Chronic renal failure (CRF) is characterized by a series of compensatory adaptations in the surviving nephrons of the diseased kidney aimed at maintaining glomerular filtration rate and tubular resorptive functions. Several lines of evidence indicate that in normal kidney growth hormone (GH) and insulin-like growth factors (IGFs) modulate the nephron, both in respect to function and size. Virtually all members of the GH/IGF axis are present in the kidney, comprising: 1) GH-receptors; 2) IGF-1 and IGF-2 mRNA; 3) distinct receptors for IGFs: the IGF-1 receptor and the IGF-2/mannose-6-phosphate receptor, and 4) specific binding proteins (IGFBPs), indicating that GH and IGFs may affect the kidney in both an endocrine and autocrine/paracrine fashion. GH and IGFs modulate renal metabolism and the kidney plays an important role in the metabolism and degradation of circulating GH and IGFs. The action of GH to enhance kidney function and size is mediated through IGF-1, and IGF-1 infusion in animals and man stimulates renal function and volume. In addition, renal growth following various pathophysiological conditions (e.g. reduction in renal mass, diabetes mellitus) is preceded by an increase in endogenous renal IGF-1. In CRF circulating levels of GH are elevated, serum IGF-1 is normal and circulating IGFBP-1, -2, and -3 are elevated. Given the ability of GH and IGF-1 to stimulate various functions of the kidney, the potential use of GH or IGF-1 in the setting of CRF has been suggested.(ABSTRACT TRUNCATED AT 250 WORDS)