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Leptin in chronic kidney disease: a link between hematopoiesis, bone metabolism, and nutrition

  • Nephrology - Review
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Abstract

Anemia, dyslipidemia, malnutrition, together with mineral and bone disorders are common complications in patients with chronic kidney disease (CKD). All are associated with increased risk of mortality. Leptin is a small peptide hormone that is mainly but not exclusively produced in adipose tissue. It is also secreted by normal human osteoblasts, subchondral osteoblasts, placental syncytiotrophoblasts, and the gastric epithelium. Leptin binds to its receptors in the hypothalamus to regulate bone metabolism and food intake. Leptin also has several other important metabolic effects on peripheral tissues, including the liver, skeletal muscle, and bone marrow. Leptin is cleared principally by the kidney. Not surprisingly, serum leptin appears to increase concurrently with declines in the glomerular filtration rate in patients with CKD. A growing body of evidence suggests that leptin might be closely related to hematopoiesis, nutrition, and bone metabolism in CKD patients. Results are conflicting regarding leptin in patients with CKD, in whom both beneficial and detrimental effects on uremia outcome are found. This review elucidates the discovery of leptin and its receptors, changes in serum or plasma leptin levels, the functions of leptin, relationships between leptin and the complications mentioned above, and pharmaceutical interventions in serum leptin levels in patients with CKD.

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Acknowledgments

This review was funded by the National Natural Science Foundation of China (81270408), RC201162, 2010(IB10), LJ201125, Chinese Society of Nephrology (13030300415). There were no financial supports or other benefits from commercial sources for this work.

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There were no interests that could create a potential conflict of interest or the appearance of a conflict of interest with regard to this work.

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Correspondence to Ningning Wang.

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Zhang, J., Wang, N. Leptin in chronic kidney disease: a link between hematopoiesis, bone metabolism, and nutrition. Int Urol Nephrol 46, 1169–1174 (2014). https://doi.org/10.1007/s11255-013-0623-8

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  • DOI: https://doi.org/10.1007/s11255-013-0623-8

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