COMPENSATORY RENAL GROWTH - ROLE OF GROWTH-HORMONE AND INSULIN-LIKE GROWTH FACTOR-I

Recent experimental evidence suggests that insulin-like growth factor-I (IGF-I) may be involved in compensatory renal growth (CRG). This study was designed to determine the relative contribution of IGF-I and growth hormone (GH) to the CRG that takes place in rats following uninephrectomy (UNx). We also studied the respective role of GH and IGF-I in the stimulation of CRG induced by a high protein diet (HPD). CRG was studied 7 days after UNx in Wistar rats and in a new mutant strain of dwarf rats, selectively deficient in GH. Prior to UNx, rats of both strains were pre-fed (14 days) either a medium-protein diet (MPD, casein 18%) or a HPD (54%). On MPD, CRG was comparable in Wistar (17.6± 3.1%, M ± SD) and dwarf (14.4 ± 4.8%) rats. The HPD enhanced CRG in the Wistars (27±3.9%, P<0.005) but not in the dwarfs (14.9 ± 2%). CRG in both experimental groups involved renal hypertrophy and hyperplasia. Control (baseline) serum, liver and kidney IGF-I were significantly less in dwarf rats. However, following UNx, on a MPD, kidney IGF-I increased significantly in both Wistar and dwarf rats: Wistar, pre-UNx, 310 ± 46 ng/g tissue; post-UNx, 405 ± 54 ng/g, P < 0.005; dwarfs, pre-UNx, 205 ± 35 ng/g; post-UNx 426 ± 90 ng/g, P< 0.001. On a HPD a further significant increase in renal IGF-I was only observed in Wistar rats (505± 46 ng/g). No change in serum or liver IGF-I was observed after UNx in either strain. Similarly, renal IGF-I remained unchanged in sham-operated rats. We conclude from this study that CRG takes place in normal and growth-hormone-deficient rats. It may be mediated by IGF-I, through an autocrine/paracrine mechanism, independently of growth hormone. On the other hand, the renotropic effect of a high-protein diet on compensatory renal growth may be GH-dependent and IGF-I-mediated. © 1990 European Dialysis and Transplant Association-European Renal Association.