Growth failure is a frequent side effect of long-term high-dose glucocorticoid therapy in children. Pharmacological doses of glucocorticoids interfere at different levels with the integrity of the somatotropic hormone axis. The majority of patients on chronic corticosteroid medication present with overt GH hyposecretion, apparently due to enhancement of hypothalamic somatostatin release. Glucocorticoids also inhibit IGF bioactivity by the induction of IGF inhibitors and stimulate the production of certain IGFBPs. In addition, glucocorticoids inhibit growth directly at the tissue level by suppressing local growth factors and skeletal tissue matrix production. In children post renal transplantation, concomitant treatment with cyclosporin A for immunosuppression allows low-dose glucocorticoid medication. Reduction of glucocorticoids, in particular when given as alternate-day therapy, improves growth in some but not all children. The new glucocorticoid deflazacort appears to have fewer side effects regarding steroid-induced osteopenia and cushingoid appearance. A beneficial effect on longitudinal growth has not been clearly established. Recent experimental and clinical data indicate that the catabolic and growth-depressing effects of glucocorticoids can be counterbalanced by concomitant anabolic treatment with rhGH. The potential role of rhIGF-I is less well investigated. Treatment with rhGH is able to antagonize several side effects of long-term glucocorticoid administration, such as growth failure, protein-wasting and osteoporosis. If catch-up growth cannot be achieved by an alternate-day steroid regimen and discontinuation of glucocorticoids appears to be an intolerable risk for graft survival, rhGH therapy may be initiated. However, rhGH therapy in this setting must still be considered experimental, because the possible interference of rhGH with the immunosuppressive action of glucocorticoids in children after organ transplantation is still incompletely defined.