The ROP [Ra/+ (ragged), Os/+ (oligosyndactyly), and Pt/+ (pintail)] mouse possessing the gene for oligosyndactylism (Os) was evaluated as a potential genetic animal model of reduced renal mass. Young male ROP mice that were heterozygotes with respect to the Os gene (Os/+) and their normal homozygote litter mates (+/+) were used in the present study. Approximately 50% fewer nephrons were present in the Os/+ mice than in the +/+ mice. Hypertrophic changes were detected in the epithelial cells in proximal convoluted and proximal straight tubules as well as in cortical collecting ducts in the kidneys of the Os/+ mice. Glomerular hypertrophy was also noted in the kidneys of these mice. After unilateral nephrectomy, further hypertrophic changes occurred in both Os/+ and +/+ mice, but the magnitude of compensatory growth was greater in the +/+ mice. From a functional standpoint, the Os/+ mice appeared to be capable of maintaining normal fluid and electrolyte homeostasis, even after unilateral nephrectomy. The findings from the present study indicate that the ROP Os/+ mouse can be a useful animal model to study the effects of reduced renal mass.