The complex pahtogenesis of certain uremic endocrinopathies is often largely due to reduced functional renal mass, because endocrine renal function includes the degradation of hormonally active peptides. Our goal is to evaluate the role of the renoprival state vs. that of uremia per se in the altered dynamics of peptide hormones in kidney failure, by investigating the renal handling of several protein - as well as glycoprotein hormones (somatostatin (SLI), glucagon (Glu), growth hormone (GH), prolactin (Prl), and the gonadotropins LH and FSH). These studies will employ several complementary techniques: i.e. measurements of renal and hepatic extraction and metabolic clearance rates of hormones both in vivo and during in vitro perfusion of isolated rat kidneys and livers, hormonal degradation and binding studies with basolateral and luminal renal tubular membranes, chromatographic separation techniques, assays of immunoreactivity and bioactivity. This comprehensive approach while addressing primarily the role of the kidney in the degradation of peptide hormones, will also allow insights on interactions between this organ and the cited hormones, which may extend beyond simple catabolic phenomena (e.g. binding of SLI, Glu, GH and Prl to specific-basolateral membrane-renal receptors); in addition it will provide information concerning the role of the kidney in gonadotropin handling and on possible derangements of their extrarenal degradation in uremia. The data to be obtained will help clarify the pathophysiology of certain uremic endocrinopathies, and provide valuable theoretical information about peptide hormone-renal interactions.
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