<i>KLK1</i> Gene Polymorphisms Are Not Associated with Lupus Nephritis in a Chinese Han Population: Table 1.

Zhou, Xu‐jie; Lv, Jicheng; Zhao, Minghui; Zhang, Hong

doi:10.3899/jrheum.091316

Cited by 19 publications

(28 citation statements)

References 10 publications

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“…Over the last year, new genes have been associated with anti-GBM disease. Specifically, in addition to HLA genes, genes of FCGR and KLK families have been found to modulate the susceptibility to the disease [36,37,56,58]. These recent findings reinforce the concept of the complexity of anti-GBM disease and emphasize the importance of investigating biologically relevant pathways [59].…”

Section: Future Directionsmentioning

confidence: 50%

“…Such pieces of evidence for a protective role for kallikrein in end-stage organ failure and autoimmune diseases support the concept of shared genetics between anti-GBM disease and lupus nephritis, and go against the belief that anti-GBM disease is radically different from other autoimmune diseases, i.e., anti-GBM disease is a somewhat organ-specific autoimmune disease that rarely relapses or coexists with other autoimmune diseases. Although these findings are very important, they should be replicated before they can be deemed valid [56,58]. Furthermore, the association of the KLK gene family with anti-GBM disease should be directly examined in human patients, not only in animal models.…”

Section: End-stage Organ Failure and Kallikrein Systemmentioning

confidence: 99%

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Advances in the Genetics of Anti-Glomerular Basement Membrane Disease

Zhou

Zhao

et al. 2010

Am J Nephrol

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Anti-glomerular basement membrane (GBM) disease is a rare but lethal autoimmune disorder. Over the past few years, the nature of the autoantigen and its epitopes has been defined, as well as the possible pathogenic role played by environmental factors, and by cellular and humoral immunity. However, the majority of data on anti-GBM disease comes from studies conducted on animal models, since human studies are relatively scarce. Genetic studies have highlighted strong positive associations of anti-GBM disease with the HLA-DRB1*1501 allele. In addition, the disease has been associated with genes of the FCGR and KLK families. Important as they are, these findings have to be considered preliminary, if not contentious. Here, we provide an overview of recent discoveries in the genetics of anti-GBM disease that may help elucidate the disease pathogenesis while improving therapeutic approaches. We also discuss the limitations of such discoveries. Finally, we suggest that extensive collaboration between investigators and novel integrative approaches are essential to the progress of our understanding of the anti-GBM disease. We attempted to summarize the current knowledge on the pathogenesis of anti-GBM disease by providing different but complementary perspectives from previous reviews.

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Section: Future Directionsmentioning

confidence: 50%

Section: End-stage Organ Failure and Kallikrein Systemmentioning

confidence: 99%

Advances in the Genetics of Anti-Glomerular Basement Membrane Disease

Zhou

Zhao

et al. 2010

Am J Nephrol

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“…Lupus nephritis (LN) is one of the most serious SLE complications due to high morbidity and mortality [1]. Although genetic variations and environmental factors have been reported to contribute to the development of LN [2,3], the precise etiology of LN remains elusive. However, sustained local inflammation has been suggested to be a common basis that leads to virtually every type of end organ damage [4,5].…”

Section: Introductionmentioning

confidence: 99%

Chemokine receptor 5 (CCR5) delta 32 polymorphism in lupus nephritis: A large case-control study and meta-analysis

et al. 2014

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“…[13] However, they could not find any difference between genotypes in terms of activity and chronicity indices, SLEDAI, C4levels or proteinuria. In contrast, a study from the UK failed to find any association between nephritis and any of the nine studied single nucleotide polymorphisms (SNPs) in the TLR9 gene.…”

Section: Discussionmentioning

confidence: 99%

Association between -1486 T>C and +1174 G>A single nucleotide polymorphisms in TLR9 gene and severity of lupus nephritis

et al. 2012

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Signaling through Toll-like receptor-9 (TLR9), a mediator of innate immune responses, could have a role in the pathogenesis of systemic lupus erythematosus (SLE). Some studies have shown an association between polymorphisms in the TLR9 gene and disease manifestations. We investigated whether two single nucleotide polymorphisms (-1486 T>C and +1174 G>A) in the TLR9 gene are associated with the risk of renal involvement in SLE. DNA samples from 112 SLE patients (62 with lupus nephritis) and 100 healthy controls were obtained. TLR9 polymorphisms (-1486 T>C and +1174 G>A) were analyzed by polymerase chain reaction–restriction fragment length polymorphism. Genotype and allelic frequencies were compared between lupus patients and healthy controls. Clinical and laboratory manifestations and activity scores on renal biopsy of patients with lupus nephritis were compared between various genotypes. There was no difference in the frequency of genotype or allele distribution at either of the two loci between lupus patients and controls and in lupus patients with or without nephritis. Patients with CC/CT genotype at the -1486 position had higher serum creatinine (P = 0.03) and Austin activity scores (P = 0.015). Patients with AA/AG genotype at +1174 position showed higher serum creatinine (P = 0.04), proteinuria (P = 0.011), anti-dsDNA titers (P < 0.001) and Austin activity scores (P = 0.003) than the GG genotype. Variations at the -1486 and +1174 positions of TLR9 gene are not associated with increased risk of SLE or that of kidney involvement in North Indians. CC/CT genotypes at -1486 and AA/AG at +1174 positions are associated with more severe kidney disease at presentation.

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KLK1 Gene Polymorphisms Are Not Associated with Lupus Nephritis in a Chinese Han Population: Table 1.

Cited by 19 publications

References 10 publications

Advances in the Genetics of Anti-Glomerular Basement Membrane Disease

Advances in the Genetics of Anti-Glomerular Basement Membrane Disease

Chemokine receptor 5 (CCR5) delta 32 polymorphism in lupus nephritis: A large case-control study and meta-analysis

Association between -1486 T>C and +1174 G>A single nucleotide polymorphisms in TLR9 gene and severity of lupus nephritis

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