Intermittent calcitriol therapy in secondary hyperparathyroidism: A comparison between oral and intraperitoneal administration

Salusky, Isidro B.; Kuizon, Beatriz D.; Belin, Thomas R.; Ramirez, Jorge A.; Gales, Barbara; Segre, Gino V.; Goodman, William G.

doi:10.1046/j.1523-1755.1998.00045.x

Cited by 113 publications

(120 citation statements)

References 30 publications

Supporting

Mentioning

119

Contrasting

Order By: Relevance

“…The absence of an increase in osteoblast number, osteoblast perimeter, and in the CKD chow-fed group indicates that with this mild level of renal insufficiency and mild hyperparathyroidism, the only manifestation of hyperparathyroid bone disease was the hyperosteoidosis. ultimate cause (5,56,66,67). We have suggested that CKD decreases skeletal anabolic factors, stimulates inhibitors of osteoblast function, or both (1,2,68).…”

Section: Discussionmentioning

confidence: 99%

“…In this setting, the development of hyperparathyroidism can be viewed as a failed adaptive attempt to maintain skeletal remodeling or modeling. The ABD is certainly more common when PTH levels are actively suppressed with high calcium dialysate and calcitriol (especially intravenous) therapy (64,66,67). Uremic bone is resistant to the actions of PTH (13), defined as release of calcium from the skeleton after a dose of PTH, and a certain amount of hyperparathyroidism is required to maintain bone turnover.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Successful Treatment of an Adynamic Bone Disorder with Bone Morphogenetic Protein-7 in a Renal Ablation Model

Lund¹,

Davies²,

Brown³

et al. 2004

Journal of the American Society of Nephrology

103

View full text Add to dashboard Cite

Abstract. An adynamic bone disorder (ABD) is an important complication of chronic kidney disease (CKD) of unknown etiology for which there is no adequate treatment. Reported is an animal model of ablative CKD complicated by an ABD characterized by the absence of secondary hyperparathyroidism and its successful treatment with a skeletal anabolic factor, bone morphogenetic protein-7 (BMP-7). Adult mice were subjected to electrocautery of the right kidney followed by left nephrectomy. Animals were randomized into groups fed normal chow or fed low-phosphate chow supplemented with calcitriol to maintain normophosphatemia in CKD. All groups were maintained on the regimens for 12 wk. Hyperphosphatemia, secondary hyperparathyroidism, and a mild osteodystrophy developed in the CKD/chow-fed group, as expected. When dietary phosphorus was restricted and calcitriol was administered in the CKD low-phosphate/calcitriol group (ABD), Ca, PO 4 , and parathyroid hormone levels were maintained normal. A significant ABD developed in the ABD group characterized by significant depressions in osteoblast number, perimeters, bone formation rates, and mineral apposition rates when compared with the sham-operated, chow-fed group. The abnormal skeletal histomorphometry was reversed by BMP-7 therapy to normal values and significantly improved from the ABD group (P Ͻ 0.05). The sham-operated low-phosphate/ calcitriol-fed control group and the CKD low-phosphate/calcitriol/BMP-7 groups had reduced phosphate levels compared with the other groups (P Ͻ 0.05). ABD produced in mice with CKD in the absence of hyperparathyroidism was successfully reversed with a bone anabolic, BMP-7, associated with a reduction in plasma phosphorus.Renal osteodystrophy is a term used to describe a heterogeneous spectrum of skeletal abnormalities found in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). Renal osteodystrophy ranges from states of high bone turnover to states of low bone turnover (1-3). Predominantly hyperparathyroid bone disease results in a high turnover osteodystrophy (osteitis fibrosa), and it is considered the most prevalent bone disorder in chronic kidney disease and ESKD. Low-turnover osteodystrophy reflects the lack of capacity to produce and mineralize bone matrix and has two main histologic forms: osteomalacia and the adynamic bone disorder (ABD). The ABD is an important complication of CKD associated with high rates of bone fractures (4), impaired growth (5,6), and probably vascular calcification (7,8). There has been an increase in the prevalence of ABD in patients with ESKD on dialysis (9).The pathogenesis of the ABD is unknown. It may occur when parathyroid hormone (PTH) levels are aggressively suppressed (10). As a result, practice standards target maintaining elevated intact PTH levels (about three to five times normal) sufficient to prevent the ABD (11,12). Therapy of the ABD besides adjustment of PTH levels is not available. Because secondary hyperparathyroidism in CKD causes a distinct osteodystrophy, in...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Successful Treatment of an Adynamic Bone Disorder with Bone Morphogenetic Protein-7 in a Renal Ablation Model

Lund¹,

Davies²,

Brown³

et al. 2004

Journal of the American Society of Nephrology

103

View full text Add to dashboard Cite

show abstract

“…All of the subjects were part of various clinical investigations to characterize the spectrum of renal osteodys-trophy in pediatric dialysis patients (3,(7)(8)(9)(10)(11); only baseline biopsies were used for the current analysis. All patients received calcium-based phosphate binders at the time of the bone biopsy, and in those treated with daily oral calcitriol, such therapy was held for 4 weeks before bone biopsy.…”

Section: Methodsmentioning

confidence: 99%

Value of the New Bone Classification System in Pediatric Renal Osteodystrophy

Bakkaloğlu

Wesseling‐Perry²,

Pereira³

et al. 2010

Clinical Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

Background and objectives: Although lesions of renal osteodystrophy have traditionally been defined by bone turnover, alterations in skeletal mineralization and volume are also prevalent and may contribute to significant morbidity in patients with chronic kidney disease (CKD). The study presented here was undertaken to compare the traditional spectrum of renal osteodystrophy defined by bone turnover to a new classification system that includes T (turnover), M (mineralization), and V (volume) and to determine the value of biochemical parameters as predictors of specific TMV lesions.Design, setting, participants, & measurements: Pediatric patients (n ‫؍‬ 161) treated with peritoneal dialysis were enrolled into the study.Results: Increased bone turnover and abnormal mineralization were prevalent (57% and 48%, respectively); bone volume was normal or increased in all subjects. Predictive algorithms for different skeletal diagnoses were established by Classification and regression tree analysis. Serum parathyroid hormone (PTH) less than 400 pg/ml in combination with alkaline phosphatase values less than 400 IU/L provided the highest correct prediction rate for patients with both normal bone turnover and normal mineralization. Levels of PTH were higher and serum calcium levels were lower in patients with defective mineralization, irrespective of bone turnover.Conclusions: Although no single biochemical marker is able to provide a complete assessment of renal osteodystrophy, a combination of serum calcium, alkaline phosphatase, and PTH levels may lead to a more precise noninvasive assessment of turnover and mineralization abnormalities in this population.

show abstract

“…Whereas early case series of bone biopsy results in children on maintenance dialysis reported high-turnover bone disease (osteitis fibrosa and mild lesions of secondary hyperparathyroidism) in the vast majority of patients [8][9][10], more recent series identified adynamic bone in a substantial proportion (27-33%) of children and adolescents [11][12][13]. The implications of low bone turnover for bone structure and strength during growth are not known; however, this bone lesion is associated with increased fracture risk in adults [14] -perhaps due to impaired microfracture repair.…”

Section: Histomorphometry Of Renal Osteodystrophymentioning

confidence: 99%

A structural approach to the assessment of fracture risk in children and adolescents with chronic kidney disease

Leonard

2007

Pediatr Nephrol

View full text Add to dashboard Cite

Children with chronic kidney disease (CKD) have multiple risk factors for impaired accretion of trabecular and cortical bone. CKD during childhood poses an immediate fracture risk and compromises adult bone mass, resulting in significantly greater skeletal fragility throughout life. Highturnover disease initially results in thickened trabeculae, with greater bone volume. As disease progresses, resorption cavities dissect trabeculae, connectivity degrades, and bone volume decreases. Increased bone turnover also results in increased cortical porosity and decreased cortical thickness. Dual-energy X-ray absorptiometry (DXA)-based measures of bone mineral density (BMD) are derived from the total bone mass within the projected bone area (g/cm 2 ), concealing distinct disease effects in trabecular and cortical bone. In contrast, peripheral quantitative computed tomography (pQCT) estimates volumetric BMD (vBMD, g/cm 3 ), distinguishes between cortical and trabecular bone, and provides accurate estimates of cortical dimensions. Recent data have confirmed that pQCT measures of cortical vBMD and thickness provide substantially greater fracture discrimination in adult dialysis patients compared with hip or spine DXA. The following review considers the structural effects of renal osteodystrophy as it relates to fracture risk and the potential advantages and disadvantages of DXA and alternative measures of bone density, geometry, and microarchitecture, such as pQCT, micro-CT (μCT), and micro magnetic resonance imaging (μMRI) for fracture risk assessment.

show abstract

Intermittent calcitriol therapy in secondary hyperparathyroidism: A comparison between oral and intraperitoneal administration

Abstract: Differences in the bioavailability of calcitriol and/or in phosphorus metabolism may account for the divergent biochemical response to p.o. and i.p. calcitriol.

Cited by 113 publications

References 30 publications

Successful Treatment of an Adynamic Bone Disorder with Bone Morphogenetic Protein-7 in a Renal Ablation Model

Successful Treatment of an Adynamic Bone Disorder with Bone Morphogenetic Protein-7 in a Renal Ablation Model

Value of the New Bone Classification System in Pediatric Renal Osteodystrophy

A structural approach to the assessment of fracture risk in children and adolescents with chronic kidney disease

Contact Info

Product

Resources

About