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Renal osteodystrophy
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Renal osteodystrophy
Renal osteodystrophy is defined as an alteration of bone in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.
The types of renal osteodystrophy have traditionally been defined on the basis of bone turnover and mineralization:
1) mild, slight increase in turnover and normal mineralization;
2) osteitis fibrosa, increased turnover and normal mineralization;
3) osteomalacia, decreased turnover and abnormal mineralization;
4) adynamic, decreased turnover and acellularity; and,
5) mixed, increased turnover with abnormal mineralization.
A Kidney Disease: Improving Global Outcomes (KDIGO) report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system).
On the other hand, CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of:
1) abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism;
2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and
3) vascular or other soft-tissue calcification.
Renal osteodystrophy may exhibit no symptoms; if it does show symptoms, they can include:
Renal osteodystrophy has been classically described as the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.[citation needed]
Low activated vitamin D3 levels are a result of the damaged kidneys' inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcemia. High levels of fibroblast growth factor 23 seem to be the most important cause of decreased calcitriol levels in CKD patients.[citation needed]
In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. However, in other situations, the initial increase in parathyroid hormone and bone remodeling may be slowed excessively by a multitude of factors, including age, ethnic origin, sex, and treatments such as vitamin D, calcium salts, calcimimetics, steroids, and so forth, leading to low bone turnover or adynamic bone disease.
Both high and low bone turnover diseases are observed equally in CKD patients treated by dialysis, and all types of renal osteodystrophy are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes.
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Renal osteodystrophy
Renal osteodystrophy is defined as an alteration of bone in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.
The types of renal osteodystrophy have traditionally been defined on the basis of bone turnover and mineralization:
1) mild, slight increase in turnover and normal mineralization;
2) osteitis fibrosa, increased turnover and normal mineralization;
3) osteomalacia, decreased turnover and abnormal mineralization;
4) adynamic, decreased turnover and acellularity; and,
5) mixed, increased turnover with abnormal mineralization.
A Kidney Disease: Improving Global Outcomes (KDIGO) report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system).
On the other hand, CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of:
1) abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism;
2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and
3) vascular or other soft-tissue calcification.
Renal osteodystrophy may exhibit no symptoms; if it does show symptoms, they can include:
Renal osteodystrophy has been classically described as the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.[citation needed]
Low activated vitamin D3 levels are a result of the damaged kidneys' inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcemia. High levels of fibroblast growth factor 23 seem to be the most important cause of decreased calcitriol levels in CKD patients.[citation needed]
In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. However, in other situations, the initial increase in parathyroid hormone and bone remodeling may be slowed excessively by a multitude of factors, including age, ethnic origin, sex, and treatments such as vitamin D, calcium salts, calcimimetics, steroids, and so forth, leading to low bone turnover or adynamic bone disease.
Both high and low bone turnover diseases are observed equally in CKD patients treated by dialysis, and all types of renal osteodystrophy are associated with an increased risk of skeletal fractures, reduced quality of life, and poor clinical outcomes.