Serum phosphorus adds to value of serum parathyroid hormone for assessment of bone turnover in renal osteodystrophy

2016 ◽  
Vol 86 (07) ◽  
pp. 9-17 ◽  
Author(s):  
Jimmy Gentry ◽  
Jonathan Webb ◽  
Daniel Davenport ◽  
Hartmut H. Malluche
Keyword(s):  
Parathyroid Hormone ◽  
Bone Turnover ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Serum Parathyroid Hormone

Renal osteodystrophy

2013 ◽  
pp. 1274-1282
Author(s):  
Thomas Bardin ◽  
Tilman Drüeke
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Alkaline Phosphatases ◽  
Calcium Phosphorus ◽  
Turnover Markers ◽  
25 Oh Vitamin D

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

Renal osteodystrophy

2013 ◽  
Author(s):  
Thomas Bardin ◽  
Tilman Drüeke
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Phosphate Binders ◽  
Type I ◽  
Vitamin D Metabolites ◽  
Alkaline Phosphatases

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

Renal osteodystrophy

2013 ◽  
pp. 1274-1282
Author(s):  
Tilman Drüeke ◽  
Thomas Bardin
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Dialysis Patients ◽  
Alkaline Phosphatases ◽  
Turnover Markers ◽  
25 Oh Vitamin D

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. Its main clinical expression is an increased propensity for fractures. It has been divided into several pathological entities based on histomorphometry criteria of bone turnover, mineralization and volume. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and α‎-klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can be schematically divided into three main types by histology: (1) osteitis fibrosa reflecting secondary hyperparathyroidism (sHP) is a high bone turnover disease which can develop early in CKD; (2) adynamic bone disease (ABD), at present the predominant type of ROD in dialysis patients, which is mainly the result of PTH resistance or excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone-specific alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus increases only in advanced CKD (stages G4-G5). Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage renal disease is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol, and in addition calcimimetics in dialysis patients, can be used to halt its progression.

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