediators Inflamm 2018;2018:1395823. Acknowledgements: This study was supported by European Union FEDER funds and “Fondo de Investigaciones Sanitarias” (grant PI18/00042) from ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). DP-P is a recipient of a Río Hortega programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CM20/00006]; SR-M is supported by funds of the RETICS Program co-funded by the European Regional Development Fund (ERDF) [grant number RD16/0012/0009]; VP-C is supported by a pre-doctoral grant from IDIVAL [grant number PREVAL 18/01]; BA-M is a recipient of a `López Albo´ Post-Residency Programme funded by Servicio Cántabro de Salud; LL-G is supported by funds of IDIVAL [grant number INNVAL20/06]; RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CP16/00033]. Disclosure of Interests: Diana Prieto-Peña: None declared, Fernanda Genre: None declared, Sara Remuzgo Martinez: None declared, Verónica Pulito-Cueto: None declared, Belén Atienza-Mateo: None declared, Belén Sevilla: None declared, Javier Llorca: None declared, Norberto Ortego: None declared, Leticia Lera-Gómez: None declared, Maite Leonardo: None declared, Ana Peñalba: None declared, Luis Martín-Penagos: None declared, Jose Alberto Miranda-Filloy: None declared, J. Narváez: None declared, LUIS CAMINAL MONTERO: None declared, PAZ COLLADO: None declared, Antonio Fernandez-Nebro: None declared, Gisela Díaz-Cordoves: None declared, Secundino Cigarrán: None declared, Jesús Calviño: None declared, Carmen Cobelo: None declared, Javier Sanchez Perez: None declared, Diego de Argila: None declared, Esteban Rubio-Romero: None declared, MANUEL LEON LUQUE: None declared, Juan María Blanco-Madrigal: None declared, E. Galindez: None declared, Javier Martin Ibanez: None declared, Santos Castañeda: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Raquel López-Mejías: None declared