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Updated: May 4, 2026

Comparative Analysis of Human Growth Hormone in Serum Using SPRi, Nano-SPRi and ELISA Assays
Published on: January 7, 2016
Growth hormone, insulin-like growth factor-1, and the kidney: pathophysiological and clinical implications
Peter Kamenický1, Gherardo Mazziotti, Marc Lombès
1Assistance Publique-Hôpitaux de Paris (P.K., M.L., P.C.), Hôpital de Bicêtre, Service d'Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Endocriniennes Rares de la Croissance, Le Kremlin Bicêtre F-94275, France; Univ Paris-Sud (P.K., M.L., P.C.), Faculté de Médecine Paris-Sud, Le Kremlin Bicêtre F-94276, France; Inserm Unité 693 (P.K., M.L., P.C.), Le Kremlin Bicêtre F-94276, France; and Department of Clinical and Experimental Sciences (A.G., G.M.), Chair of Endocrinology, University of Brescia, 25125 Brescia, Italy.
Abstract:
Besides their growth-promoting properties, GH and IGF-1 regulate a broad spectrum of biological functions in several organs, including the kidney. This review focuses on the renal actions of GH and IGF-1, taking into account major advances in renal physiology and hormone biology made over the last 20 years, allowing us to move our understanding of GH/IGF-1 regulation of renal functions from a cellular to a molecular level. The main purpose of this review was to analyze how GH and IGF-1 regulate renal development, glomerular functions, and tubular handling of sodium, calcium, phosphate, and glucose. Whenever possible, the relative contributions, the nephronic topology, and the underlying molecular mechanisms of GH and IGF-1 actions were addressed. Beyond the physiological aspects of GH/IGF-1 action on the kidney, the review describes the impact of GH excess and deficiency on renal architecture and functions. It reports in particular new insights into the pathophysiological mechanism of body fluid retention and of changes in phospho-calcium metabolism in acromegaly as well as of the reciprocal changes in sodium, calcium, and phosphate homeostasis observed in GH deficiency. The second aim of this review was to analyze how the GH/IGF-1 axis contributes to major renal diseases such as diabetic nephropathy, renal failure, renal carcinoma, and polycystic renal disease. It summarizes the consequences of chronic renal failure and glucocorticoid therapy after renal transplantation on GH secretion and action and questions the interest of GH therapy in these conditions.
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