the potential influence of SLE susceptibility variants in our tests of association with LN. To account for potential population substructure, principal component analyses were computed using SNPs that passed quality control.35 All tests of association were computed and adjusted for five principal components in the set I samples and four principal components in the set II and set III samples. Within each GWAS set, autosomal SNPs that passed quality control filters and exhibited a minor allele frequency .0.01 were used to impute the approximately 2.5 million SNPs in HapMap2 (Build 35) using IMPUTE.36 The reference set for imputation was theUtah residents with ancestry from northern and western Europe available via the HapMap. Within each GWASset,logistic regression models included theabovestated principal components and accounted for the imputation uncertainty via the poster iorge notypeprobabilities.36Dominant,additive, and recessivegenetic models were computed assuming at least 10 and 20 individuals homozygous for the minor allele were observed. Because of the modest sample size, this requirement caused many SNPs tonothaveatestcomputedinsetIII.Theevidenceofassociationfrom each of the three GWAS sets was weighted by sample size and combined using the weighted inverse normal method as implemented in METAL.37 To account for any inflation, the genomiccontrol-adjusted P value was reported