GH receptors, IGFs, and IGF-receptors are expressed in the kidney. Their location in the different parts of the nephron suggests autocrine or paracrine as well as endocrine modes of action. A lack of GH receptors and probably of IGF-I synthesis in glomeruli in vivo suggest that all glomerular GH and IGF-I effects are mediated by circulating IGF-I through endocrine modes. GH and IGF-I increase GFR in normal rats and humans, and increase phosphate and possibly sodium reabsorption in normal and diabetic subjects. During normal renal development GH, IGF-I, and IGF-II appear to play a role. GH and IGF-I cause kidney growth, and circulating and/or renal IGF-I appear to contribute to renal hypertrophy and compensatory renal growth in experimental animal models. GH may contribute also to glomerular sclerosis and progression of renal failure in experimental models. In patients with chronic renal failure such a role of endogenous or exogenous GH has not yet been convincingly proven. In chronic or acute renal failure and in the nephrotic syndrome there are complex abnormalities in the systemic and renal IGF/IGFBP-system. In chronic renal failure there is resistance to GH and IGF-I that can be overridden by pharmacological administration of each of the peptides. GH is used therapeutically in children with chronic renal failure to accelerate growth. GH and IGF-I may be useful agents to improve nitrogen balance and nutritional status in patients with chronic renal failure. In rats with ARF, administration of IGF-I accelerates the recovery of renal function. Whether this treatment is also successful in patients with ARF remains to be demonstrated by ongoing clinical trials.