Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)

Moe, Sharon M.; Drüeke, Tilman B.; Cunningham, John A.; Goodman, William G.; Martin, Kévin; Ølgaard, Klaus; Ott, Susan M.; Sprague, Stuart M.; Lameire, Norbert; Eknoyan, Garabed

doi:10.1038/sj.ki.5000414

Cited by 1,663 publications

(1,340 citation statements)

References 31 publications

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“…Serum phosphate has been shown to strongly correlate with these cardiovascular events, with emerging evidence that poor bone health may also contribute to phosphate imbalance. (5,7) Individuals with CKD-MBD exhibit a range of renal osteodystrophies with defects ranging from LTO to HTO bone disease. (27,48,49) Classic radiolabel studies performed in the mid-1990s suggest that at either extreme of bone turnover, there is a loss of buffering capacity such that bone cannot accept or retain the increased burden of calcium and presumably phosphate that results from reduced bone mineralization.…”

Section: Discussionmentioning

confidence: 99%

“…(4) Evidence suggests that vascular disease is at least partially related to poor bone health. (5)(6)(7)(8) Importantly, deviation from the normal range of serum bone biomarkers predicts an increased risk of cardiovascular events, (9) and impaired bone remodeling is associated with increased vascular calcification. (10) In the general population, individuals with osteoporosis have increased atherosclerosis and coronary artery calcification (11)(12)(13)(14) and there is an inverse relationship between coronary artery calcification and bone mineral density (BMD) in both normal and CKD patients.…”

Section: Introductionmentioning

confidence: 99%

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Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Sabbagh

Graciolli

O’Brien

et al. 2012

Journal of Bone and Mineral Research

232

219

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Chronic kidney disease–mineral bone disorder (CKD‐MBD) is defined by abnormalities in mineral and hormone metabolism, bone histomorphometric changes, and/or the presence of soft‐tissue calcification. Emerging evidence suggests that features of CKD‐MBD may occur early in disease progression and are associated with changes in osteocyte function. To identify early changes in bone, we utilized the jck mouse, a genetic model of polycystic kidney disease that exhibits progressive renal disease. At 6 weeks of age, jck mice have normal renal function and no evidence of bone disease but exhibit continual decline in renal function and death by 20 weeks of age, when approximately 40% to 60% of them have vascular calcification. Temporal changes in serum parameters were identified in jck relative to wild‐type mice from 6 through 18 weeks of age and were subsequently shown to largely mirror serum changes commonly associated with clinical CKD‐MBD. Bone histomorphometry revealed progressive changes associated with increased osteoclast activity and elevated bone formation relative to wild‐type mice. To capture the early molecular and cellular events in the progression of CKD‐MBD we examined cell‐specific pathways associated with bone remodeling at the protein and/or gene expression level. Importantly, a steady increase in the number of cells expressing phosphor‐Ser33/37‐β‐catenin was observed both in mouse and human bones. Overall repression of Wnt/β‐catenin signaling within osteocytes occurred in conjunction with increased expression of Wnt antagonists (SOST and sFRP4) and genes associated with osteoclast activity, including receptor activator of NF‐κB ligand (RANKL). The resulting increase in the RANKL/osteoprotegerin (OPG) ratio correlated with increased osteoclast activity. In late‐stage disease, an apparent repression of genes associated with osteoblast function was observed. These data confirm that jck mice develop progressive biochemical changes in CKD‐MBD and suggest that repression of the Wnt/β‐catenin pathway is involved in the pathogenesis of renal osteodystrophy. © 2012 American Society for Bone and Mineral Research.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Sabbagh

Graciolli

O’Brien

et al. 2012

Journal of Bone and Mineral Research

232

219

View full text Add to dashboard Cite

show abstract

“…Although bone histomorphometry is not routinely recommended or executed in uremic patients, it is the gold standard and the only way to evaluate the type of renal osteodystrophy in CKD‐MBD 97, 98. The bone histologic findings in CKD range from low to high bone turnover, mineralization troubles, and changes in bone volume.…”

Section: Bone and Musculoskeletal Abnormalities In Chronic Kidney Dismentioning

confidence: 99%

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Molina

Carrero

Bover

et al. 2017

J cachexia sarcopenia muscle

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The spectrum of activity of vitamin D goes beyond calcium and bone homeostasis, and growing evidence suggests that vitamin D contributes to maintain musculoskeletal health in healthy subjects as well as in patients with chronic kidney disease (CKD), who display the combination of bone metabolism disorder, muscle wasting, and weakness. Here, we review how vitamin D represents a pathway in which bone and muscle may interact. In vitro studies have confirmed that the vitamin D receptor is present on muscle, describing the mechanisms whereby vitamin D directly affects skeletal muscle. These include genomic and non‐genomic (rapid) effects, regulating cellular differentiation and proliferation. Observational studies have shown that circulating 25‐hydroxyvitamin D levels correlate with the clinical symptoms and muscle morphological changes observed in CKD patients. Vitamin D deficiency has been linked to low bone formation rate and bone mineral density, with an increased risk of skeletal fractures. The impact of low vitamin D status on skeletal muscle may also affect muscle metabolic pathways, including its sensitivity to insulin. Although some interventional studies have shown that vitamin D may improve physical performance and protect against the development of histological and radiological signs of hyperparathyroidism, evidence is still insufficient to draw definitive conclusions.

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“…In Stage 1 through 3 chronic kidney disease (CKD), the metabolic changes that accompany early CKD are intermittent hyperphosphotemia and a mild increase of parathyroid hormone 77. Fractures in Stage 1 through 3 CKD are most likely caused by osteoporosis than CKD-related metabolic bone disease 76.…”

Section: Specific Types Of Osteoporosismentioning

confidence: 99%

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

Raef

Al-Bugami

Balharith

et al. 2011

Annals of Saudi Medicine

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Postmenopausal osteoporosis and osteoporosis in elderly men are major health problems, with a significant medical and economic burden. Although osteopenia and osteoporosis are more common locally than in the West, fracture rates are generally less than in Western countries. Vitamin D deficiency is common in the region and contributes adversely to bone health. Vitamin D deficiency should be suspected and treated in all subjects with ostopenia or osteoporosis. The use of risk factors to determine fracture risk has been adopted by the World Health Organization and many international societies. Absolute fracture risk methodology improves the use of resources by targeting subjects at higher risk of fractures for screening and management. The King Faisal Specialist Hospital Osteoporosis Working Group recommends screening for women 65 years and older and for men 70 years and older. Younger subjects with clinical risk factors and persons with clinical evidence of osteoporosis or diseases leading to osteoporosis should also be screened. These guidelines provide recommendations for treatment for postmenopausal women and men older than 50 years presenting with osteoporotic fractures for persons having osteoporosis—after excluding secondary causes—or for persons having low bone mass and a high risk for fracture. The Working Group has suggested an algorithm to use at King Faisal Specialist Hospital that is based on the availability, cost, and level of evidence of various therapeutic modalities. Adequate calcium and vitamin D supplement are recommended for all. Weekly alendronate (in the absence of contraindications) is recommended as first-line therapy. Alternatives to alendronate are raloxifene or strontium ranelate. Second-line therapies are zoledronic acid intravenously once yearly, when oral therapy is not feasible or complicated by side effects, or teriparatide in established osteoporosis with fractures.

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Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)

Cited by 1,663 publications

References 31 publications

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Updated Recommendations for the Diagnosis and Management of Osteoporosis: A Local Perspective

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