Bone metabolism and disease in chronic kidney disease

Eknoyan, Garabed; Levin, Adeera; Levin, Nathan W.

doi:10.1016/s0272-6386(03)00905-3

Cited by 1,184 publications

(408 citation statements)

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“…Treatment with vitamin D corrects these impairments [14,30] as well as restoring strength and improving balance in vitamin D deficient humans [16,29,31]. Despite the fact that vitamin D deficiency is associated with muscle loss [12,13] and weakness [16,28,29], which may contribute to the significant muscle atrophy, weakness, and widespread disability experienced by patients with ESRD, the current focus of vitamin D treatment for the control of SHPT, as outlined in the current K/DOQI guidelines [5], is on measuring its effects on bone metabolism and tissue calcification.…”

Section: Discussionmentioning

confidence: 99%

“…Secondary hyperparathyroidism (SHPT) develops in chronic kidney disease (CKD) and ESRD in response to disruptions in the homeostatic control of parathyroid hormone (PTH) secretion related to alterations in serum phosphorous, calcium (Ca 2+ ), and declining 1,25 dihydroxyvitamin D (1,25 (OH) 2 D) levels, which occur with diminishing renal function. Although the molecular actions of vitamin D in skeletal muscle are well known, the current focus of vitamin D treatment in ESRD is the prevention and treatment of SHPT and its effects on bone metabolism and tissue calcification, as outlined in the current Kidney Disease Quality Outcomes Initiatives (K/DOQI) guidelines [5].…”

Section: Introductionmentioning

confidence: 99%

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Relationship Between Vitamin D and Muscle Size and Strength in Patients on Hemodialysis

Gordon

Sakkas

Doyle

et al. 2007

Journal of Renal Nutrition

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OBJECTIVE-Vitamin D has various actions in skeletal muscle. The purpose of this study was to compare lower limb muscle size and strength in hemodialysis (HD) patients being treated with 1,25-dihydroxyvitamin D (calcitriol) or a 1,25-dihydroxyvitamin D analog (paricalcitol) to HD patients who were receiving none.DESIGN-This was a retrospective cross-sectional study. SETTING-Outpatient hemodialysis centers.PATIENTS-HD patients receiving calcitriol or paricalcitol (active vitamin D) for control of secondary hyperparathyroidism (VitD, n = 49) were compared to HD patients who were not (n = 30).MAIN OUTCOME MEASURES-Cross-sectional areas (CSA) of thigh and tibialis anterior muscles by magnetic resonance imaging (MRI), and three measures of strength; three-repetition maximum (3RM) for knee extension (isotonic), peak torque of knee extensors (isokinetic), and maximal voluntary contraction (MVC) of the ankle dorsiflexor muscles (isometric).RESULTS-There were no differences in age, weight, dialysis vintage, or intact parathyroid hormone levels between the groups, although serum albumin was higher in the VitD group (p <0.05). Patients in the VitD group had larger thigh muscle CSA (p < 0.05) and were stronger across all strength measures (p< 0.05) after controlling for age and gender (ANCOVA). When all analyses were subsequently adjusted for serum albumin concentration, only the difference in 3RM knee extension strength lost significance. There were no significant differences in any measurements between patients who received calcitriol or paricalcitol.CONCLUSION-Treatment with active vitamin D was associated with greater muscle size and strength in this cohort of HD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Relationship Between Vitamin D and Muscle Size and Strength in Patients on Hemodialysis

Gordon

Sakkas

Doyle

et al. 2007

Journal of Renal Nutrition

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“…(30) In renal patients, persisting hyperphosphatemia is a strong contraindication for vitamin D therapy. (31) As a vitamin D analog, the potentially adverse effect on vascular calcification also applies to paricalcitol. In this study, the NTX rats received paricalcitol despite prevailing hyperphosphatemia, which may explain the increased the calcifications in the aorta of the paricalcitoltreated NTX rats.…”

Section: Discussionmentioning

confidence: 99%

Paricalcitol [19-Nor-1,25-(OH)2D2] in the Treatment of Experimental Renal Bone Disease

Jokihaara

Pörsti

Pajamäki

et al. 2006

Journal of Bone and Mineral Research

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Paricalcitol is a less hypercalcemic vitamin D analog that has been shown to suppress secondary hyperparathyroidism and to prevent the associated histomorphometric changes in bone. In this study, we show that paricalcitol also ameliorates the renal insufficiency-induced loss of bone mineral and the mechanical competence of bone.Introduction: Renal bone disease is a common consequence of chronic renal insufficiency and the associated secondary hyperparathyroidism (SH). Paricalcitol [19-nor-1,25(OH) 2 D 2 ] has been shown to ameliorate SH and prevent renal failure-induced histomorphometric changes in bone with minimal calcemic and phosphatemic activity. However, information about its efficacy on restoration of bone structural strength is lacking. In this study, we explored the effects of paricalcitol treatment on bone structure and strength in a model of advanced renal disease. Materials and Methods: Forty-five 8-week-old rats were randomly assigned to either surgical 5/6 nephrectomy (NTX) or Sham-operation. After a 15-week postoperative disease progression period, the NTX rats were further allocated to uremic control (NTX) and treatment (NTX + paricalcitol) groups, the latter of which received paricalcitol for the subsequent 12 weeks. After 27 weeks, the animals were killed, plasma samples were collected, and both femora were excised for comprehensive analysis of the femoral neck and midshaft (pQCT and biomechanical testing). Results: High mortality that exceeded 30% was observed in both NTX groups. NTX induced over a 13-fold increase in plasma PTH, whereas this increase was only 5-fold after paricalcitol treatment. At the femoral neck, NTX was associated with an 8.1% decrease (p < 0.05) in vBMD and a 16% decrease in breaking load (p < 0.05) compared with the Sham group, whereas paricalcitol treatment completely prevented these changes. At the femoral midshaft, the NTX resulted in a 6.6% decrease in cortical BMD (p < 0.01 versus Sham), and this change was also prevented by paricalcitol. Conclusions: Paricalcitol administration prevented renal insufficiency-associated decreases in BMD in the femoral neck and the femoral midshaft and restored bone strength in the femoral neck. Therefore, paricalcitol can efficiently ameliorate renal insufficiency-induced loss of bone mineral and mechanical competence of bone.

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“…However, in the USA, the National Kidney Foundation have proposed a single target for dialysis patients of o300 ng/L, irrespective of the PTH assay used. 11 Other management thresholds may be a¡ected. For example, cinacalcet hydrochloride, a calcimimetic agent that increases the sensitivity of the calciumsensing receptor, thereby inhibiting the release of PTH, is under review by the National Institute for Health and Clinical Excellence (NICE) for use in secondary hyperparathyroidism.…”

mentioning

confidence: 99%

“…Patients'eligibility for this therapy could be compromised by the characteristics of the local PTH assay in a'post-code' lottery of exactly the kind that NICE guidelines are intended to circumvent. UK guidelines for the management of renal osteodystrophy among patients with stage 3 CKD, 13 partly in£uenced by the earlier US guidelines, 11 have also indirectly used PTH targets linked to the second-generation Nichols Allegro IRMA. For example, evaluation of vitamin D status and correction of any underlying de¢ciency is recommended when PTH exceeds 70 ng/ L in patients with stage 3 CKD.…”

mentioning

confidence: 99%