Bone and the kidney: it's complex

Susan J. Allison

doi:10.1038/nrneph.2013.184

Nature Reviews Nephrology 9, 623 (2013)

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FGF-23 and secondary hyperparathyroidism in chronic kidney disease

Justin Silver & Tally Naveh-Many

doi:10.1038/nrneph.2013.147

Nature Reviews Nephrology 9, 641-649 (2013)

Chronic kidney disease (CKD) is associated with high levels of serum phosphate, fibroblast growth factor (FGF)-23 and parathyroid hormone (PTH). FGF-23 acts in the kidney to induce phosphaturia and inhibit the synthesis of 1,25-dihydroxyvitamin D₃. Here, the authors discuss the pathogenesis of increased FGF-23 levels in secondary hyperparathyroidism associated with CKD.

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Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism

Makoto Kuro-o

doi:10.1038/nrneph.2013.111

Nature Reviews Nephrology 9, 650-660 (2013)

In this Review, the author discusses new insights into the pathogenesis of chronic kidney disease and describes a novel mechanism of ageing, both in the context of the fibroblast growth factor (FGF)–Klotho endocrine axis. In addition, the author proposes a new paradigm for dietary phosphate restriction in which phosphate restriction is started when serum FGF-23 level starts to rise, regardless of serum phosphate level.

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Mechanisms of vascular calcification in CKD—evidence for premature ageing?

Catherine M. Shanahan

doi:10.1038/nrneph.2013.176

Nature Reviews Nephrology 9, 661-670 (2013)

Cardiovascular mortality is very high in young patients with chronic kidney disease (CKD), and it has been suggested that patients with CKD exhibit a 'premature ageing' phenotype. This Review discusses data showing that uraemic toxins can drive vascular smooth muscle cell damage and phenotypic changes that promote vascular calcification. It also describes emerging data indicating that uraemic toxins may also promote DNA damage, which drives cellular ageing.

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Evaluating bone quality in patients with chronic kidney disease

Hartmut H. Malluche, Daniel S. Porter & David Pienkowski

doi:10.1038/nrneph.2013.198

Nature Reviews Nephrology 9, 671-680 (2013)

Changes in bone quality and quantity are associated with an increased risk of fracture in patients with chronic kidney disease–mineral and bone disorder (CKD–MBD). Here, methods used to assess bone quality abnormalities across different hierarchical levels are outlined, as well as the results, such as abnormalities in structural parameters and bone material or mechanical properties, which are linked to an increased risk of fracture. Such assessment will improve our understanding of CKD–MBD and aid therapeutic development.

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Therapy for patients with CKD and low bone mineral density

Susan M. Ott

doi:10.1038/nrneph.2013.182

Nature Reviews Nephrology 9, 681-692 (2013)

Patients with chronic kidney disease (CKD) have a high risk of bone fracture and low bone mineral density, which resembles osteoporosis. However, the mineral and bone disorder associated with CKD (CKD–MBD) is more complex than osteoporosis and the same treatments might not be appropriate in these patients. In this Review, Susan Ott discusses therapies for osteoporosis, and the evidence for their use in patients with CKD–MBD.

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