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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">The term adynamic bone disease &#40;ABD&#41; or aplastic bone disease was first described in early 1980s&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">1&#44;2</span></a> ABD is defined by faulty rate of collagen synthesis and mineralization i&#46;e&#46; low-bone turnover without osteoid accumulation &#40;thin osteoid seam&#41;&#46; It needs to be differentiated from osteomalacia which is also a low turnover disease but their defect in mineralization exceeds the defects in bone formation and therefore&#44; there is a relative osteoid excess in osteomalacia&#46; In ABD&#44; there are few or no osteoblasts&#44; minimal or no peri-trabecular fibrosis&#44; substantially low bone formation rate &#40;BFR&#41; and the number of re-modeling sites is also low&#46;<a class="elsevierStyleCrossRefs" href="#bib0365"><span class="elsevierStyleSup">3&#44;4</span></a> Here&#44; we would be briefly summarizing ABD in the following sections with special focus on newer treatment strategies&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">ABD in course of CKD and prevalence</span><p id="par0010" class="elsevierStylePara elsevierViewall">ABD is most common of all CKD associated MB disorders &#40;osteitis fibrosa&#44; osteomalacia&#44; mixed turnover disorder&#41;&#44; and requires preventive care even from early stages of CKD&#46; Though&#44; advances CKD stages are at high risk of ABD with prevalence rate variable from 10 to 40&#37; in advanced stages to 10&#8211;50&#37; in dialysis patients but it is also not uncommon to see in earlier CKD stages 3&#8211;5 with a prevalence rate showed rising trends and reaches to about 18&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0375"><span class="elsevierStyleSup">5&#44;6</span></a> In one study of patients with pre-dialysis CKD&#44; ABD was seen in 12&#37; of bone biopsies&#46; Increased average age&#44; percentage of patient with diabetes and high vitamin D and oral calcium supplements are important contributor to the rising trends&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">7</span></a> Peritoneal dialysis &#40;PD&#41; is more commonly associated with ABD &#40;almost in 50&#37;&#41; than hemodialysis &#40;HD&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">8</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Risk factors</span><p id="par0015" class="elsevierStylePara elsevierViewall">The risk factors for ABD are multifactorial &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Elderly individuals&#44; diabetes&#44; high calcium load&#44; vitamin D excess&#44; overzealous treatment of hyperparathyroidism&#44; low parathyroid hormone &#40;PTH&#41; levels&#44; parathyroidectomy&#44; systemic inflammation&#44; calcimimetics&#44; and bisphosphonates have all been commonly implicated&#46;<a class="elsevierStyleCrossRefs" href="#bib0395"><span class="elsevierStyleSup">9&#44;10</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">High concentrations of glucose and insulin deficiency suppresses PTH secretion in parathyroid cell cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">11</span></a> In a study of rats with streptozocin-induced diabetes&#44; bone histology was characterised by low bone formation&#44; reduced osteoid measurements&#44; decreased osteoclast number&#44; and less bone collagen synthesis&#46;<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">12</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">High calcium load&#44; whether oral dietary intake or in dialysis solution and low phosphate diet suppresses parathyroid gland hyperplasia by induction of p21 and reduction of transforming growth factor alpha&#46; In addition&#44; calcitriol also induces p21 and act via membrane trafficking of the epithelial growth factor receptor &#40;EGFR&#41; and down regulated signaling&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">13</span></a> Adynamic bone is thus a result of over-suppression of PTH synthesis and secretion&#46;<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">14</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">CKD progression is coupled with PTH resistance due to changes in the tissue expression of their regulators&#44; disturbances of hepatic and renal PTH catabolism and downregulation or desensitization of PTH1R&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">15</span></a> It is also affected by serum level of phosphate&#44; indoxyl sulphate and paracresyl sulphate&#46; In addition&#44; treatment resulting excess of CaSR and vitamin D receptor activation along with FGF23-Klotho endocrine axis suppresses PTH secretion&#46; FGF23 binds to the Klotho to activate MAPK-pathway and there is also an early inhibition of the Wnt pathway with an increase in the expression of sclerostin&#46;<a class="elsevierStyleCrossRefs" href="#bib0430"><span class="elsevierStyleSup">16&#44;17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Bisphosphonates are risk factor in advanced CKD for ABD in presence of abnormal laboratory parameters&#46; Metanalysis of bisphosphonates in age related CKD 1&#8211;3 concluded it as a safe therapy in absence of laboratory features of CKD-MBD&#46;<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">18</span></a> In another study of 31 CKD stage 5 hemodialysis patients&#44; short term usage of bisphosphonates did no harm and bone biopsy was not advised&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">19</span></a> However&#44; study of thirteen CKD patients &#40;stage 2&#8211;4&#41; treated from 4 to &#62;60 months with bisphosphonates for osteopenia or osteoporosis&#44; underwent trabecular bone biopsies from the iliac crest and all were diagnosed with adynamic bone on biopsy evaluation&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">20</span></a> It is therefore necessary to warn for a possible harm before administering bisphosphonates in this patient population&#46; KDIGO suggests that treatment choices including bisphosphonates take into account the magnitude and reversibility of the biochemical abnormalities and the progression of CKD&#44; with consideration of a bone biopsy in patients with CKD G3a-G5D with biochemical abnormalities of CKD-MBD and low BMD and&#47;or fragility fractures&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">21</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Other potential mechanisms of low bone formation include elevated circulating cytokine levels &#40;interleukin &#40;IL&#41;-I&#44; tumor necrosis factor &#40;TNF&#41;&#44; low estrogen and testosterone levels&#44; decreased osteoblast proliferation from the direct effect of accumulated uremic inhibitors&#44; and decreased circulating insulin-like growth factor &#40;IGF&#41;-I activity either from low IGF-I and&#47;or IGF-binding protein &#40;IGFBP&#41;-5 levels or from excess IGFBPs that inhibit the action of IGF-I&#46;<a class="elsevierStyleCrossRefs" href="#bib0460"><span class="elsevierStyleSup">22&#8211;29</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">ABD pathophysiology</span><p id="par0045" class="elsevierStylePara elsevierViewall">Three elements of bone characterize different types of CKD&#8211;MBD&#46; These are bone turnover&#44; bone mineralization and fibrosis quantification assessment&#46; The practiced metric for ABD includes &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0455"><span class="elsevierStyleSup">21&#44;30&#44;31</span></a><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Bone formation rate less than 97 to 108<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0055" class="elsevierStylePara elsevierViewall">Osteoid volume less than 12&#8211;15&#37;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#46;</span><p id="par0060" class="elsevierStylePara elsevierViewall">No &#40;minimal&#41; fibrosis&#46;</p></li></ul></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">Osteoblastic proteins stimulate mineralization&#46; Fibroblast growth factor-23 FGF-23 is formed by osteoblasts and osteocytes in bone and keep a physiological check on mineral levels by its action on parathyroid&#44; kidney and bone and therefore affecting calcium&#44; phosphorus&#44; calcitriol and parathormone synthesis&#46; It gets activated after its binding to a transmembrane protein&#44; klotho and combination then result in suppression of both PTH and 1&#44;25-dihydroxyvitamin D through downregulating action on NaPi-2a &#40;SLC34A1&#41; and NaPi-2c &#40;SLC34A3&#41; channels in the proximal tubules and distal tubule and suppression of 1&#945;-hydroxylase &#40;thus lower down phosphorous level and calcitriol&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0510"><span class="elsevierStyleSup">32&#44;33</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Bone turnover is also affected by many local factors as growth factors and cytokines and interleukins by their action on PTH&#46; Cytokines regulate osteoclastogenesis and osteoprotegerin &#40;OPG&#41;&#44; which is a complex system to regulate bone resorption&#46;<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">34</span></a> It has a negative association with PTH in ABD&#46; Osteoprotegerin is also a soluble member of the tumor necrosis factor and associated with atherogenesis and endothelial dysfunction&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Clinical features</span><p id="par0075" class="elsevierStylePara elsevierViewall">There are no pathognomonic clinical signs of ABD&#46; The two most common symptoms are skeletal pain and fractures&#46;<a class="elsevierStyleCrossRefs" href="#bib0525"><span class="elsevierStyleSup">35&#44;36</span></a> Although&#44; biopsy proven adynamic bone as a risk factor for fracture has not been demonstrated in the studies but recent guidelines do not recommend routine bone biopsy for making diagnosis&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Diagnosis</span><p id="par0080" class="elsevierStylePara elsevierViewall">No biochemical markers can accurately define ABD&#46; Bone alkaline phosphatase &#40;BAP&#41; is the most useful parameter for bone formation as elevated levels&#44; exclude ABD while low PTH levels distinguishes it from high turnover CKD-MBD&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">37</span></a> Relatively low&#47;normal PTH served as a surrogate marker of low bone turnover and identifies fracture risk in ABD&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">The histomorphometric examination of an under calcified bone sample is the gold standard for the diagnosis of ABD&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">38</span></a> The requisites include pre-biopsy in-vivo tetracycline double labelling&#44; amyloid and aluminium staining&#46; Both cortical and trabecular bone should be assessed for static and dynamic parameters to interpret bone metabolism in totality&#46; Favoured site of biopsy is 2<span class="elsevierStyleHsp" style=""></span>cm posterior and 2<span class="elsevierStyleHsp" style=""></span>cm inferior to the anterior iliac crest&#46; The instrument is specifically planned to obtain a core of bone of at least 4&#8211;5<span class="elsevierStyleHsp" style=""></span>mm diameter&#46;<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">39</span></a></p><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Ectopic calcification</span><p id="par0090" class="elsevierStylePara elsevierViewall">A notable feature of ABD is diminished assimilation of serum calcium into the bone&#46; In a study of 101 hemodialysis patients&#44; 52&#37; had moderate or severe coronary artery calcification &#40;CAC&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">40</span></a> This association was pronounced with older age&#44; higher BMI&#44; inflammation&#44; reduced trabecular volume and with higher osteoprotegerin levels&#46; Asci et al&#46; noted that when only HD patients with CAC were included for analysis&#44; there was a U-shaped relationship between CAC and bone turnover&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">41</span></a> London et al concluded that a high arterial calcification score is defined by bone histo-morphometry suggestive of low bone activity and ABD&#46;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">42</span></a> Studies have shown that anabolic bone stimulating agents such as bone morphogenic protein 7 &#40;BMP-7&#41; or synthetic PTH &#40;1&#8211;34&#41; improved bone turnover and skeletal mineralization and decreased calcium deposition in the aorta&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">43</span></a> The mechanism of action of PTH &#40;1-34&#41; seems to be mediated through a combination of both direct and osteopontin effects&#46;</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">ABD and mortality</span><p id="par0095" class="elsevierStylePara elsevierViewall">Multiple studies have documented relation between low and very high PTH &#40;U-shaped pattern&#41; and risk of sudden death&#46;<a class="elsevierStyleCrossRefs" href="#bib0570"><span class="elsevierStyleSup">44&#8211;46</span></a> In a multi-centric French ARNOS cohort of 1&#44;348 prevalent HD patients&#44; very low PTH levels &#40;&#60;50<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#41; was associated with poor survival rates &#40;HR&#58; 1&#46;4 &#40;1&#46;07&#8211;1&#46;8&#41;&#44; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;006&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">47</span></a> Also Korean multicenter prospective cohort study of 1&#44;771 incident dialysis patients&#44; revealed association of low serum PTH level &#40;&#60;150<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#41; and infection-related mortality &#40;hazard ratio &#91;HR&#93;&#44; 2&#46;52&#59; 95&#37; CI&#44; 1&#46;06&#8211;5&#46;99&#59; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;04&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">48</span></a> With the understanding of rise of PTH level with CKD progression&#44; KDIGO suggest maintaining intact PTH levels in the range of approximately two to nine times the upper normal limit for the assay&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">21</span></a> Guidelines gave emphasis for keeping higher targets for PTH as per the stages of CKD and minimise over usage of calcium-based binders and Vitamin D analogues&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Key measures in the management of ABD</span><p id="par0100" class="elsevierStylePara elsevierViewall">The chief management strategy aims to increase PTH synthesis&#46; The following measures may be useful&#58;<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">1&#46;</span><p id="par0105" class="elsevierStylePara elsevierViewall">Switch from calcium-containing phosphate binders to non-calcium&#44; non-aluminium-containing binders&#58;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Sevelamer therapy increases osteoblast surfaces of long bones and bone formation rates and shown to reverse CKD related osteopenia&#46;<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">49</span></a> A randomized&#44; prospective&#44; open label study&#44; evaluated 119 HD patients with bone biopsies &#40;59&#37; having ABD at baseline&#41; at the beginning and after 1-year treatment period with sevelamer or calcium compound&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">50</span></a> Sevelamer group resulted in no statistically significant changes in bone turnover or mineralization compared with calcium&#44; but bone formation rate increased and trabecular architecture improved only with sevelamer &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;019&#41;&#46; In another Japanese study of 40 HD patients who were switched from calcium to sevelamer&#44; showed improvement in bone turnover markers over a period of one year&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">51</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">The treatment with lanthanum has also shown beneficial effects in bone histology in various studies&#46; There has been a normalization of the bone histo-morphometric parameters and almost no evolution toward low bone turnover after one year of treatment with lanthanum &#40;compared to calcium carbonate treated patients&#41; in a multi-centric randomized study&#46;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">52</span></a> An additional follow up in a subset of patients &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>20&#41; showed that bone deposition of lanthanum is low after one year&#46;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">53</span></a> Furthermore&#44; there is a slow release of lanthanum from its bone deposits two years after stopping the treatment without any features of aluminium-like bone toxicity&#46; The results of lanthanum treatment were also encouraging in a Japanese prospective dialysis study where two patients with ABD improved after one year of lanthanum treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">54</span></a> The beneficial effects of lanthanum on bone histology persisted for three years&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">2&#46;</span><p id="par0120" class="elsevierStylePara elsevierViewall">Oral daily dietary calcium intake should be evaluated and reduced to 1200<span class="elsevierStyleHsp" style=""></span>mg&#46; As per current guidelines&#44; daily calcium intake of men aged 19&#8211;70 and women aged 19&#8211;50 should be up to 1000 and beyond that up to 1200<span class="elsevierStyleHsp" style=""></span>mg&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">55</span></a></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">3&#46;</span><p id="par0125" class="elsevierStylePara elsevierViewall">Stop&#47;reduce active vitamin D medications&#46;</p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">4&#46;</span><p id="par0130" class="elsevierStylePara elsevierViewall">Lower dialysate calcium to 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;L or below&#58; In a study&#44; fifty-one biopsy-proven ABD patients treated with PD were randomized to treatment with control calcium &#40;1&#46;62<span class="elsevierStyleHsp" style=""></span>mM&#41;&#44; or low calcium &#40;1&#46;0<span class="elsevierStyleHsp" style=""></span>mM&#41; dialysate over a 16-month period&#46;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">56</span></a> Bone formation rates increased from18&#46;1<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>5&#46;6<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day to 159<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>59&#46;4<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41; in the low calcium group&#46; There was also a reduction in hypercalcemic episodes&#44; which resulted in increased PTH levels and normalization of bone turnover in patients with ABD&#46; In another&#44; randomized&#44; controlled trial of 52 hemodialysis patients over a period of 6 months&#44; all bone parameters in the low calcium dialysate &#40;1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#41; group were significantly higher than in the group with dialysate calcium of 1&#46;75<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">57</span></a> Preventing an overall positive calcium balance and resultant PTH stimulation is useful in these patients&#46; Thus&#44; a low calcium dialysate might be regarded a valuable therapeutic option for ABD patients&#46;</p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">5&#46;</span><p id="par0135" class="elsevierStylePara elsevierViewall">A bone biopsy to confirm diagnosis and to assess bone aluminium content and distribution should be done in only indicated patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0640"><span class="elsevierStyleSup">58&#44;59</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">6&#46;</span><p id="par0140" class="elsevierStylePara elsevierViewall">Bisphosphonates administration with monitoring for biomarkers&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">60</span></a></p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">7&#46;</span><p id="par0145" class="elsevierStylePara elsevierViewall">Calcilytics are currently of undetermined value&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">61</span></a> Ronacaleret&#44; a calcilytic which allows bone formation by serving as a CASR antagonist and increasing endogenous production of PTH showed initial encouraging results in post-menopausal women&#46;<a class="elsevierStyleCrossRef" href="#bib0660"><span class="elsevierStyleSup">62</span></a> This agent is yet to be tested in ABD&#46;</p></li><li class="elsevierStyleListItem" id="lsti0055"><span class="elsevierStyleLabel">8&#46;</span><p id="par0150" class="elsevierStylePara elsevierViewall">Teriparatide &#40;PTH &#40;1&#8211;34&#41;&#41; as a bone stimulating agent&#58; Teriparatide &#40;recombinant human parathyroid hormone&#41; is an anabolic agent approved for the treatment of patients at high risk for fracture&#46;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">63</span></a> It has been hypothesized that teriparatide would be effective for ABD based on its ability to promote both osteoblast and osteoclast activity&#46; Because teriparatide promotes bone formation&#44; it should also allow the skeleton to recover its function as a reservoir for excess calcium and phosphorus&#46; However&#44; it is not recommended in children with open epiphysis and in those with risk for osteosarcoma&#46; Dose and duration dependent risk of malignant bone tumor was found in rat studies&#44; and therefore&#44; warning for osteosarcoma and hypercalcemia have been added for its usage beyond 2 years&#46; In an open-label&#44; prospective&#44; 6-month observational pilot-study of seven HD patients with ABD and a median iPTH level of 22<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#44; all patients received 20<span class="elsevierStyleHsp" style=""></span>&#956;g teriparatide&#47;day subcutaneously&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">64</span></a> At 6 months&#44; compared to pre-treatment values&#44; calculated monthly changes in BMD improved significantly in both the lumbar spine and femoral neck &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;02&#41;&#46; Sumida et al administered teriparatide 56&#46;5<span class="elsevierStyleHsp" style=""></span>&#956;g subcutaneous once weekly to 22 HD patients with serum PTH<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>60<span class="elsevierStyleHsp" style=""></span>pg&#47;mL&#46;<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">65</span></a> BMD at lumbar spine increased by 3&#46;3<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>1&#46;9&#37; &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41; and 3&#46;0<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>1&#46;8&#37; at 24 and 48 weeks respectively&#44; without significant changes in femoral neck and distal radius BMD&#46; Further clinical studies are needed to establish teriparatide as a therapeutic option for dialysis patients with ABD&#46;</p></li><li class="elsevierStyleListItem" id="lsti0060"><span class="elsevierStyleLabel">9&#46;</span><p id="par0155" class="elsevierStylePara elsevierViewall">Abaloparatide&#58; a PTH-related peptide analogue that specifically activates PTH receptor type I pathway was developed as another anabolic drug&#46;<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">66</span></a> In a phase 3 Abaloparatide Comparator Trial In Vertebral Endpoints &#40;ACTIVE&#41; trial&#44; treatment with abaloparatide for 18 months significantly increased BMD and decreased the risk of vertebral&#44; nonvertebral&#44; clinical&#44; and major osteoporotic fractures compared with a placebo&#46;<a class="elsevierStyleCrossRef" href="#bib0685"><span class="elsevierStyleSup">67</span></a> Abaloparatide is approved in the US for the treatment of postmenopausal women with osteoporosis at high risk for fracture&#46; However&#44; potential benefits of this drug in ABD needs to be explored&#46;</p></li><li class="elsevierStyleListItem" id="lsti0065"><span class="elsevierStyleLabel">10&#46;</span><p id="par0160" class="elsevierStylePara elsevierViewall">Romosozumab&#58; Romosozumab is a monoclonal antibody that binds and inhibits sclerostin&#46; &#40;The wingless in Drosophila and integrated in vertebrate &#40;Wnt&#41; signaling pathway is a crucial regulator of osteoblast recruitment&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">68</span></a> Sclerostin is an endogenous inhibitor of this pathway&#44; thereby inhibiting osteoblast recruitment and decreasing bone formation&#46;<a class="elsevierStyleCrossRef" href="#bib0695"><span class="elsevierStyleSup">69</span></a> The resultant effects include increase in bone formation and decrease in bone resorption&#46; The beneficial effects of this drug compared to placebo in increasing BMD and reducing vertebral fractures in postmenopausal osteoporotic women have been seen in clinical studies&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">70</span></a> Identical triumph in using romosozumab to improve bone density in patients with ABD&#44; although might be promising in coming years&#44; but it&#39;s important not to overlook the potential risk of myocardial infarction&#44; stroke&#44; and cardiovascular death and should not be initiated in patient with such risk factors&#46;</p></li></ul></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conclusion</span><p id="par0165" class="elsevierStylePara elsevierViewall">ABD is a complex disease process which is associated with increased morbidity and mortality&#46; Prevention through the judicious use of calcium containing phosphate binders and antiparathyroid agents is likely to be more effective than the treatment of established disease&#46; However&#44; there are promising therapeutic interventions whose role needs to be established in appropriate trials&#46;</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Compliance with ethical standards</span><p id="par0170" class="elsevierStylePara elsevierViewall">This article does not contain any studies with human participants or animals performed by any of the authors&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Informed consent</span><p id="par0175" class="elsevierStylePara elsevierViewall">Not applicable for this review article&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Financial disclosure</span><p id="par0180" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Conflicts of interest</span><p id="par0185" class="elsevierStylePara elsevierViewall">None&#46;</p></span></span>"
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          "titulo" => "Introduction"
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          "identificador" => "sec0010"
          "titulo" => "ABD in course of CKD and prevalence"
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          "titulo" => "Risk factors"
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          "titulo" => "ABD pathophysiology"
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          "titulo" => "Diagnosis"
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              "titulo" => "Ectopic calcification"
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          "identificador" => "sec0040"
          "titulo" => "ABD and mortality"
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          "identificador" => "sec0045"
          "titulo" => "Key measures in the management of ABD"
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        12 => array:2 [
          "identificador" => "sec0050"
          "titulo" => "Conclusion"
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          "titulo" => "Compliance with ethical standards"
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          "titulo" => "Informed consent"
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    "fechaRecibido" => "2020-08-21"
    "fechaAceptado" => "2020-11-16"
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            0 => "Adynamic bone disease"
            1 => "CKD-MBD"
            2 => "Bone biopsy"
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        0 => array:4 [
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          "palabras" => array:3 [
            0 => "Enfermedad &#243;sea adin&#225;mica"
            1 => "ERC-TMO"
            2 => "Biopsia &#243;sea"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The bone and mineral disorders form an integral part of the management of a chronic kidney disease &#40;CKD&#41; patient&#46; Amongst various types of bone pathologies in chronic kidney disease-mineral bone disorder &#40;CKD-MBD&#41;&#44; the prevalence of adynamic bone disease &#40;ABD&#41; is increasing&#46; The present review discusses the updated pathophysiology&#44; risk factors&#44; and management of this disorder&#46;</p></span>"
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        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Los trastornos &#243;seos y minerales son una parte fundamental del tratamiento del paciente con enfermedad renal cr&#243;nica &#40;ERC&#41;&#46; Entre los distintos tipos de patolog&#237;as &#243;seas en la enfermedad renal cr&#243;nica-trastorno mineral &#243;seo &#40;ERC-TMO&#41;&#44; la prevalencia de la enfermedad &#243;sea adin&#225;mica &#40;EOA&#41; est&#225; aumentando&#46; En esta revisi&#243;n se analizan los datos actuales sobre la fisiopatolog&#237;a&#44; los factores de riesgo y el tratamiento de este trastorno&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Risk factors for adynamic bone disease&#46;</p>"
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        "fuente" => "&#40;Permission from Sista SK&#44; Arum SM&#46; Management of adynamic bone disease in chronic kidney disease&#58; A brief review&#46; J Clin Transl Endocrinol&#46; 2016 Jul 25&#59;5&#58;32&#8211;5&#46; <span class="elsevierStyleInterRef" id="intr0005" href="doi:10.1016/j.jcte.2016.07.002">doi&#58;10&#46;1016&#47;j&#46;jcte&#46;2016&#46;07&#46;002</span>&#46; eCollection 2016 Sep under-Open access article under the CC BY-NC-ND license &#40;<span class="elsevierStyleInterRef" id="intr0010" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http&#58;&#47;&#47;creativecommons&#46;org&#47;licenses&#47;by-nc-nd&#47;4&#46;0&#47;</span>&#41;&#46;"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Adynamic bone disease&#46; Depicts a classic bone biopsy featuring minimal osteoid &#40;black arrow&#41; and nearly no activity of osteoblasts or osteoclasts&#46; Image courtesy of Avudai Maran&#44; PhD and Bart Clarke&#44; MD &#8211; Biomaterials and Histomorphometry Core Lab&#44; Mayo Clinic&#44; Rochester&#44; MN&#46;</p>"
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                    0 => array:2 [
                      "titulo" => "Aluminum-associated bone disease in chronic renal failure&#58; high prevalence in a long-term dialysis population"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "D&#46;L&#46; Andress"
                            1 => "N&#46;A&#46; Maloney"
                            2 => "D&#46;B&#46; Endres"
                            3 => "D&#46;J&#46; Sherrard"
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Brief review
Adynamic bone disease: Revisited
Enfermedad ósea adinámica: Una revisión
Sonia Sharmaa, Ankur Guptab,
Autor para correspondencia
parthankur@yahoo.com

Corresponding author.
a Pediatric Nephrology, Max Superspeciality Hospital, Shalimar Bagh, New Delhi, India
b Department of Medicine, Whakatane Hospital, Whakatane, New Zealand
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    "titulo" => "Adynamic bone disease&#58; Revisited"
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        "fuente" => "&#40;Permission from Sista SK&#44; Arum SM&#46; Management of adynamic bone disease in chronic kidney disease&#58; A brief review&#46; J Clin Transl Endocrinol&#46; 2016 Jul 25&#59;5&#58;32&#8211;5&#46; <span class="elsevierStyleInterRef" id="intr0005" href="doi:10.1016/j.jcte.2016.07.002">doi&#58;10&#46;1016&#47;j&#46;jcte&#46;2016&#46;07&#46;002</span>&#46; eCollection 2016 Sep under-Open access article under the CC BY-NC-ND license &#40;<span class="elsevierStyleInterRef" id="intr0010" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http&#58;&#47;&#47;creativecommons&#46;org&#47;licenses&#47;by-nc-nd&#47;4&#46;0&#47;</span>&#41;&#46;"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Adynamic bone disease&#46; Depicts a classic bone biopsy featuring minimal osteoid &#40;black arrow&#41; and nearly no activity of osteoblasts or osteoclasts&#46; Image courtesy of Avudai Maran&#44; PhD and Bart Clarke&#44; MD &#8211; Biomaterials and Histomorphometry Core Lab&#44; Mayo Clinic&#44; Rochester&#44; MN&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">The term adynamic bone disease &#40;ABD&#41; or aplastic bone disease was first described in early 1980s&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">1&#44;2</span></a> ABD is defined by faulty rate of collagen synthesis and mineralization i&#46;e&#46; low-bone turnover without osteoid accumulation &#40;thin osteoid seam&#41;&#46; It needs to be differentiated from osteomalacia which is also a low turnover disease but their defect in mineralization exceeds the defects in bone formation and therefore&#44; there is a relative osteoid excess in osteomalacia&#46; In ABD&#44; there are few or no osteoblasts&#44; minimal or no peri-trabecular fibrosis&#44; substantially low bone formation rate &#40;BFR&#41; and the number of re-modeling sites is also low&#46;<a class="elsevierStyleCrossRefs" href="#bib0365"><span class="elsevierStyleSup">3&#44;4</span></a> Here&#44; we would be briefly summarizing ABD in the following sections with special focus on newer treatment strategies&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">ABD in course of CKD and prevalence</span><p id="par0010" class="elsevierStylePara elsevierViewall">ABD is most common of all CKD associated MB disorders &#40;osteitis fibrosa&#44; osteomalacia&#44; mixed turnover disorder&#41;&#44; and requires preventive care even from early stages of CKD&#46; Though&#44; advances CKD stages are at high risk of ABD with prevalence rate variable from 10 to 40&#37; in advanced stages to 10&#8211;50&#37; in dialysis patients but it is also not uncommon to see in earlier CKD stages 3&#8211;5 with a prevalence rate showed rising trends and reaches to about 18&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0375"><span class="elsevierStyleSup">5&#44;6</span></a> In one study of patients with pre-dialysis CKD&#44; ABD was seen in 12&#37; of bone biopsies&#46; Increased average age&#44; percentage of patient with diabetes and high vitamin D and oral calcium supplements are important contributor to the rising trends&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">7</span></a> Peritoneal dialysis &#40;PD&#41; is more commonly associated with ABD &#40;almost in 50&#37;&#41; than hemodialysis &#40;HD&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">8</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Risk factors</span><p id="par0015" class="elsevierStylePara elsevierViewall">The risk factors for ABD are multifactorial &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Elderly individuals&#44; diabetes&#44; high calcium load&#44; vitamin D excess&#44; overzealous treatment of hyperparathyroidism&#44; low parathyroid hormone &#40;PTH&#41; levels&#44; parathyroidectomy&#44; systemic inflammation&#44; calcimimetics&#44; and bisphosphonates have all been commonly implicated&#46;<a class="elsevierStyleCrossRefs" href="#bib0395"><span class="elsevierStyleSup">9&#44;10</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">High concentrations of glucose and insulin deficiency suppresses PTH secretion in parathyroid cell cultures&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">11</span></a> In a study of rats with streptozocin-induced diabetes&#44; bone histology was characterised by low bone formation&#44; reduced osteoid measurements&#44; decreased osteoclast number&#44; and less bone collagen synthesis&#46;<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">12</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">High calcium load&#44; whether oral dietary intake or in dialysis solution and low phosphate diet suppresses parathyroid gland hyperplasia by induction of p21 and reduction of transforming growth factor alpha&#46; In addition&#44; calcitriol also induces p21 and act via membrane trafficking of the epithelial growth factor receptor &#40;EGFR&#41; and down regulated signaling&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">13</span></a> Adynamic bone is thus a result of over-suppression of PTH synthesis and secretion&#46;<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">14</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">CKD progression is coupled with PTH resistance due to changes in the tissue expression of their regulators&#44; disturbances of hepatic and renal PTH catabolism and downregulation or desensitization of PTH1R&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">15</span></a> It is also affected by serum level of phosphate&#44; indoxyl sulphate and paracresyl sulphate&#46; In addition&#44; treatment resulting excess of CaSR and vitamin D receptor activation along with FGF23-Klotho endocrine axis suppresses PTH secretion&#46; FGF23 binds to the Klotho to activate MAPK-pathway and there is also an early inhibition of the Wnt pathway with an increase in the expression of sclerostin&#46;<a class="elsevierStyleCrossRefs" href="#bib0430"><span class="elsevierStyleSup">16&#44;17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Bisphosphonates are risk factor in advanced CKD for ABD in presence of abnormal laboratory parameters&#46; Metanalysis of bisphosphonates in age related CKD 1&#8211;3 concluded it as a safe therapy in absence of laboratory features of CKD-MBD&#46;<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">18</span></a> In another study of 31 CKD stage 5 hemodialysis patients&#44; short term usage of bisphosphonates did no harm and bone biopsy was not advised&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">19</span></a> However&#44; study of thirteen CKD patients &#40;stage 2&#8211;4&#41; treated from 4 to &#62;60 months with bisphosphonates for osteopenia or osteoporosis&#44; underwent trabecular bone biopsies from the iliac crest and all were diagnosed with adynamic bone on biopsy evaluation&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">20</span></a> It is therefore necessary to warn for a possible harm before administering bisphosphonates in this patient population&#46; KDIGO suggests that treatment choices including bisphosphonates take into account the magnitude and reversibility of the biochemical abnormalities and the progression of CKD&#44; with consideration of a bone biopsy in patients with CKD G3a-G5D with biochemical abnormalities of CKD-MBD and low BMD and&#47;or fragility fractures&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">21</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Other potential mechanisms of low bone formation include elevated circulating cytokine levels &#40;interleukin &#40;IL&#41;-I&#44; tumor necrosis factor &#40;TNF&#41;&#44; low estrogen and testosterone levels&#44; decreased osteoblast proliferation from the direct effect of accumulated uremic inhibitors&#44; and decreased circulating insulin-like growth factor &#40;IGF&#41;-I activity either from low IGF-I and&#47;or IGF-binding protein &#40;IGFBP&#41;-5 levels or from excess IGFBPs that inhibit the action of IGF-I&#46;<a class="elsevierStyleCrossRefs" href="#bib0460"><span class="elsevierStyleSup">22&#8211;29</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">ABD pathophysiology</span><p id="par0045" class="elsevierStylePara elsevierViewall">Three elements of bone characterize different types of CKD&#8211;MBD&#46; These are bone turnover&#44; bone mineralization and fibrosis quantification assessment&#46; The practiced metric for ABD includes &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0455"><span class="elsevierStyleSup">21&#44;30&#44;31</span></a><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Bone formation rate less than 97 to 108<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0055" class="elsevierStylePara elsevierViewall">Osteoid volume less than 12&#8211;15&#37;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#46;</span><p id="par0060" class="elsevierStylePara elsevierViewall">No &#40;minimal&#41; fibrosis&#46;</p></li></ul></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">Osteoblastic proteins stimulate mineralization&#46; Fibroblast growth factor-23 FGF-23 is formed by osteoblasts and osteocytes in bone and keep a physiological check on mineral levels by its action on parathyroid&#44; kidney and bone and therefore affecting calcium&#44; phosphorus&#44; calcitriol and parathormone synthesis&#46; It gets activated after its binding to a transmembrane protein&#44; klotho and combination then result in suppression of both PTH and 1&#44;25-dihydroxyvitamin D through downregulating action on NaPi-2a &#40;SLC34A1&#41; and NaPi-2c &#40;SLC34A3&#41; channels in the proximal tubules and distal tubule and suppression of 1&#945;-hydroxylase &#40;thus lower down phosphorous level and calcitriol&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0510"><span class="elsevierStyleSup">32&#44;33</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Bone turnover is also affected by many local factors as growth factors and cytokines and interleukins by their action on PTH&#46; Cytokines regulate osteoclastogenesis and osteoprotegerin &#40;OPG&#41;&#44; which is a complex system to regulate bone resorption&#46;<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">34</span></a> It has a negative association with PTH in ABD&#46; Osteoprotegerin is also a soluble member of the tumor necrosis factor and associated with atherogenesis and endothelial dysfunction&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Clinical features</span><p id="par0075" class="elsevierStylePara elsevierViewall">There are no pathognomonic clinical signs of ABD&#46; The two most common symptoms are skeletal pain and fractures&#46;<a class="elsevierStyleCrossRefs" href="#bib0525"><span class="elsevierStyleSup">35&#44;36</span></a> Although&#44; biopsy proven adynamic bone as a risk factor for fracture has not been demonstrated in the studies but recent guidelines do not recommend routine bone biopsy for making diagnosis&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Diagnosis</span><p id="par0080" class="elsevierStylePara elsevierViewall">No biochemical markers can accurately define ABD&#46; Bone alkaline phosphatase &#40;BAP&#41; is the most useful parameter for bone formation as elevated levels&#44; exclude ABD while low PTH levels distinguishes it from high turnover CKD-MBD&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">37</span></a> Relatively low&#47;normal PTH served as a surrogate marker of low bone turnover and identifies fracture risk in ABD&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">The histomorphometric examination of an under calcified bone sample is the gold standard for the diagnosis of ABD&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">38</span></a> The requisites include pre-biopsy in-vivo tetracycline double labelling&#44; amyloid and aluminium staining&#46; Both cortical and trabecular bone should be assessed for static and dynamic parameters to interpret bone metabolism in totality&#46; Favoured site of biopsy is 2<span class="elsevierStyleHsp" style=""></span>cm posterior and 2<span class="elsevierStyleHsp" style=""></span>cm inferior to the anterior iliac crest&#46; The instrument is specifically planned to obtain a core of bone of at least 4&#8211;5<span class="elsevierStyleHsp" style=""></span>mm diameter&#46;<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">39</span></a></p><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Ectopic calcification</span><p id="par0090" class="elsevierStylePara elsevierViewall">A notable feature of ABD is diminished assimilation of serum calcium into the bone&#46; In a study of 101 hemodialysis patients&#44; 52&#37; had moderate or severe coronary artery calcification &#40;CAC&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">40</span></a> This association was pronounced with older age&#44; higher BMI&#44; inflammation&#44; reduced trabecular volume and with higher osteoprotegerin levels&#46; Asci et al&#46; noted that when only HD patients with CAC were included for analysis&#44; there was a U-shaped relationship between CAC and bone turnover&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">41</span></a> London et al concluded that a high arterial calcification score is defined by bone histo-morphometry suggestive of low bone activity and ABD&#46;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">42</span></a> Studies have shown that anabolic bone stimulating agents such as bone morphogenic protein 7 &#40;BMP-7&#41; or synthetic PTH &#40;1&#8211;34&#41; improved bone turnover and skeletal mineralization and decreased calcium deposition in the aorta&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">43</span></a> The mechanism of action of PTH &#40;1-34&#41; seems to be mediated through a combination of both direct and osteopontin effects&#46;</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">ABD and mortality</span><p id="par0095" class="elsevierStylePara elsevierViewall">Multiple studies have documented relation between low and very high PTH &#40;U-shaped pattern&#41; and risk of sudden death&#46;<a class="elsevierStyleCrossRefs" href="#bib0570"><span class="elsevierStyleSup">44&#8211;46</span></a> In a multi-centric French ARNOS cohort of 1&#44;348 prevalent HD patients&#44; very low PTH levels &#40;&#60;50<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#41; was associated with poor survival rates &#40;HR&#58; 1&#46;4 &#40;1&#46;07&#8211;1&#46;8&#41;&#44; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;006&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">47</span></a> Also Korean multicenter prospective cohort study of 1&#44;771 incident dialysis patients&#44; revealed association of low serum PTH level &#40;&#60;150<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#41; and infection-related mortality &#40;hazard ratio &#91;HR&#93;&#44; 2&#46;52&#59; 95&#37; CI&#44; 1&#46;06&#8211;5&#46;99&#59; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;04&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">48</span></a> With the understanding of rise of PTH level with CKD progression&#44; KDIGO suggest maintaining intact PTH levels in the range of approximately two to nine times the upper normal limit for the assay&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">21</span></a> Guidelines gave emphasis for keeping higher targets for PTH as per the stages of CKD and minimise over usage of calcium-based binders and Vitamin D analogues&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Key measures in the management of ABD</span><p id="par0100" class="elsevierStylePara elsevierViewall">The chief management strategy aims to increase PTH synthesis&#46; The following measures may be useful&#58;<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">1&#46;</span><p id="par0105" class="elsevierStylePara elsevierViewall">Switch from calcium-containing phosphate binders to non-calcium&#44; non-aluminium-containing binders&#58;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Sevelamer therapy increases osteoblast surfaces of long bones and bone formation rates and shown to reverse CKD related osteopenia&#46;<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">49</span></a> A randomized&#44; prospective&#44; open label study&#44; evaluated 119 HD patients with bone biopsies &#40;59&#37; having ABD at baseline&#41; at the beginning and after 1-year treatment period with sevelamer or calcium compound&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">50</span></a> Sevelamer group resulted in no statistically significant changes in bone turnover or mineralization compared with calcium&#44; but bone formation rate increased and trabecular architecture improved only with sevelamer &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;019&#41;&#46; In another Japanese study of 40 HD patients who were switched from calcium to sevelamer&#44; showed improvement in bone turnover markers over a period of one year&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">51</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">The treatment with lanthanum has also shown beneficial effects in bone histology in various studies&#46; There has been a normalization of the bone histo-morphometric parameters and almost no evolution toward low bone turnover after one year of treatment with lanthanum &#40;compared to calcium carbonate treated patients&#41; in a multi-centric randomized study&#46;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">52</span></a> An additional follow up in a subset of patients &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>20&#41; showed that bone deposition of lanthanum is low after one year&#46;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">53</span></a> Furthermore&#44; there is a slow release of lanthanum from its bone deposits two years after stopping the treatment without any features of aluminium-like bone toxicity&#46; The results of lanthanum treatment were also encouraging in a Japanese prospective dialysis study where two patients with ABD improved after one year of lanthanum treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">54</span></a> The beneficial effects of lanthanum on bone histology persisted for three years&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">2&#46;</span><p id="par0120" class="elsevierStylePara elsevierViewall">Oral daily dietary calcium intake should be evaluated and reduced to 1200<span class="elsevierStyleHsp" style=""></span>mg&#46; As per current guidelines&#44; daily calcium intake of men aged 19&#8211;70 and women aged 19&#8211;50 should be up to 1000 and beyond that up to 1200<span class="elsevierStyleHsp" style=""></span>mg&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">55</span></a></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">3&#46;</span><p id="par0125" class="elsevierStylePara elsevierViewall">Stop&#47;reduce active vitamin D medications&#46;</p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">4&#46;</span><p id="par0130" class="elsevierStylePara elsevierViewall">Lower dialysate calcium to 1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;L or below&#58; In a study&#44; fifty-one biopsy-proven ABD patients treated with PD were randomized to treatment with control calcium &#40;1&#46;62<span class="elsevierStyleHsp" style=""></span>mM&#41;&#44; or low calcium &#40;1&#46;0<span class="elsevierStyleHsp" style=""></span>mM&#41; dialysate over a 16-month period&#46;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">56</span></a> Bone formation rates increased from18&#46;1<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>5&#46;6<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day to 159<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>59&#46;4<span class="elsevierStyleHsp" style=""></span>&#956;m<span class="elsevierStyleSup">2</span>&#47;mm<span class="elsevierStyleSup">2</span>&#47;day &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41; in the low calcium group&#46; There was also a reduction in hypercalcemic episodes&#44; which resulted in increased PTH levels and normalization of bone turnover in patients with ABD&#46; In another&#44; randomized&#44; controlled trial of 52 hemodialysis patients over a period of 6 months&#44; all bone parameters in the low calcium dialysate &#40;1&#46;25<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#41; group were significantly higher than in the group with dialysate calcium of 1&#46;75<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">57</span></a> Preventing an overall positive calcium balance and resultant PTH stimulation is useful in these patients&#46; Thus&#44; a low calcium dialysate might be regarded a valuable therapeutic option for ABD patients&#46;</p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">5&#46;</span><p id="par0135" class="elsevierStylePara elsevierViewall">A bone biopsy to confirm diagnosis and to assess bone aluminium content and distribution should be done in only indicated patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0640"><span class="elsevierStyleSup">58&#44;59</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">6&#46;</span><p id="par0140" class="elsevierStylePara elsevierViewall">Bisphosphonates administration with monitoring for biomarkers&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">60</span></a></p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">7&#46;</span><p id="par0145" class="elsevierStylePara elsevierViewall">Calcilytics are currently of undetermined value&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">61</span></a> Ronacaleret&#44; a calcilytic which allows bone formation by serving as a CASR antagonist and increasing endogenous production of PTH showed initial encouraging results in post-menopausal women&#46;<a class="elsevierStyleCrossRef" href="#bib0660"><span class="elsevierStyleSup">62</span></a> This agent is yet to be tested in ABD&#46;</p></li><li class="elsevierStyleListItem" id="lsti0055"><span class="elsevierStyleLabel">8&#46;</span><p id="par0150" class="elsevierStylePara elsevierViewall">Teriparatide &#40;PTH &#40;1&#8211;34&#41;&#41; as a bone stimulating agent&#58; Teriparatide &#40;recombinant human parathyroid hormone&#41; is an anabolic agent approved for the treatment of patients at high risk for fracture&#46;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">63</span></a> It has been hypothesized that teriparatide would be effective for ABD based on its ability to promote both osteoblast and osteoclast activity&#46; Because teriparatide promotes bone formation&#44; it should also allow the skeleton to recover its function as a reservoir for excess calcium and phosphorus&#46; However&#44; it is not recommended in children with open epiphysis and in those with risk for osteosarcoma&#46; Dose and duration dependent risk of malignant bone tumor was found in rat studies&#44; and therefore&#44; warning for osteosarcoma and hypercalcemia have been added for its usage beyond 2 years&#46; In an open-label&#44; prospective&#44; 6-month observational pilot-study of seven HD patients with ABD and a median iPTH level of 22<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#44; all patients received 20<span class="elsevierStyleHsp" style=""></span>&#956;g teriparatide&#47;day subcutaneously&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">64</span></a> At 6 months&#44; compared to pre-treatment values&#44; calculated monthly changes in BMD improved significantly in both the lumbar spine and femoral neck &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;02&#41;&#46; Sumida et al administered teriparatide 56&#46;5<span class="elsevierStyleHsp" style=""></span>&#956;g subcutaneous once weekly to 22 HD patients with serum PTH<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>60<span class="elsevierStyleHsp" style=""></span>pg&#47;mL&#46;<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">65</span></a> BMD at lumbar spine increased by 3&#46;3<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>1&#46;9&#37; &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41; and 3&#46;0<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>1&#46;8&#37; at 24 and 48 weeks respectively&#44; without significant changes in femoral neck and distal radius BMD&#46; Further clinical studies are needed to establish teriparatide as a therapeutic option for dialysis patients with ABD&#46;</p></li><li class="elsevierStyleListItem" id="lsti0060"><span class="elsevierStyleLabel">9&#46;</span><p id="par0155" class="elsevierStylePara elsevierViewall">Abaloparatide&#58; a PTH-related peptide analogue that specifically activates PTH receptor type I pathway was developed as another anabolic drug&#46;<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">66</span></a> In a phase 3 Abaloparatide Comparator Trial In Vertebral Endpoints &#40;ACTIVE&#41; trial&#44; treatment with abaloparatide for 18 months significantly increased BMD and decreased the risk of vertebral&#44; nonvertebral&#44; clinical&#44; and major osteoporotic fractures compared with a placebo&#46;<a class="elsevierStyleCrossRef" href="#bib0685"><span class="elsevierStyleSup">67</span></a> Abaloparatide is approved in the US for the treatment of postmenopausal women with osteoporosis at high risk for fracture&#46; However&#44; potential benefits of this drug in ABD needs to be explored&#46;</p></li><li class="elsevierStyleListItem" id="lsti0065"><span class="elsevierStyleLabel">10&#46;</span><p id="par0160" class="elsevierStylePara elsevierViewall">Romosozumab&#58; Romosozumab is a monoclonal antibody that binds and inhibits sclerostin&#46; &#40;The wingless in Drosophila and integrated in vertebrate &#40;Wnt&#41; signaling pathway is a crucial regulator of osteoblast recruitment&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">68</span></a> Sclerostin is an endogenous inhibitor of this pathway&#44; thereby inhibiting osteoblast recruitment and decreasing bone formation&#46;<a class="elsevierStyleCrossRef" href="#bib0695"><span class="elsevierStyleSup">69</span></a> The resultant effects include increase in bone formation and decrease in bone resorption&#46; The beneficial effects of this drug compared to placebo in increasing BMD and reducing vertebral fractures in postmenopausal osteoporotic women have been seen in clinical studies&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">70</span></a> Identical triumph in using romosozumab to improve bone density in patients with ABD&#44; although might be promising in coming years&#44; but it&#39;s important not to overlook the potential risk of myocardial infarction&#44; stroke&#44; and cardiovascular death and should not be initiated in patient with such risk factors&#46;</p></li></ul></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conclusion</span><p id="par0165" class="elsevierStylePara elsevierViewall">ABD is a complex disease process which is associated with increased morbidity and mortality&#46; Prevention through the judicious use of calcium containing phosphate binders and antiparathyroid agents is likely to be more effective than the treatment of established disease&#46; However&#44; there are promising therapeutic interventions whose role needs to be established in appropriate trials&#46;</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Compliance with ethical standards</span><p id="par0170" class="elsevierStylePara elsevierViewall">This article does not contain any studies with human participants or animals performed by any of the authors&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Informed consent</span><p id="par0175" class="elsevierStylePara elsevierViewall">Not applicable for this review article&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Financial disclosure</span><p id="par0180" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Conflicts of interest</span><p id="par0185" class="elsevierStylePara elsevierViewall">None&#46;</p></span></span>"
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          "titulo" => "Introduction"
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        5 => array:2 [
          "identificador" => "sec0010"
          "titulo" => "ABD in course of CKD and prevalence"
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        6 => array:2 [
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          "titulo" => "Risk factors"
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        7 => array:2 [
          "identificador" => "sec0020"
          "titulo" => "ABD pathophysiology"
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          "identificador" => "sec0025"
          "titulo" => "Clinical features"
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          "identificador" => "sec0030"
          "titulo" => "Diagnosis"
          "secciones" => array:1 [
            0 => array:2 [
              "identificador" => "sec0035"
              "titulo" => "Ectopic calcification"
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        10 => array:2 [
          "identificador" => "sec0040"
          "titulo" => "ABD and mortality"
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        11 => array:2 [
          "identificador" => "sec0045"
          "titulo" => "Key measures in the management of ABD"
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        12 => array:2 [
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          "titulo" => "Conclusion"
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          "titulo" => "Compliance with ethical standards"
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          "titulo" => "Informed consent"
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            0 => "Adynamic bone disease"
            1 => "CKD-MBD"
            2 => "Bone biopsy"
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        0 => array:4 [
          "clase" => "keyword"
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          "palabras" => array:3 [
            0 => "Enfermedad &#243;sea adin&#225;mica"
            1 => "ERC-TMO"
            2 => "Biopsia &#243;sea"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The bone and mineral disorders form an integral part of the management of a chronic kidney disease &#40;CKD&#41; patient&#46; Amongst various types of bone pathologies in chronic kidney disease-mineral bone disorder &#40;CKD-MBD&#41;&#44; the prevalence of adynamic bone disease &#40;ABD&#41; is increasing&#46; The present review discusses the updated pathophysiology&#44; risk factors&#44; and management of this disorder&#46;</p></span>"
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      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Los trastornos &#243;seos y minerales son una parte fundamental del tratamiento del paciente con enfermedad renal cr&#243;nica &#40;ERC&#41;&#46; Entre los distintos tipos de patolog&#237;as &#243;seas en la enfermedad renal cr&#243;nica-trastorno mineral &#243;seo &#40;ERC-TMO&#41;&#44; la prevalencia de la enfermedad &#243;sea adin&#225;mica &#40;EOA&#41; est&#225; aumentando&#46; En esta revisi&#243;n se analizan los datos actuales sobre la fisiopatolog&#237;a&#44; los factores de riesgo y el tratamiento de este trastorno&#46;</p></span>"
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        "fuente" => "&#40;Permission from Sista SK&#44; Arum SM&#46; Management of adynamic bone disease in chronic kidney disease&#58; A brief review&#46; J Clin Transl Endocrinol&#46; 2016 Jul 25&#59;5&#58;32&#8211;5&#46; <span class="elsevierStyleInterRef" id="intr0005" href="doi:10.1016/j.jcte.2016.07.002">doi&#58;10&#46;1016&#47;j&#46;jcte&#46;2016&#46;07&#46;002</span>&#46; eCollection 2016 Sep under-Open access article under the CC BY-NC-ND license &#40;<span class="elsevierStyleInterRef" id="intr0010" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http&#58;&#47;&#47;creativecommons&#46;org&#47;licenses&#47;by-nc-nd&#47;4&#46;0&#47;</span>&#41;&#46;"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Adynamic bone disease&#46; Depicts a classic bone biopsy featuring minimal osteoid &#40;black arrow&#41; and nearly no activity of osteoblasts or osteoclasts&#46; Image courtesy of Avudai Maran&#44; PhD and Bart Clarke&#44; MD &#8211; Biomaterials and Histomorphometry Core Lab&#44; Mayo Clinic&#44; Rochester&#44; MN&#46;</p>"
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