Limits...
Chronic kidney disease and the skeleton.

Miller PD - Bone Res (2014)

Bottom Line: Differentiations among the disorders of renal osteodystrophy, CKD-MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry.Management of fractures in stages 1-3 CKD does not differ in persons with or without CKD with osteoporosis assuming that there is no evidence for CKD-MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD.Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence-based, with the exception of post-hoc analysis suggesting efficacy and safety of specific osteoporosis therapies (alendronate, risedronate and denosumab) in stage 4 CKD.

View Article: PubMed Central - PubMed

Affiliation: Colorado Center for Bone Research , Lakewood, CO, USA.

ABSTRACT
Fractures across the stages of chronic kidney disease (CKD) could be due to osteoporosis, some form of renal osteodystrophy defined by specific quantitative histomorphometry or chronic kidney disease-mineral and bone disorder (CKD-MBD). CKD-MBD is a systemic disease that links disorders of mineral and bone metabolism due to CKD to either one or all of the following: abnormalities of calcium, phosphorus, parathyroid hormone or vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth or strength; or vascular or other soft-tissue calcification. Osteoporosis, as defined by the National Institutes of Health, may coexist with renal osteodystrophy or CKD-MBD. Differentiation among these disorders is required to manage correctly the correct disorder to reduce the risk of fractures. While the World Health Organization (WHO) bone mineral density (BMD) criteria for osteoporosis can be used in patients with stages 1-3 CKD, the disorders of bone turnover become so aberrant by stages 4 and 5 CKD that neither the WHO criteria nor the occurrence of a fragility fracture can be used for the diagnosis of osteoporosis. The diagnosis of osteoporosis in stages 4 and 5 CKD is one of the exclusion-excluding either renal osteodystrophy or CKD-MBD as the cause of low BMD or fragility fractures. Differentiations among the disorders of renal osteodystrophy, CKD-MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry. Management of fractures in stages 1-3 CKD does not differ in persons with or without CKD with osteoporosis assuming that there is no evidence for CKD-MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD. Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence-based, with the exception of post-hoc analysis suggesting efficacy and safety of specific osteoporosis therapies (alendronate, risedronate and denosumab) in stage 4 CKD. This review also discusses how to diagnose and manage fragility fractures across the five stages of CKD.

No MeSH data available.


Related in: MedlinePlus

The physiological interactions between bone, the kidney, parathyroid glands and vasculature. Miller PD, Sprague S, Shane E. (original) 2014.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4472138&req=5

fig1: The physiological interactions between bone, the kidney, parathyroid glands and vasculature. Miller PD, Sprague S, Shane E. (original) 2014.

Mentions: The kidney and the skeleton have intimate biological relationships that can affect bone strength as well as renal physiological functions (Figure 1).1,2 The individual or collective roles of each of these interactions will be detailed in this manuscript, but from the figure, one can see how molecules regulated or produced by the kidney, the parathyroid glands, the bone and the vasculature all contribute to bone metabolism. Both intrinsic primary renal diseases such as diabetic nephropathy, as well as changes in renal function associated with the aging-kidney, affect systemic (including bone) metabolism which, in the case of skeletal interactions with the kidney, can lead to a heterogeneous group of bone diseases all of which are associated with skeletal fragility and increased risk for fractures.


Chronic kidney disease and the skeleton.

Miller PD - Bone Res (2014)

The physiological interactions between bone, the kidney, parathyroid glands and vasculature. Miller PD, Sprague S, Shane E. (original) 2014.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4472138&req=5

fig1: The physiological interactions between bone, the kidney, parathyroid glands and vasculature. Miller PD, Sprague S, Shane E. (original) 2014.
Mentions: The kidney and the skeleton have intimate biological relationships that can affect bone strength as well as renal physiological functions (Figure 1).1,2 The individual or collective roles of each of these interactions will be detailed in this manuscript, but from the figure, one can see how molecules regulated or produced by the kidney, the parathyroid glands, the bone and the vasculature all contribute to bone metabolism. Both intrinsic primary renal diseases such as diabetic nephropathy, as well as changes in renal function associated with the aging-kidney, affect systemic (including bone) metabolism which, in the case of skeletal interactions with the kidney, can lead to a heterogeneous group of bone diseases all of which are associated with skeletal fragility and increased risk for fractures.

Bottom Line: Differentiations among the disorders of renal osteodystrophy, CKD-MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry.Management of fractures in stages 1-3 CKD does not differ in persons with or without CKD with osteoporosis assuming that there is no evidence for CKD-MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD.Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence-based, with the exception of post-hoc analysis suggesting efficacy and safety of specific osteoporosis therapies (alendronate, risedronate and denosumab) in stage 4 CKD.

View Article: PubMed Central - PubMed

Affiliation: Colorado Center for Bone Research , Lakewood, CO, USA.

ABSTRACT
Fractures across the stages of chronic kidney disease (CKD) could be due to osteoporosis, some form of renal osteodystrophy defined by specific quantitative histomorphometry or chronic kidney disease-mineral and bone disorder (CKD-MBD). CKD-MBD is a systemic disease that links disorders of mineral and bone metabolism due to CKD to either one or all of the following: abnormalities of calcium, phosphorus, parathyroid hormone or vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth or strength; or vascular or other soft-tissue calcification. Osteoporosis, as defined by the National Institutes of Health, may coexist with renal osteodystrophy or CKD-MBD. Differentiation among these disorders is required to manage correctly the correct disorder to reduce the risk of fractures. While the World Health Organization (WHO) bone mineral density (BMD) criteria for osteoporosis can be used in patients with stages 1-3 CKD, the disorders of bone turnover become so aberrant by stages 4 and 5 CKD that neither the WHO criteria nor the occurrence of a fragility fracture can be used for the diagnosis of osteoporosis. The diagnosis of osteoporosis in stages 4 and 5 CKD is one of the exclusion-excluding either renal osteodystrophy or CKD-MBD as the cause of low BMD or fragility fractures. Differentiations among the disorders of renal osteodystrophy, CKD-MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry. Management of fractures in stages 1-3 CKD does not differ in persons with or without CKD with osteoporosis assuming that there is no evidence for CKD-MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD. Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence-based, with the exception of post-hoc analysis suggesting efficacy and safety of specific osteoporosis therapies (alendronate, risedronate and denosumab) in stage 4 CKD. This review also discusses how to diagnose and manage fragility fractures across the five stages of CKD.

No MeSH data available.


Related in: MedlinePlus