Both uteroglobin knockout and antisense transgenic mice develop pathological and clinical features similar to immunoglobulin A (IgA) nephropathy. However, several association studies of uteroglobin G38A polymorphism and IgA nephropathy showed controversial findings. We used meta-analysis to assess the impact of the uteroglobin G38A polymorphism on susceptibility to and progression of IgA nephropathy. Six studies involving uteroglobin G38A genotyping of 930 patients with IgA nephropathy and 768 healthy controls were included. No significant publication bias was found (Egger's linear regression, P = 0.763; 95% confidence interval [CI], -0.610 to 0.476). All control samples were in Hardy-Weinberg proportion. No association between the AA genotype and risk for IgA nephropathy relative to both other genotypes (odds ratio [OR], 1.05; 95% CI, 0.71 to 1.54) or A allele and risk for IgA nephropathy (OR, 0.96; 95% CI, 0.84 to 1.11) were shown in the total meta-analysis. In both Asian and European subgroups, the overall effect of the AA genotype and A allele also showed no significant difference. There also was no significant association between uteroglobin AA genotype or A allele and IgA nephropathy progression (OR, 3.62; 95% CI, 0.59 to 22.34; OR, 2.19, 95% CI, 0.37 to 13.14, respectively). We suggest that uteroglobin G38A polymorphism is not related to the development and progression of IgA nephropathy.