In this paper, we describe the results of a dense genome-wide scan in two small groups of individuals with FSGS, one African American, and the other European American. We were unable to identify any reproducible associations between FSGS and common genetic variants in European cases compared with unselected controls, which suggests that there are no common variants in the European population of large effect in the susceptibility to disease. (Because our sample size was small, we cannot exclude the existence of genetic variants of small effect.) We replicated the signal originating from the MYH9 locus that has been previously observed [14,15]. This signal did not replicate in European samples, although the statistical power to detect a true association was limited by the relatively small number of cases available for study. We did not find any other signal outside of the MYH9 locus. Given the strong association at this locus for African Americans, this association explains most of FSGS in this cohort, and therefore we were extremely underpowered to identify any additional and independent association.
