Variant of Adynamic Bone Disease in Hemodialysis Patients: Fact or Fiction?

Rocha, Lillian Andrade da; Higa, Andrea; Barreto, Fellype Carvalho; Reis, Luciene M. dos; Jorgetti, Vanda; Draibe, Sérgio Antônio; Carvalho, Aluízio Barbosa de

doi:10.1053/j.ajkd.2006.05.028

Cited by 19 publications

(15 citation statements)

References 23 publications

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“…Perhaps the Bayer assay measured fewer fragments and the hypercalcemia with the lower PTH levels found in was merely from higher 1-84/7-84 PTH. Similarly, although most have correlated low BFR with low PTH levels [27][28][29], some investigators have argued from their remnant kidney model that low BFR is unrelated to PTH levels [30]. They argue that the low osteoblast production is due to hypercholesterolemia and can be reversed with sevelamer.…”

Section: Discussionmentioning

confidence: 97%

Can the combination of calcium and parathormone levels above k/doqi guidelines be used as a marker of adynamic bone disease in African Americans?

et al. 2010

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We did not find hypercalcemia predictive of adynamic bone in patients of African American descent at levels of parathormone where low bone formation rates have been documented to occur. Since no parameter predicted bone histology, perhaps bone biopsies will be necessary to distinguish hyperparathyroidism from adynamic bone disease in African Americans with ESRD, hypercalcemia, and moderately elevated levels of PTH. Further studies are needed to determine appropriate therapy.

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Section: Discussionmentioning

confidence: 97%

Can the combination of calcium and parathormone levels above k/doqi guidelines be used as a marker of adynamic bone disease in African Americans?

et al. 2010

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“…One potentially relevant observation is that increased osteoclast activity was a common finding irrespective of the type of renal osteodystrophy. (36,71) Additional studies will be required to confirm this hypothesis.…”

Section: Discussionmentioning

confidence: 98%

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

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237

225

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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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“…Specifically, the process of remodeling must replace effete bone with new to prevent brittleness. Thus, arrested remodeling in conditions such as chronic renal failure 85 results in qualitatively and structurally compromised bone. The same occurs in some patients treated for many years with resorption-inhibiting bisphosphonates, which dampen remodeling.…”

Section: Glucocorticoids and The Osteoclastmentioning

confidence: 99%

Osteoclasts: What Do They Do and How Do They Do It?

Teitelbaum

2007

The American Journal of Pathology

615

474

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As Americans live longer, degenerative skeletal diseases, such as osteoporosis, become increasingly prevalent. Regardless of cause, osteoporosis reflects a relative enhancement of osteoclast activity. Thus, this unique bone resorptive cell is a prominent therapeutic target. A number of key observations provide insights into the mechanisms by which precursors commit to the osteoclast phenotype and how the mature cell degrades bone. The osteoclast is a member of the monocyte/macrophage family that differentiates under the aegis of two critical cytokines, namely RANK ligand and M-CSF. Tumor necrosis factor (TNF)-␣ also promotes osteoclastogenesis, particularly in states of inflammatory osteolysis such as that attending rheumatoid arthritis. Once differentiated, the osteoclast forms an intimate relationship with the bone surface via the ␣v␤3 integrin, which transmits matrix-derived, cytoskeleton-organizing, signals. These integrin-transmitted signals include activation of the associated proteins, c-src, syk, Vav3, and Rho GTPases. The organized cytoskeleton generates an isolated microenvironment between the cell's plasma membrane and the bone surface in which matrix mineral is mobilized by the acidic milieu and organic matrix is degraded by the lysosomal protease, cathepsin K. This review focuses on these and other molecules that mediate osteoclast differentiation or function and thus serve as candidate anti-osteoporosis therapeutic targets.

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Variant of Adynamic Bone Disease in Hemodialysis Patients: Fact or Fiction?

Cited by 19 publications

References 23 publications

Can the combination of calcium and parathormone levels above k/doqi guidelines be used as a marker of adynamic bone disease in African Americans?

Can the combination of calcium and parathormone levels above k/doqi guidelines be used as a marker of adynamic bone disease in African Americans?

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

Osteoclasts: What Do They Do and How Do They Do It?

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