scholarly journals The use of bone turnover markers in chronic kidney disease-mineral and bone disorders

Nephrology ◽  
2017 ◽  
Vol 22 ◽  
pp. 11-13 ◽  
Author(s):  
Cherie Chiang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Bone Disorders ◽  
Turnover Markers

Assessment of bone turnover markers to predict mineral and bone disorder in men with pre-dialysis non-diabetic chronic kidney disease

2017 ◽  
Vol 469 ◽  
pp. 195-200 ◽  
Author(s):  
Joseph Jessy Davina ◽  
M. Priyadarssini ◽  
Medha Rajappa ◽  
Sreejith Parameswaran ◽  
Jayaprakash Sahoo ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Mineral And Bone Disorder ◽  
Bone Disorder ◽  
Turnover Markers

Corrigendum to “Association of bone turnover markers and arterial stiffness in pre-dialysis chronic kidney disease (CKD)” [Bone 48 (2011) 1127–1132]

Bone ◽  
2011 ◽  
Vol 49 (3) ◽  
pp. 588
Author(s):  
P. Manghat ◽  
I. Souleimanova ◽  
J. Cheung ◽  
A.S. Wierzbicki ◽  
D.J. Harrington ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Turnover Markers

Corrigendum to “Association of bone turnover markers and arterial stiffness in pre-dialysis chronic kidney disease (CKD)” [Bone 48 (2011) 1127–1132]

Bone ◽  
2013 ◽  
Vol 53 (1) ◽  
pp. 319
Author(s):  
P. Manghat ◽  
I. Souleimanova ◽  
J. Cheung ◽  
A.S. Wierzbicki ◽  
D.J. Harrington ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Turnover Markers

scholarly journals P0874THE IMPACT OF CHRONIC EXPOSURE TO INDOXYL SULFATE ON BONE TURNOVER MARKERS, PTH, VITAMIN D3, AND BIOMECHANICAL AND DENSITOMETRIC PROPERTIES OF BONES IN RAT MODEL

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Malgorzata Karbowska ◽  
Beata Sieklucka ◽  
Alicja Roszczenko ◽  
Joanna Rogalska ◽  
Krystyna Pawlak ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Turnover ◽  
Cortical Bone ◽  
Vitamin D3 ◽  
Bone Turnover Markers ◽  
Chronic Exposure ◽  
Bending Test ◽  
Femoral Diaphysis ◽  
Turnover Markers

Abstract Background and Aims Chronic kidney disease (CKD) is a crucial risk factor for biochemical and bone disturbances, as well as non-skeletal calcifications known as Chronic Kidney Disease – Mineral and Bone Disorders (CKD-MBD). Etiopathogenesis of CKD-MBD still remains unknown and arouses much controversy. Indoxyl sulfate (IS) is one of the most potent protein-bound uremic toxin that accumulates during CKD, and exerts aggressive and multidirectional effect on the body. In vitro studies indicate that IS modulates the differentiation and activation of osteoblasts and osteoclasts, however IS impact on bone and mineral disorders still remains unclear. The purpose of the study was to assess IS effect on bone turnover markers, parathyroid hormone (PTH), vitamin D3, and densitometric and biomechanical properties of bones in rat model. Method Male Wistar rats weighting 180 – 210 g (n=48) were divided into three groups – control group that received pure water and two experimental groups. Experimental groups were exposed to IS in the doses of 100 or 200 mg/kg of b.w. (200 IS) in the drinking water during 4 weeks. At the end of experiment, rats were anesthetized and samples of blood, as well as tibiae, femurs and lumbar spines were collected. Next, the IS bone (cortical and trabecular), plasma and urine levels were determined by high-performance liquid chromatography (HPLC). We also assessed IS influence on bone turnover markers (alkaline phosphatase – ALP, and tartrate-resistant acid phosphatase - TRAP), and level of vitamin D3, and PTH. Furthermore, we evaluated densitometric parameters of tibiae, femurs and lumbar spines using Horizon QDR Series X-ray Bone Densitometer, and performed biomechanical parameters analysis of the cortical bone of the femoral diaphysis using three-point bending test, and the mixed cortico-trabecular structure of the proximal femur by the bending test of the femoral neck. Results Chronic exposure to IS led to statistically significant increase in plasma, urine, cortical and trabecular bone IS concentrations. We observed reduction in bone turnover markers – bone formation marker ALP in trabecular and cortical bone, and bone resorption marker TRAP in cortical bone. Moreover, the highest dose of IS increased PTH. None of tested IS doses affected vitamin D3. From data obtained due to biomechanical tests, the highest dose of IS decreased the main indicators of bone strength: yield load (Fy) and displacement at yield [dl(Fy)] of femoral diaphysis and femoral neck, and ultimate load (Fu) and displacement at ultimate [dl(Fu)] of femoral diaphysis. Furthermore, we observed the decrease in elasticity of femoral diaphysis (increased Young’s modulus of elasticity E). Additionally, densitometric measurements revealed reduction only in the bone mineral density (BMD) and BMD of diaphyseal area (BMD R2) of tibiae, BMD R2 of femurs in 200 IS group, as well as BMD and BMD R2 of tibiae in 100 IS group. Conclusion Obtained data confirm that IS affects bones. We observed reduced bone metabolism and strength after exposure to IS. On the basis of the results, we concluded that IS can be one of crucial uremic factors responsible for increased risk of fracture during CKD.

Association of bone turnover markers and arterial stiffness in pre-dialysis chronic kidney disease (CKD)

Bone ◽  
2011 ◽  
Vol 48 (5) ◽  
pp. 1127-1132 ◽  
Author(s):  
P. Manghat ◽  
I. Souleimanova ◽  
J. Cheung ◽  
A.S. Wierzbicki ◽  
D.J. Harrington ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Turnover Markers

Rationale for Raising Current Clinical Practice Guideline Target for Serum 25-Hydroxyvitamin D in Chronic Kidney Disease

2019 ◽  
Vol 49 (4) ◽  
pp. 284-293 ◽  
Author(s):  
Stephen A. Strugnell ◽  
Stuart M. Sprague ◽  
Akhtar Ashfaq ◽  
Martin Petkovich ◽  
Charles W. Bishop
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Clinical Practice ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Hydroxyvitamin D ◽  
Calcium Phosphorus ◽  
Safety Parameters ◽  
25 Hydroxyvitamin D ◽  
Turnover Markers

Background: Vitamin D repletion is recommended for secondary hyperparathyroidism (SHPT) and associated vitamin D insufficiency (VDI) in chronic kidney disease (CKD), but optimal levels of serum total 25-hydroxyvitamin D remain undefined. Clinical practice guidelines target sufficiency, whereas recent data indicate that higher levels are required to control the elevation of intact parathyroid hormone (iPTH) as CKD advances. This secondary analysis of 2 randomized controlled trials seeks to identify the minimum level of mean serum 25-hydroxyvitamin D required to control SHPT arising from VDI in stage 3 or 4 CKD. Methods: Adult subjects (n = 429) with SHPT, VDI, and stage 3 or 4 CKD were stratified by stage and treated daily with either extended-release calcifediol (ERC) or placebo in 2 identical, parallel, randomized, double-blind studies. After treatment for 26 weeks, all subjects were ranked by the level of serum total 25-hydroxyvitamin D and divided into quintiles in order to examine the relationships between the degree of vitamin D repletion and the associated changes in plasma iPTH, serum bone turnover markers, calcium, phosphorus, intact fibroblast growth factor 23 (FGF23) and vitamin D metabolites, estimated glomerular filtration rate (eGFR), and urine calcium:creatinine (Ca:Cr) ratio. Results: Progressive increases in serum 1,25-dihydroxyvitamin D and reductions in plasma iPTH and serum bone turnover markers were observed as mean posttreatment serum 25-hydroxyvitamin D rose from 13.9 ng/mL (in Quintile 1) to 92.5 ng/mL (in Quintile 5), irrespective of CKD stage. Mean serum calcium, phosphorus and FGF23, eGFR, and urine Ca:Cr ratio (collectively “safety parameters”) did not significantly change from Quintile 1. Suppression of iPTH and bone turnover markers was not observed until serum 25-hydroxyvitamin D rose to at least 50.8 ng/mL (Quintile 3). Conclusion: ERC therapy produced exposure-dependent reductions in plasma iPTH and bone turnover markers only when mean serum total 25-hydroxyvitamin D reached at least 50.8 ng/mL, indicating that current targets for vitamin D repletion therapy in CKD are too low. Gradual elevation of mean serum 25-hydroxyvitamin D to 92.5 ng/mL was not associated with significant adverse changes in safety parameters.

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