Impairment of longitudinal growth in children with chronic renal failure (CRF) is multifactorial. It is mainly due to disturbances in the growth hormone (GH)/insulin-like growth factor (IGF)/IGF-binding protein axis. Growth failure can be managed by optimizing nutrition and fluid/electrolyte homeostasis, and overcoming the growth-inhibiting effects of uremia by high-dose recombinant human (rh) GH treatment. A sufficient catch-up growth is one of the determining issues for the overall success of pediatric kidney transplantation (Tx). However, despite satisfactory renal function, spontaneous catch-up growth is often insufficient as glucocorticoid treatment is the main inhibiting factor for longitudinal growth after Tx. In addition, longitudinal growth may be jeopardized by low glomerular filtration rate (GFR) and African American or Hispanic background. Supraphysiological doses of GH and/or IGF-I in vitro and in vivo can partially overcome the growth-inhibiting effects of glucocorticoid treatment. GH-associated increase of leukocyte proliferation and cytotoxicity with stimulated interferon synthesis have been demonstrated. However, it is not clear whether such stimulatory effects on leukocyte function are a transitory or a constant risk factor after organ Tx. Clinical trials of GH in children after renal Tx have suggested a rather moderate or transient effect of rhGH on the immune system, and corticosteroids induce a hyporesponsiveness to the action of GH. As long as corticosteroids are believed to be essential after renal Tx, rhGH should be considered to optimize longitudinal growth in children.