Uremia is associated with reduced hepatic GHr mRNA which is hypothesized to contribute to uremic growth retardation. Similar reductions of GHr gene expression in other target tissue(s) have been hypothesized. To address this we evaluated TEGP morphometrics and GHr gene expression in uremic (U), uremic-GH treated (UGH), pair-fed (PF), and control (C) rats using video computer measurements and in situ hybridization histochemistry and immunohistochemistry. Uremia was created by standard two stage 5/6 nephrectomy, and verified by elevation of serum creatinine in U animals vs PF/C rats (mean±SD U: 0.9 vs PF/C: 0.4 mg/dL,p<0.05). At 42d of age rats were matched for length and placed into four groups: U (n=8), UGH (n=8), PF (n=7), C (n=6). Treatment (Rx) with intraperitoneal (IP) rat GH 10 IU/kg/d, an equal volume of IP saline [U, PF rats], and limitation of chow intake to that of a matched U mate [PF rats] were continued for 14d. GH Rx resulted in longer length, a wider total TEGP width, and a wider proliferative zone (PRO) width vs U and PF rats (TEGP width C: 417.5±24 vs U: 361.8±12 and PF: 374.4±13 μ, p<0.05, and PRO C: 140.3± 8.8 vs U:111.6±4.7 and PF:119.6±7.6 μ, p<0.05). Visual inspection of the in situ hybridization revealed reduced GHr mRNA abundance and more faint GHr peptide immunoreactivity (IR) in the PRO zone of the U TEGP vs C rats. GH Rx did not significantly alter GHr mRNA abundance or peptide IR. Nutritional limitation was associated with GHr mRNA abundance similar to C TEGPs, but more faint GHr peptide IR in the PRO zone. We conclude (1) uremia is associated with reduced GHr gene expression in the TEGP which likely contributes to uremic growth retardation, and (2) nutritional limitation and uremia exert differeing influences on GHr gene expression.