GROWTH-RETARDATION IN CHILDREN WITH CHRONIC RENAL-INSUFFICIENCY - CURRENT ASPECTS OF PATHOPHYSIOLOGY AND TREATMENT

The pathogenesis of growth retardation in children with chronic renal failure (CRF) is clearly multifactorial involving malnutrition, metabolic acidosis, renal osteodystrophy and hormonal disturbances. In particular, alterations of the growth hormone (GH)/insulin-like growth factor (IGF)-axis are pathogenic. Insensitivity to the somatotropic action of GB, decreased IGF-I secretion rate and decreased IGF bioactivity are operative in children with CRF, while in children post transplantation, glucocorticoid-induced GH hyposecretion and local inhibition of IGF action play a pivotal role besides the consequences of graft dysfunction, Optimization of nutritional support, supplementation with oral bicarbonate preparations, prevention of renal osteodystrophy by phosphate restriction and vitamin D therapy, and in end-stage renal disease initiation of dialysis are the basis of therapy. These methods can at most stabilize growth, but cannot induce true catch-up growth, apart from nutritional support in early infancy. In children posttransplant, catch-up growth is restricted to young patients with near-normal graft function and a lo cv-dose, preferably alternate-day glucocorticoid regimen, The perspective for growth-retarded children with CRF has improved only recently by the introduction of rhGH therapy, RhGH has proven to be an effective, safe and well tolerated new treatment modality for growth retarded children at all stages of CRF, There is strong evidence that final height will increase in these children. In children posttransplant, rhGH is also effective, but the potential risk of interference with graft function has not yet been sufficiently defined.