Sclerostin and CKD-MBD

Schiavi, Susan C.

doi:10.1007/s11914-015-0263-2

Cited by 5 publications

(2 citation statements)

References 55 publications

(42 reference statements)

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“…The Wnt/β‐catenin pathway is essential for normal osteoblast differentiation and function and therefore normal bone formation. Sclerostin and Dickkopf‐1 (DKK1) are two circulating inhibitors of this pathway; these inhibit lipoprotein receptor‐related protein 5/6 activation of Wnt signaling and impair normal osteoblast differentiation . Sclerostin is primarily expressed in skeletal tissue, and its expression is maintained during aging; in contrast, expression of DKK1 is more general and decreases in bone with age .…”

Section: Pathophysiology Of Renal Osteodystrophymentioning

confidence: 99%

“…Furthermore, animal studies suggest that DKK1 overexpression negatively impacts bone healing, suggesting a role for DKK1 inhibition during the fracture repair process . Sclerostin and DKK1 levels are elevated in CKD, with sclerostin levels increased early in CKD, and generally preceding the rise of FGF‐23 and β‐catenin . In a study of ESKD patients, sclerostin levels were inversely associated with reduced bone formation and bone loss over a 1‐year period .…”

Section: Pathophysiology Of Renal Osteodystrophymentioning

confidence: 99%

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Rethinking Bone Disease in Kidney Disease

Damasiewicz

Nickolas

2018

JBMR Plus

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Renal osteodystrophy (ROD) is the bone component of chronic kidney disease mineral and bone disorder (CKD‐MBD). ROD affects bone quality and strength through the numerous hormonal and metabolic disturbances that occur in patients with kidney disease. Collectively these disorders in bone quality increase fracture risk in CKD patients compared with the general population. Fractures are a serious complication of kidney disease and are associated with higher morbidity and mortality compared with the general population. Furthermore, at a population level, fractures are at historically high levels in patients with end‐stage kidney disease (ESKD), whereas in contrast the general population has experienced a steady decline in fracture incidence rates. Based on these findings, it is clear that a paradigm shift is needed in our approach to diagnosing and managing ROD. In clinical practice, our ability to diagnose ROD and initiate antifracture treatments is impeded by the lack of accurate noninvasive methods that identify ROD type. The past decade has seen advances in the noninvasive measurement of bone quality and strength that have been studied in kidney disease patients. Below we review the current literature pertaining to the epidemiology, pathology, diagnosis, and management of ROD. We aim to highlight the pressing need for a greater awareness of this condition and the need for the implementation of strategies that prevent fractures in kidney disease patients. Research is needed for more accurate noninvasive assessment of ROD type, clinical studies of existing osteoporosis therapies in patients across the spectrum of kidney disease, and the development of CKD‐specific treatments. © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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Section: Pathophysiology Of Renal Osteodystrophymentioning

confidence: 99%

Section: Pathophysiology Of Renal Osteodystrophymentioning

confidence: 99%

Rethinking Bone Disease in Kidney Disease

Damasiewicz

Nickolas

2018

JBMR Plus

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The role of bone biopsy for the diagnosis of renal osteodystrophy: a short overview and future perspectives

2016

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Chronic kidney disease (CKD) patients present specific bone and mineral metabolism disturbances, which account for important morbidity and mortality. The term renal osteodystrophy, classically used for the nomination of CKD-associated bone disorder, has been limited to the histologic description of bone lesions, requiring the use of bone biopsy. Biochemical markers and imaging tools do not adequately predict the complex bone changes that are observed in renal osteodystrophy. Parathyroid hormone, which is a universally used biomarker of bone turnover in clinical practice, lacks specificity and sensitivity. Therefore, tetracycline double-labelled transiliac bone biopsy, with bone histology and histomorphometric evaluation, remains the best clinical tool to discriminate bone turnover and to evaluate the other dimensions of renal osteodystrophy. This review will focus on the value of classic bone histomorphometric analysis of trabecular bone in CKD patients and unfold new perspectives of this diagnostic tool, including cortical bone evaluation and bone tissue immunohistochemistry.

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