<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Munroe ME</submitter><funding>NIAID NIH HHS</funding><funding>NIAMS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>396-409</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4653095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>35(5)</volume><pubmed_abstract>Systemic lupus erythematosus is a heterogeneous autoimmune disease marked by the presence of pathogenic autoantibodies, immune dysregulation, and chronic inflammation that may lead to increased morbidity and early mortality from end-organ damage. More than half of all systemic lupus erythematosus patients will develop lupus nephritis. Genetic-association studies have identified more than 50 polymorphisms that contribute to lupus nephritis pathogenesis, including genetic variants associated with altered programmed cell death and defective immune clearance of programmed cell death debris. These variants may support the generation of autoantibody-containing immune complexes that contribute to lupus nephritis. Genetic variants associated with lupus nephritis also affect the initial phase of in</pubmed_abstract><journal>Seminars in nephrology</journal><pubmed_title>Genetics of Lupus Nephritis: Clinical Implications.</pubmed_title><pmcid>PMC4653095</pmcid><funding_grant_id>U54 GM104938</funding_grant_id><funding_grant_id>U54GM104938</funding_grant_id><funding_grant_id>U19AI082714</funding_grant_id><funding_grant_id>P30GM103510</funding_grant_id><funding_grant_id>P30 AR053483</funding_grant_id><funding_grant_id>U19 AI082714</funding_grant_id><funding_grant_id>P30AR053483</funding_grant_id><funding_grant_id>P30 GM103510</funding_grant_id><funding_grant_id>U01AI101934</funding_grant_id><funding_grant_id>U01 AI101934</funding_grant_id><pubmed_authors>James JA</pubmed_authors><pubmed_authors>Munroe ME</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetics of Lupus Nephritis: Clinical Implications.</name><description>Systemic lupus erythematosus is a heterogeneous autoimmune disease marked by the presence of pathogenic autoantibodies, immune dysregulation, and chronic inflammation that may lead to increased morbidity and early mortality from end-organ damage. More than half of all systemic lupus erythematosus patients will develop lupus nephritis. Genetic-association studies have identified more than 50 polymorphisms that contribute to lupus nephritis pathogenesis, including genetic variants associated with altered programmed cell death and defective immune clearance of programmed cell death debris. These variants may support the generation of autoantibody-containing immune complexes that contribute to lupus nephritis. Genetic variants associated with lupus nephritis also affect the initial phase of in</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Sep</publication><modification>2025-04-22T14:24:05.062Z</modification><creation>2019-03-27T02:02:25Z</creation></dates><accession>S-EPMC4653095</accession><cross_references><pubmed>26573543</pubmed><doi>10.1016/j.semnephrol.2015.08.002</doi></cross_references></HashMap>