Blocking the action of insulin‐like growth factor I (IGF I) impairs kidney development in vitro. However, no renal developmental abnormalities have been reported in newborn transgenic mice that do not express IGF I (Igf1^−/−) mice. Ninety‐five percent of Igf1^−/− mice die immediately following birth. Kidney development continues following birth in rodents. To readdress the question of the participation of IGF I in the process of kidney development, we measured nephron numbers in developed kidneys from Igf1^−/− mice that survived past birth, and using a second model of kidney development, characterized the effect of IGF I infused into rat hosts on the renal function of transplanted metanephroi. Igf1^−/− mice were born with grossly normal kidneys. At 77 ± 10 days after birth, Igf1^−/− mice that survived were approximately 28% the weight of wild‐type (WT) littermates and had proportionally smaller kidneys. The number of nephrons per kidney was reduced by approximately 20% in Igf1^−/− mice. Glomerular size was also reduced in Igf1^−/− mice. In untreated host rats, neither the size nor inulin clearance of transplanted metanephroi changed significantly from 12–28 weeks postimplantation. The administration of IGF I to hosts did not affect the size of transplanted metanephroi measured at 12–16 weeks following implantation. However, inulin clearances were increased significantly by the administration of IGF I to hosts. Our findings 1) indicate that IGF I plays a role in determining nephron number, 2) suggest that it enhances function in developing kidneys, and 3) establish the potential for the pharmacological use of IGF I to enhance the growth and function of transplanted metanephroi. Dev. Genet. 24:293–298, 1999. © 1999 Wiley‐Liss, Inc.