scholarly journals Sevelamer and the bone–vascular axis in chronic kidney disease: bone turnover, inflammation, and calcification regulation

2009 ◽  
Vol 76 ◽  
pp. S26-S33 ◽  
Author(s):  
Vincent M. Brandenburg ◽  
Willi Jahnen-Dechent ◽  
Markus Ketteler
2017 ◽  
Vol 469 ◽  
pp. 195-200 ◽  
Author(s):  
Joseph Jessy Davina ◽  
M. Priyadarssini ◽  
Medha Rajappa ◽  
Sreejith Parameswaran ◽  
Jayaprakash Sahoo ◽  
...  

Bone ◽  
2011 ◽  
Vol 49 (3) ◽  
pp. 588
Author(s):  
P. Manghat ◽  
I. Souleimanova ◽  
J. Cheung ◽  
A.S. Wierzbicki ◽  
D.J. Harrington ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250438
Author(s):  
Corinne E. Metzger ◽  
Elizabeth A. Swallow ◽  
Alexander J. Stacy ◽  
Matthew R. Allen

Chronic kidney disease (CKD) causes bone loss, particularly in cortical bone, through formation of cortical pores which lead to skeletal fragility. Animal models of CKD have shown variability in the skeletal response to CKD between males and females suggesting sex may play a role in this variation. Our aim was to compare the impact of adenine-induced CKD on cortical parameters in skeletally mature male and female C57Bl/6 mice. After 10-weeks of adenine-induced CKD, both male and female adenine mice had high serum parathyroid hormone (PTH), high bone turnover, and cortical porosity compared to non-CKD controls. Both sexes had lower cortical thickness, but only male mice had lower cortical bone area. CKD imparted greater deficits in mechanical properties of male mice compared to female mice. These data demonstrate that both male and female mice develop high PTH/high bone turnover in response to adenine-induced CKD and that cortical bone phenotypes are slightly more severe in males, particularly in mechanical properties deficits.


2019 ◽  
Vol 23 (6) ◽  
pp. 83-91 ◽  
Author(s):  
E. O. Bogdanova ◽  
O. N. Beresneva ◽  
I. M. Zubina ◽  
G. T. Ivanova ◽  
M. M. Parastaeva ◽  
...  

BACKGROUND. The molecular mechanisms of the initial stages of inorganic phosphate (Pi) metabolic disorders in chronic kidney disease (CKD) remain poorly understood.THE AIM. To test the hypothesis about changes in canonical Wnt signaling pathway inhibitors biosynthesis and a concomitant decrease in bone turnover as one of early mechanisms of Pi imbalance in CKD.MATERIAL AND METHODS. Creatinine (Cr), inorganic phosphate (Pi), serum parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), osteoprotegerin (OPG), sclerostin (SOST) and Dickkopf-1 (DKK), renal SOST and DKK mRNA expression, albuminuria (Alb), proteinuria (uTP) levels, fractional (FEPi) and daily (uPi24) Pi excretion were analyzed in SHR rats (N = 52) with 3/4 nephrectomy (NE) or sham operation (SO) and observation periods of 2, 4, and 6 months.RESULTS. Experimental model was comparable with 1-2 stages of CKD. In groups NE4 and NE6, the concentration of sPi and renal Pi excretion (FEPi and uPi24) were significantly higher vs corresponding controls SO4 (p = 0.006, p <0.010) and SO6 (p = 0.002, p = 0.028). Serum concentrations of FGF23 and PTH in NE and SO animals did not change significantly. In NE4 and NE6 groups, serum SOST and DKK concentrations were significantly higher vs controls (p <0.049, p <0.043), while the kidney expression SOST and DKK mRNA in NE rats did not change significantly or decreased (p = 0.002, p <0.011). The serum concentration of OPG was higher in the NE6 vs SO6 control (p = 0.028).CONCLUSION. The initial stages of experimental CKD are characterized by an increase in serum concentrations of Dikkopf-1, sclerostin and osteoprotegerin. The obtained data suggest the possible role of canonical Wnt signaling inhibition and reduction of bone turnover in the pathogenesis of Pi metabolic disorders in early stages of CKD.


2020 ◽  
Vol 105 (8) ◽  
pp. e2903-e2911 ◽  
Author(s):  
Jan M Hughes-Austin ◽  
Ronit Katz ◽  
Richard D Semba ◽  
Stephen B Kritchevsky ◽  
Douglas C Bauer ◽  
...  

Abstract Background We sought to identify biomarkers that indicate low turnover on bone histomorphometry in chronic kidney disease (CKD) patients, and subsequently determined whether this panel identified differential risk for fractures in community-dwelling older adults. Methods Among CKD patients who underwent iliac crest bone biopsies and histomorphometry, we evaluated candidate biomarkers to differentiate low turnover from other bone disease. We applied this biomarker panel to 641 participants in the Health Aging and Body Composition Study (Health ABC) study with estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2 who were followed for fracture. Cox proportional hazards models evaluated the association of bone mineral density (BMD) with fracture risk and determined whether biomarker-defined low bone turnover modified fracture risk at any level of BMD. Results In 39 CKD patients age 64 ± 13 years, 85% female, with mean eGFR 37 ± 14 mL/min/1.73 m2 who underwent bone biopsy, lower fibroblast growth factor (FGF)-23, higher ɑ-Klotho, and lower parathyroid hormone (PTH) indicated low bone turnover in accordance with bone histomorphometry parameters (individual area under the curve = 0.62, 0.73, and 0.55 respectively; sensitivity = 22%, specificity = 100%). In Health ABC, 641 participants with CKD were age 75 ± 3 years , 49% female, with mean eGFR 48 ± 10 mL/min/1.73 m2. For every SD lower hip BMD at baseline, there was an 8-fold higher fracture risk in individuals with biomarker-defined low turnover (hazard ratio 8.10 [95% CI, 3.40-19.30]) vs a 2-fold higher risk in the remaining individuals (hazard ratio 2.28 [95% CI, 1.69-3.08]) (Pinteraction = .082). Conclusions In CKD patients who underwent bone biopsy, lower FGF-23, higher ɑ-Klotho, and lower PTH together had high specificity for identifying low bone turnover. When applied to older individuals with CKD, BMD was more strongly associated with fracture risk in those with biomarker-defined low turnover.


2010 ◽  
Vol 21 (3) ◽  
pp. 230-232 ◽  
Author(s):  
Ramin Tolouian ◽  
German T. Hernandez ◽  
Wen-Yuan Chiang ◽  
Ajay Gupta

2020 ◽  
Vol 33 (11) ◽  
pp. 1383-1390
Author(s):  
Sercin Guven ◽  
Ibrahim Gokce ◽  
Neslihan Cicek ◽  
Ali Yaman ◽  
Pinar Vatansever ◽  
...  

AbstractBackgroundSclerostin and osteoprotegerin (OPG) are new markers of chronic kidney disease (CKD) mediated mineral bone disease (CKD-MBD) which were extensively evaluated in adult population. We aimed to evaluate the associations between serum levels of sclerostin/OPG and parameters of bone turnover and compare the serum levels of sclerostin/OPG in different stages of CKD in children.Methods70 children with CKD stage 1-5, aged 2-21 years were examined. Serum levels of alkaline phosphatase (ALP), creatinine, total calcium, phosphorus , intact parathyroid hormone (iPTH) and vitamin D were measured. Serum sclerostin and OPG levels were measured in children with different levels of CKD stage and their association with bone turnover parameters were noted.ResultsWe did not observe any significant correlation between serum levels of sclerostin and OPG and stages of CKD. A negative relationship was present between serum sclerostin and 25-OH vitamin D levels. Osteoprotegerin was positively and significantly correlated with ALP but serum sclerostin was negatively correlated with ALP.ConclusionOur study, which includes only children and adolescents with a growing skeleton under uremic conditions and excluding diabetes and atherosclerosis interference, is very valuable. We couldn't find any significant relationship between either sclerostin or OPG levels among different stages of CKD. Also our study demonstared a strong negative relationship between ALP and sclerostin levels and a strong positive relationship between ALP and OPG levels, reminding the importance of ALP levels to predict the bone-mineral status of the children with CKD.


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