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    8 views7 pages

    Osteodistrophy

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    ricardoatejass

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    © All Rights Reserved
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    22)9122, 2:57 Renal Osteodystrophy - StatPearls- NCBI Bookshelf Renal Osteadystrophy Shah A. Reddula NR Continuing Education Activity Renal osteodystrophy i one ofthe main complications of end-stage ren dicate that lao skeletal and exraskeetal manifestations Although it ray be unavoidable inpatients undergoing hemodilyis, approprat and timely interventions can help alleviate the sypoms experienced bythe patients and als reduce the osteodysuophy-rlated comorbidities. Thi activity reviews the evaluation and management of rena osteodytophy and explains the ole ofthe interproessonal team in improving the eat of patents with this condition, Objectives: + Identity the stiology of real osteodystrophy. + Outline the physic findings ofa patient with renal osteodystrophy, + Describe the management considerations fr paints with real osteodystrophy. + Summarize the importance of improving ear coordination amongst the iterpofesioal tam to move outcomes for patients feted by enaloneodyatrohy. Access ee multiple choice question on this tpi Introduction Renal osteodystrophy i router that incorporates al the biochemical abaormaitis and skeletal manifestations inpatient suring fom lz Kidney disease or end-stage real dieae. The derangements in the serum Ievels of easiun, phosphorous, PTH, vitain D along with their effects on bone tumover, mincalizstio, and extaskeltl calcifications, ae all important componcnts ofthis condition. Reports sugest hes abnormalities ae mos likely to Be seen ata GFR bso 60min 1.752.112 ‘Thehistopatiologieal findings of renal ostodystopy are commonly used to farther lst his condition int: + High bone turover states ike eset rosa and hyperparaiyidism + Low bone turnover states, suchas adymamie bone disease or heavy mell-induced oxtcomalacia “The development of renal osteodystrophy as a complication of end-stage real disease has also infuenced changes in he reatment protocols aod Aisi regimens in patents, Etiology Renal osteodystrophy is invariably sen inpatients of chronic kidney disease, atbough the disease processes may differ inpatients, Histologically, ther it lasicaton ito high o low bone turnover stats igh bone turnover stats: They led Yo inereased rte of bone resorption and formation Increased parathyroid hormone (PTH) levels pay & major role nthe pathogenetis of igh bone turnover sates. lyperparathyroidim en be primary, secondary, or etary, Neoplasms ofthe parathyroid lands secreting PTH autonomously, an exarpl of tetany hyperparahyridis, can lead to «high hone turnover sate Secondary hypeparathyroidism isthe predominant cause of osteodystophy The lferent factors involved inthe pathway building up to secondary hyperprathyroiism are also worth mentioning nthe elogy of real otendsstrohy: + Phoephae retention: High phosphate levels inthe blood can simulate PTH secretion more ways than on, I en ether dict ncresse PTH mRNA levels or decrense the level of calc and cleo, indirectly causing a surge in PTH lve] + Calium: The relationship between calcium and PTH levels swell established. decrease in serum eau wil alo stile PTH + Role of acto: Caleivil and PTH both increase serum cleium ovl, and in cass of decreased ealetol in tho body, scondary ayperparathyroidism ensues due 1 decreased calcium absorption trough the intestine anda eflex increase in PTH. Cail s also required for suppressing PTH secretion by the parathyroid glands. + ibroblas growth factor 28: FGF-28 is responsible for decreasing phospate levels in the boy, and a decrease in FGF-23 can lead to secondary hyperparatyroidim, htpsswwwcnebi nim nin govlbooksiNBKS507421 wr 22)9122, 2:57 Renal Osteodystrophy - SttPearls- NCBI Bookshelf “The predominant histological bone pater in renal osteodystrophy is ost fbosa, which su product of igh bone tumover duet secondary hyperprathyroidism. Along with he PTH lev, secondary ficton hat pay olen the development of otis ross inelae neleukns 1 6, sd ‘TNFalpha 4) Low hone tumover sates: Disetsesnchadd hee are mainly osteomalacia and dynamic bone digas, both sen in pints with end-stage rel seas (ESRD). The important fctor that ply roe in the pathogenesis are Crtcomalacia: Heavy mea intoxication, mainly aluminum, cas eado dysfunction of both osteoblasts and osteoclasts. A dees in bone mineralization due tothe dyfinstonalosteabis leds to an excess of accumulated bone matrix, Other metals implicated inchde ion and exami. dynamic bone disase (ABD): The pathogenesis of adynamic bone disease mainly revolves aound the suppression of PTH, leading to low bone ‘tumover and inadequate bone mineralization but no escumultion of ences oso in contrat oostomalci, Factors which lead tothe inch!) wi + Calsium and vitamin D: Aggressive treatment with these inpatients of chronic kidney disease (CKD) causes a chonic suppression of PTH, + Continuous ambulatory peritoneal dalsis (CAPD): This eas to a large inh of aleium int the body through the dialysate. + ishetes melts: Evidence sugges that elevated gincose and decreased insulin levels together suppress PTH sserstion 7 + Other factors: Interleukin 4 and a deficiency of osteogcnic-protein | play secondary roles in the pathogenesis of ABD (4) “Mixed uremic ostcodystophy includes components of the high turnover estes fbrosa and low turover mineralization defects, es een in stoomalacin (3) Epidemiology Inthe last couple of decades, dynamic bane disease as become the most prominent subtype of real osteodystrophy seen inpatients undergoing isis, Bark, the aluinumnded low bone lamover disease was frguenty seen before heaven of alsminumafice dst solutions and the use of nom aluminum phosphate binders ‘The oven rend has alo shifted from hyperparathyroidism induced high hone tumover diseases to adynamic one disease [) Vrious factors have boon hypothesized to ave eased this, The ovens of itamin D analogs that cate suppression of PTL sone of them 9] Caleum-contsning phosphate binders ako have similar mechanism, Pathophysiology is important to understand he ongoing bone remodeling that takes place andthe elements involved in ito get a more complete petre of he pathophysiology of eal astcodysrophy. The two main cells in tis proces te osteoclast that cut down or esd the Bone and osteoblast that bl up or form new tons] Osteoblast produce the organic marx of te bone consisting of typeI collagen like ataline phosphatase and osteocalcin 1 ng with other non-cllagenous proteins “The process begins withthe esrpion of bane by the osteoclast, which ae setivated by osteoblasts through a RANK-RANK ligand complex and Inicaely epuated by several factors ike PTH, vitamin D, osteoprotegerin (OP), et. ln ali, this complex fst activates ostoocasts precursor cells, which in tam provoke the gene wansripton by nuclear factor kappa B leading to an increase in osteoclasts and bone resorption. Factors hat stimulate the complex and im to inrease osteoclasts formation are PTH, vitamin D, and aciosis. neleuins ike HL 6, tumor necrosis factor, and MIF-I alpha also activate osteoclasts. Tis wil ineeas serum clsium levels by increasing bone resorption, Oseoprotegerin isan cstcocasiogsneisnbitory factor an itimatsly decrease bone resorption 12] “The derangement inthe levels of thet factors mentioned, especialy PTH, ithe ult in real osteodystrophy: Patients suffering fom conic iuey disease (CKD) have an aoseerte dscae proces due to the alteration in levels of ther factors like phosphate, calcium, and vitamin D along With PTE, High bone tumover tats involving an increased PTH act through the RANK complex to activate more osteoclasts. On the other hand, ow bone tumover fs have lower than normal PH levels, which renders the boe incapable of integrating calcium ito the new bone thai being formed. History and Physical tis not uncommon for patients with renal steodystopty tobe asympiomatic, hough some may present wih bone pin or Rctures Low turnover slate leading to defective mineralization nd the inability to reps anyomgoing damage, ae more commonly symptom. Thi i een patents With edyramie bone disease who ne pain a the predominant symptom,/5) The higher ncidenesof facture in these pacts ca ls be htpsswwwcnebinim nin govlbooksiNBKS507421 aT 22)9122, 2:57 Renal Osteodystrophy - StatPearls- NCBI Bookshelf sributed tothe poor structural integrity ofthe bones in patents with ABD. Proximal muscle and axa skeleton involvement point towards aluminum toxicity andthe reslking osteomalacia | Patients with ABD ar likey to have an overy-supressed PTH along with an inability to bute calcium onto the bone leading to hypecalemia [5] Vaseular eae sttines and puke presse, slong with chronic hypertension, This ould result ina higher incidence of cardiovascular evens, stroke, and 30 tions are an imporant complication and cus lead to site-

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