The role of glomerular hyperfiltration as a risk factor for renal outcome in diabetes is not clear (O'Donnell et al. 1988; Anderson and Vora 1995; Yip et al. 1996; Pitrosch et al. 2005; Sallstrom et al. 2007), but the lessening of urinary nephrin, podocalyxin, and βig-h3 as well as albumin without change in creatinine clearance in animals receiving test compound indicates that these decreases do not reflect effects on the glomerular filtration rate and that hyperfiltration is not a principal contributor to the increases in control diabetic animals. This evidence concerns the gene PODXL and diabetes mellitus.