Uremic growth retardation is associated with normal to elevated serum concentrations of GH, IGF-I, and IGFBP-3. Treatment with exogenous GH further raises the serum concentrations of IGF-I and IGFBP-3. The IGFBPs impart tissue-and cell-specific selectivity to the growth promoting actions of the IGFs. We therefore characterized the gene expression of IGF-I and IGFBP-3 in an end-organ mediating longitudinal growth, the TEGP. Uremia was created by standard 5/6 ths subtotal nephrectomy (Nx) as previously published at 25d age. Controls received decapsulization. At 42d age 6 Nx and 3 control (S) rats were matched for length. 10 IU/Kg/d rat GH (rGH) was injected intraperitoneally (IP) in 3 Nx rats (UGH) for 14d. The remaining 3 Nx rats (U) received an equal volume of IP saline. Sacrifice by transcardial fixation took place at 56d age. Serum urea nitrogen and creatinine did not differ U vs UGH, but were higher than S (p<0.05). Treatment of the U rat with rGH resulted in an increase in linear length such that UGH rats did not differ from the S rats in nose to tail tip length. The S rats were significantly longer than the U rats (UGH: 17.4± 0.5 vs S: 18.4±0.7 vs U: 15.5±0.3 cm, p<0.05). Treatment with rGH resulted in an increase in total growth plate width (TPW, U: 363.6 ± 9.3, UGH: 402.4 ± 21.7, S: 400.2 ± 3.8 μ, p<0.05) and in the width of the proliferative zone vs U rats(U:114.9 ± 8.8, UGH: 132.6 ± 3.4 μ, p<0.05). These increases were associated with concomitant enhancement of IGF-I and IGFBP-3 TEGP gene expression most notable in the younger chondrocytes of the proliferative zone. We conclude GH treatment of the uremic rat promotes an increase in longitudinal length and total growth plate width which coincides with enhancedTEGP IGF-I and IGFBP-3 gene expression.