Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multiple system involvement and positive serum autoantibodies. Lupus nephritis (LN) is the most common and serious complication of SLE, and it is the main cause of death in patients with SLE. Abnormalities in the immune system lead to LN and involve a variety of cells (T cells, B cells, macrophages, NK cells, etc.), cytokines (interleukin, tumor necrosis factor α, etc.) and their related pathways. Previous studies have shown that the interactions of genetic, epigenetic and environmental factors contribute to the pathogenesis and development of LN. In recent years, one genome-wide association study (GWAS) and a number of gene association studies have explored the susceptibility genes of LN, including immunization-, inflammation-, adhesion- and other pathway-related genes. These genes participate in or suggest the pathogenesis and progression of LN. In this review, we summarize the genetic susceptibility of LN and discuss the possible mechanism underlying the susceptibility genes of LN.

系统性红斑狼疮（SLE）是一种慢性自身免疫性疾病，其特征在于多系统参与和阳性血清自身抗体。狼疮性肾炎（LN）是SLE的最常见和最严重的并发症，它是SLE患者死亡的主要原因。免疫系统异常会导致LN，并涉及多种细胞（T细胞，B细胞，巨噬细胞，NK细胞等），细胞因子（白介素，肿瘤坏死因子α等）及其相关途径。先前的研究表明，遗传，表观遗传和环境因素的相互作用促进了LN的发病和发展。近年来，一项全基因组关联研究（GWAS）和许多基因关联研究已经探索了LN的易感基因，包括免疫，炎症，粘附和其他途径相关的基因。这些基因参与或提示LN的发病机理和进展。在这篇综述中，我们总结了LN的遗传易感性，并讨论了LN易感性基因的潜在机制。