Bone and Mineral Guidelines for Patients with Chronic Kidney Disease

Andress, Dennis L.

doi:10.2215/cjn.01310307

Cited by 18 publications

(17 citation statements)

References 43 publications

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“…It is well accepted that elevations in PTH are primarily responsible for the high bone turnover in the majority of individuals with late-stage CKD, and PTH measurements are used to predict HTO renal osteodystrophy. (58,(60)(61)(62)(63)(64) Although we cannot exclude the possibility that assay sensitivity may have limited our ability to detect the earliest rise in PTH, several recent clinical observations support our preclinical result because PTH levels do not uniformly predict bone turnover when diagnosed via a bone biopsy. (65)(66)(67) These findings raise the possibility that PTH may not be the sole determinant of elevated bone turnover.…”

Section: Discussionmentioning

confidence: 66%

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

240

224

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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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Section: Discussionmentioning

confidence: 66%

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

240

224

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“…The dialysis patient has very few outlets for calcium loss (i.e., they are not regulating calcium balance through their kidney, and many are not very physically active; therefore, little calcium is lost in sweat). A small amount (200 mg) will be lost in gastrointestinal secretions (19) or through efflux during dialysis, although in studies of the dialysate calcium concentrations used in this study (2.5 mEq/L or 1.25 mmol/L), there is either no transfer of calcium (20) or a small transfer of 100-200 mg elemental calcium to the patient per dialysis session (21). As in a healthy person, calcium input will be derived from the gastrointestinal tract and bone.…”

Section: Discussionmentioning

confidence: 98%

Calcium Absorption Response to Cholecalciferol Supplementation in Hemodialysis

Armas

Zena

Lund

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Recent understanding of extrarenal production of calcitriol has led to the use of more vitamin D supplementation in CKD populations. This paper reports the effect of cholecalciferol supplementation on calcium absorption.Design, setting, participants, & measurements Paired calcium absorption tests were done before and after 12-13 weeks of 20,000 IU weekly cholecalciferol supplementation in 30 participants with stage 5 CKD on hemodialysis. The study was conducted from April to December of 2011. Calcium absorption was tested with a standardized meal containing 300 mg calcium carbonate intrinsically labeled with 45 Ca; 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured.Results 25-Hydroxyvitamin D rose from 14.2 ng/ml (11.5-18.5) at baseline to 49.3 ng/ml (42.3-58.1) at the end of the study (P,0.001). 1,25-Dihydroxyvitamin D rose from 15.1 (10.5-18.8) pg/ml at baseline to 20.5 (17.0-24.7) pg/ml at the end of the study (P,0.001). The median baseline calcium absorption was 12% (7%-17%) and 12% (7%-16%) at the end of study.Conclusions Patients with stage 5 CKD on hemodialysis had very low calcium absorption values at baseline, and cholecalciferol supplementation that raised 25(OH)D levels to 50 ng/ml had no effect on calcium absorption.

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“…Serum calcium and phosphate levels were monitored every 2 weeks during the 8-week calcitriol treatment. The calcitriol dose was maintained as long as the patients did not develop the following conditions: serum PTH levels at or below 300 pg/ml; calcium-phosphate products > 75 mg 2 /dl 2 ; serum phosphate levels > 7.0 mg/dl; or serum calcium levels > 10.5 mg/dl (Andress 2008).…”

Section: Calcitriol Treatmentmentioning

confidence: 99%

Calcitriol Treatment Increases Serum Levels of the Soluble Receptor of Advanced Glycation End Products in Hemodialysis Patients with Secondary Hyperparathyroidism

Sung

Chung

Kim

et al. 2013

Tohoku J. Exp. Med.

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Cardiovascular disease is common in the patients with end-stage renal disease, who often suffer from secondary hyperparathyroidism (SHP). Vitamin D is considered for the first-line therapy managing SHP in hemodialysis (HD) patients and has a beneficial effect in the chronic inflammation and development of cardiovascular disease. The soluble receptor for advanced glycation end products (sRAGE) may be protective by binding AGE in the pathogenesis of atherosclerotic vascular complications, whereas extracellular RAGE-binding protein (EN-RAGE) represents pro-inflammatory ligands for RAGE. We have hypothesized that vitamin D treatment may alter the levels of sRAGE and EN-RAGE in HD patients. Therefore, this prospective observational study was performed in 51 HD patients with SHP who had low serum 1,25 dihydroxyvitamin D 3 (1,25D) levels and elevated intact parathyroid hormone (PTH) levels. We evaluated the changes in the values of sRAGE, EN-RAGE, and other inflammatory marker, interleukin-6 (IL-6), before and at the end of the 8-week calcitriol treatment. After calcitriol treatment, the serum levels of 1,25D were increased, whereas the serum intact PTH levels were decreased. In addition, the sRAGE levels were increased, whereas those of IL-6 were decreased after calcitriol treatment. A positive correlation between 1,25D and sRAGE levels (r = 0.609, P < 0.001) and a negative correlation between sRAGE and EN-RAGE levels (r = −0.368, P = 0.020) were detected after calcitriol treatment. This study suggests that calcitriol treatment could play an anti-inflammatory role through the increasing sRAGE in HD patients with SHP.

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Bone and Mineral Guidelines for Patients with Chronic Kidney Disease

Cited by 18 publications

References 43 publications

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

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

Calcium Absorption Response to Cholecalciferol Supplementation in Hemodialysis

Calcitriol Treatment Increases Serum Levels of the Soluble Receptor of Advanced Glycation End Products in Hemodialysis Patients with Secondary Hyperparathyroidism

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