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    CKD

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    Jay Ar
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    Cardoranal nema paberyloy ‘Sadun nae ‘Tut eons dt ey oe ws Tope _ art ‘BADE THe ‘Nee PA. Di 1 MCNGO200 wera ac, cote ach 208 Ny abe Figure || Cariorenal syndrome pathophysiology. AH, antec hormone ANP al native pepe BNP, ype natvetic ep; CHD cone aise OM, diets lus FO, etopoet HTN, yprensn: Lue; KN dy molec LV, et vena; GAL, nop celtnaseasocted Epc NSAD, nono arbfammatry dg; O44 osc sp pa spc; pty hme 6 ppt anos eT, a secs eters -araiovascuilar disease In cnronic Kkianey disease. 4 clinical update from Kidney Disease: Improving Global Outcomes (KDIGO) charles A. Herzog’, Richard W. Asinger"4, Alan K Berger, David M. Charytan’, Javier Diez’ lover G. Hart’, Kal Uwe Eckardt®, Bertam L. Kasiske"”, Peter A. McCullough’, Rod S. Passman*, itephanie $. DeLoach®, Patrick H. Pun" and Eberhard Ritz"? Hennepin County Medea Cente, Minneapolis, Mionessta, USK: “Univesity of Minesote, Minneapolis, Minnesota, USK; "Bigham and YVomer's Hospital, Bosion, Massachusets, USA “University of Navarra, Pamplona, Spain; “Population Health Research isiutey ‘ettaser Univer, Hamiton, Ontrio,Cenade; *Universty of Erangen-hurembeg,Irlangen, Germany; St John Providence Heath stem, Novi, Michigan USA; *Nonhwestem Univesity Chicaco, ino, USA: “Jefersen Medical College, hledelphia, Peanssvania, ‘Geman 14: "uke University, Durham, North Caroling, USA and "Univesity of Heidelberg, Heidelberg, -ardiovascular morbidity and mortaity in patients with ‘ironic kidney disease (CKD) is high, ard the presence of. "KD worsens outcomes of cardiovascular disease (CVD). CKD + associated with specific risk factors. Emerging evidence ndfcatoe thatthe pathology and manifestation of CVD lifer in the presence of CKD. During a clinical update ‘onference convened by the Kidney Disease: Improving Slobal Outcomes (KDIGO}, an international group of experts lefned the current state of lnowledge and the implications oF patent care in important topic areas, inclucing coronary irtery disease and myocardial lnfarcion, congestive heart allure, carebrovatcular iseate, atal flat, peripheral eral disease, and sudden cardiac death. Although optimal trategies for prevention, diagnesis, and management of ‘hese complications ltely should be modified in the presence CKD, the evidence base fer decision making i Imited. ‘als targeting CVD in patients with CKD have a larae rotential to improve outcomes. ey emt arc pub, 1 Hy 21 EYHORDS: sl Nbr heat lu; myocar pepe ‘arespondence: Chaves A-Henoa, Chane Dice esearch owe, Uinoopal ia Reach Faundoan 93 South Bh Sot Sate S06 inopals, Minesou 3908, USA Eel derngeearyorg lecsved 22 March 2011; revined 17 May 2011 acepted 31 May 2011 sen nen In October 2010, the KDIGO (Kidney Disease: Improving Global Outcomes) convened a Clinical Update Conference i London, United Kingdem, ttle “Cardiovascular Ditease in CKD: What it and what can we do about it? The objective wat to define the carrent tate of knowledge about cardiovascular disease (CVD) in patients with chronic kidney dicate (CKD) stages 1-5 (cee Table 1 for terminology) Topics included epidemiology, pathophysiology, disgnosis, prevention, and treatment, focusing on areas of elisical relevance: (1) coronary artery disease (CAD) and myocanlial infarction (1); (2) congestive heart flue (CHF); (3) cerebrovatcular dseste,strake, atrial elation, peripheral arterial disease (PAD); andl (4) sudden cardiac death (SCD). ‘A total of 90 inlerrational experts in thete arent attended, including nephrologists cardiologists, neurologists, and represeatstives of other disciplines, This is a report on con- ference proceedings and recommendations: it is not intended sv critical review of availble literature. Conference detaila fate posted on the KDIGO website, htp//iww klgo.crg! ‘mectings_event/Cardiovascuar_Disease_in_Chronic_Kidney__ Disente-pip. Growing evidence exggedts that CKD is an fmportant, independent risk factor for CVD. Many paticnts with CKD die prematurely before or aftr beginning dials Reasons for these adverse associations are not well under- stood ars are thus the subject of controveny. Whether CVD events differ in patients with and without CKD is poorly fined. Similasly, whether diferences ia CVD in CKD patients aigget preventative or therapeutic attics unique to this population is unclear. (cAD AND mt Fnidemiclogy and pathophysiology The incidence snd severty Of obeiucive CAD increases as glomerular fttion rate (GFR) declines! CAD shows pattem of die muilievessel involvement with coronary lebcations™ smal angiographic studies suggest that thie (Ab sage of OD, clang days Specie ager of CHD Diayst- and nareie-dependet CHO sage 5 Nomtayi-depenint CKD. ‘Diae-dependort CRD stage 5, etc hemodtas ‘cl pentane! ai equivalent 9 endtage renal Hermodiie Perkonenl chips incidence exceeds 50% in unselected CKD SD patients? ‘Among patients with CAD, concomitant CKD portends a ‘worse prognosis. Cardiovascular morbidity and mortality are inversely and independently associated with kidney function, particularly at estimated GFR-~<15 ml/min pee 173m" ‘Although the absolute incidence and mortality rate of Mt is dearly elevated in advanced CKD." standard cardiovascular risk factors are common in the setting of CKD. and the degree to which CKD is independently associated with the risk of inital MI is not well defined. Standard cardiovascular risk factors are common in CKD, but do not fully explain the high incidence of cardiovascular events or incresed mortality rates." their association with cardiovascular ‘outcomes is attenuated or even reversed atthe most advanced (CKD stages tnilarmmation and oxidative stress have been linked to the pathogenesis of plague formation and plague rupture: both are associated with worse cardiovascular outcomes” The role of mineralocorticaid excess in the development af cardiovascular complications is increasingly recognized * Revent studies have implicated disordered ‘mineral and bone metabolism in the pathogenesis of coronary disease and CVD in CKD patients Diagnosis Although early detection of coronary plague may permit tisk factor modification and pharmacological intervention, the increased prevalence of CAD among CKD. patients diminishes the negative predictive value of diagnostic studies in this population. CKD patients are underrepresented in cohort studies evaluating the diagnostic sensitivities and specificities of non-invasive tests, Exercise elecrocardiogra- hy is limited by lack of specificity of the ST-segment response and by inability of many CKD patients to exercise 10 4 diagnostic workload." The risks of contrast agents limit the use of perfusion magnetic resonance imaging and computed tomography coronary angiography, and the later is compromised by a high prevalence of coronary calcifica- tion among CKD patients” Radionuclide perfusion imaging is more, sensitive but less specific than stress echocardio- srphy.* but may be problematic in the seting of elevated leftoventricular (IV) mass index and frank LV hypertrophy (LVH) because limited spatial resolotion and disturbed coronary flow reserve may lead to false results ~ The acc racy of exercise and of pharmacological myocardial pefusie jmaging is reduced in CKD patients compared with general population, and sensitivities and specificities < 80 Ihave been reported “>” Conversely, stress echocardiograpl may be compromised by small IV cavity size in patien with elevated LY mass index.” Sensitivity and specifci for pharmacological stress echocardiography is 69-95% ar 16-5406, vespectively 7 Diagnosis of acute coronary syndrome may abso | problematic in CKD. The clase triad of ischemic symptom elevated cardiac biomarkers, and electrocardiograph changes is frequently absent in CKD patients"°? who a more likely to present with systolic or diastolic dysfanctc causing hear failure symptoms, or with syncope.” LVH wi a strain pattern may musk diagnostic ST depressio Convenely, creatine kinase MB isoform and eardise trope nin (cTas) may be devated in the absence of true myocar ‘necrosis, posibly because of myocardial apoptosis oF sm: vessel disease” This mandates careful attention to tren lover time and! reduces the value of single tests, 2 problem th ‘may be exacerbated by increased sensitivity of next-pener tion troponin assays, Prevention “The altered relationship of typical risk factors with cardi ‘waitalle atoms Mad the voctina aaclankene of pie with advanced CKD from most clinical trials testing CV ‘diaeapien!* panalerdlsehe docu she eeleweace WE casa standards of care to these patients. Evidence of the efica ff glycemic or bload pressure (BP) control or lifety ‘modification to reduce cardiovascular events in patients wi advanced CKD remains limited Strict glycemic contr sx zhot benefit CKD SD patienta"“*" Randomized data on #1 efficacy of specific BP goals in CKD SD patients ae lackin “The labile nature of BP and the absence of clear association berween hypertension and adverse cardiovascular outcom in CKD SD preclude definitive recommendations about E ‘dear Riesaghc oaiticstntn “howe sah Mose nad Studied in CKD patients, in a small tal, multfactori intervention that included smoking cessation war 1 associated with significant cardiovascular benefits. Neve theless, smoking cesation, exercise, dietary salt eduction and weight lose are reasonable interventions at all CK stages, and contrl of hypertension to usual goals or lower indicated to slow CKD progresion in patients with pr dialysis CKD. ‘Data are sparse regarding efficacy of prophylactic aspir jn advanced CKD. Subgroup analyses of randomiz tials have demonstrated convincing cardiovascular 1 reduction from daly asprin in individuals with estimats GFReASmilmin per 173m4, induding CKD SD patient despite higher incidence of bleeding in CKD patients *!$* ‘With release of initial results from the SHARP (Study + Heart and Renal Protection) trial, statins may now be t beest-studied medical therapy in the context of advanci ey memonr +2 [Future directions for cardiovascular disease in chronic kidney disease: 1-23) may be relevant The hutadienolides (steroid Roowindge som ‘Sarening maybe beret bat ata ar ruler fo mavocate atecring srymtomatie pater. Eee nang ern mary and scone Clronasiar tab have hequenty exes CKO ‘Basen rom eevlimere Prone dit on non-surgical therapies Dea vegedingperetaneous ws ural ‘Sirand octos fred rm the ges popaation may nt pe. Few utopoy aut ‘ey peace ect ry ned secondary prevetion tik, tones circulating inthe blood and excreted in urine) are ted in CKD. They inhibit preferentially the 21 Boform *-K? "ATPase, resulting in volume expansion and ‘Rension™ Histopathological studies indicate that capl- density i reduced in the hypertiophied myocardium, Dronaunced intestial fibrosis isa dominant featare of Tieociated structural myocardial remodeling " diastolic dysfunction is Bequent among CKD patients ‘i aswocated with the risk of CHF and increased (Generate management guideline. ‘Rect: amputation frequency my progam that o and do not arom Preventive toot ene Sosy bactenslogy of dabei patent fee. Danasesetie brge-saie prospective cohort uch fr rk rata Stay hetrogerwocs CKD populotors at alstage ing al aval re Sutheseen tere Femave buries preveriing dit linkage to allow for popustin-ise cot and case-control mutes. Fandom tal ataenang the spectum of interven: lockers (et ‘rvediol CDs sympatiete aban. ‘Gerpcrte SOD a spec cecoe sir ccd il dn Invonignte te poveri oe flee apes SCD. mortality; impaired diastolic function may occur ex in CKD, even without IVE Myocardial fibrosis rest from an imbalance between exaggerated collagen ol ented or dqpeaed calles degedates 16 patients, it i a major determinant of LV stiffness, increa: IV filing pressure, and disturbances in diastolic fli Predisposing to development of diastolic dysfunc In CKD patients, resting IY systolic function is wsus normal or even hyperdynamic, at least in the absence ey eae >. Nevertheless, debate continues regarding their appro- ve role. A subgroup analysis of several randomized cal trials suggests benefit in patients with moderate > Conversely, evo large tial comparing statins with 2bo_ in is patients did not “demonstrate ‘U2 More recently, in the SHARP tral, the combina ‘of simvastatin and eaetimibe in CKD patients (including SD) reduced major atherosclerotic events by 17%, but tot appear to reduce overall mortality*" As-no significant 2 from statin use was demonstrated in any of the tials, reduction in non-fatal events provides a rationale for the of statins in CKD patients despite the apparent lack ‘cacy in reducing the risk of death. Jomized data on treatment of acute MI in CKD patients ‘parse, but treatment approaches using aspirin, clopido- ‘Brblockers, and angiotensin-converting enzyme inhibi (ACEIS\PARBs (angiotensin receptor blockers) seem 10 ‘similar benefits in CKD and non-CKD patients:”** ‘al antiplatelet and anticoagulant agents are metabolized ugh the kidneys and warrant dose adjustment in CKD ants and low-molecular weight heparins and epifbatie not be safe in CKD 5D patients: heve is litle reason to Believe that kidney impairment imishes the benefits of immediate reperfusion therapy in f ST-elevation MI, but there are no randomized trials spetfusion therapy in CKD. A recent analysis suggests when immediately available, primary percutancous ‘nary intervention (PCI) should be the testment of ce irrespective of CKD status ‘mong patients with mon-ST elevation acute coronary ‘rome (unstable angina and non-ST-elevation MI), the ay Uecion §i betes Kenebcoacopahey sal nservative approach. In the general population, an carly she strategy reduces post-acute coronary syndrome bidity and mortality ‘by 20-309%°" and guidelines mimcnd early angiography in high-risk patients! A 1 meta-analysis suggested similar benefits in CKD 3-4 sats but CKD 4 was underrepresented (n-< 300) and "SD patients were not included. Conversely, a recent spective analysis of all non-ST-devation MI patients in fen suggested that an early ivasve strategy was harmful ORD 5 patiemss* heve is 2 paucity of data regarding revascularization in > patients with stable angina. Surgical coronary revascu- ation is generally recommended for non-CKD patients high-risk features such as left-main CAD, and PCI is ally recommended for symptomatic ngle- or two-vessel ) or when a significant amount of myocardium is at ‘#6 No randomized clinical tials compare coronary secularization strategies in advanced CKD _ patients ibgroup analysis of the COURAGE (Clinical Outcomes zing Revascularization and Aggresive Drug Evaluation)

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