Renal insufficiency and bone lossOtt, Susan M.Current Opinion in Rheumatology: July 2019 - Volume 31 - Issue 4 - p 394–399 doi: 10.1097/BOR.0000000000000626 METABOLIC BONE DISEASE: Edited by Stephen Honig Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review Patients with chronic kidney disease have a high risk of fractures and no established treatments that have been shown to prevent the bone disease. The physiology of renal osteodystrophy is complex and recently more factors have been found that complicate the mineral metabolism. The recognition that vascular calcifications are related to bone disease has made treatment even more challenging. Recent findings The most exciting new findings relate to the signaling pathways that are seen in kidney disease and how they cause abnormalities in bone physiology. In particular, wnt and activin signaling pathways are seen early in the course of renal disease. The bones react by increasing FGF-23, which targets both renal phosphate secretion and a variety of other systemic effects. Secreted klotho is another newly described hormone with effects on several systems. Clinical studies have focused on treatments for hyperparathyroidism and phosphate, and frustrating limitations of the treatments used for ordinary osteoporosis. Summary Treatment of bone disease in patients with chronic kidney disease is challenging, and understanding the physiological pathways could lead to novel therapies. Department of Medicine, University of Washington, Seattle, Washington, USA Correspondence to Susan M. Ott, Professor of Medicine, Department of Medicine, University of Washington, Seattle, WA 98195, USA. Tel: +1 206 598 4288; e-mail: firstname.lastname@example.org Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.