A specific model for CFHR5 nephropathy was also developed, in which mice lacking mFH and murine FHRs but coexpressing human FH and mutant FHR-5 (with duplicated CCP1-2) developed glomerular deposition of C3 fragments, while those coexpressing human FH and wild type FHR-5 did not (283). This evidence concerns the gene FH and kidney disorder.