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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThis article addresses the relationship between the heart and kidney. Individuals with chronic kidney disease (CKD) are twice as likely to have cardiovascular disease (CVD) than individuals with normal kidney function, with 40% also being diagnosed with coronary artery disease and\/or congestive heart failure. CVD progresses at twice the rate in those with CKD as in those without CKD.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ECardiology Genomics\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHypertension \u0026amp; Kidney Disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPrevention \u0026amp; Screening\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ERenal Disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EMyocardial Infarction\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHeart Failure\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EBetween 8% and 10% of individuals within the Medicare and the dual-eligible Medicare\/Medicaid programs have chronic kidney disease (CKD) or end-stage renal disease (ESRD) [Collins AJ et al. \u003Cem\u003EAm J Kidney Dis\u003C\/em\u003E 2009]. CKD is defined by either a glomerular filtration rate (GFR) of less than 60 ml\/min\/1.73 m\u003Csup\u003E2\u003C\/sup\u003E of body surface area or the presence of kidney damage, regardless of the cause, for 3 or more months. Together with ESRD, the two conditions account for more than one-third of overall expenditures in the two health care programs [Foundation NK. \u003Cem\u003EAm J Kidney Dis\u003C\/em\u003E 2002].\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EDick De Zeeuw, MD, PhD, University Medical Center, Groningen, The Netherlands, addressed the relationship between the heart and kidney. Individuals with CKD are twice as likely to have cardiovascular disease (CVD) than individuals with normal kidney function, with 40% also being diagnosed with coronary artery disease and\/or congestive heart failure (CHF). CVD progresses at twice the rate in those with CKD as in those without CKD. In addition, patients with CKD are hospitalized for heart failure 5 times more often than those without CKD, while the major cause of death in patients with CKD is cardiovascular in nature [Collins AJ et al. \u003Cem\u003EKidney Int Suppl\u003C\/em\u003E 2003; Sarnak MJ et al. \u003Cem\u003EAm J Kidney Dis\u003C\/em\u003E 2000].\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EThere is ample evidence that renal dysfunction predicts CVD progression. However, the impact of CVD on the progression of renal disease has not been studied extensively, and limited data are available from subgroup and\/or post hoc analyses. In a secondary analysis from the Prevention of Renal and Vascular End-stage Disease (PREVEND) cohort, renal function declined more rapidly in patients after myocardial infarction (MI; p=0.005; \u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Eijkelkamp WB et al. \u003Cem\u003EAm J Cardiol\u003C\/em\u003E 2007].\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022PREVEND: Effect of MI on Renal Function in General Population.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-961739237\u0022 data-figure-caption=\u0022PREVEND: Effect of MI on Renal Function in General Population.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/11413\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n            \u003Cp id=\u0022p-5\u0022 class=\u0022first-child\u0022\u003EPREVEND: Effect of MI on Renal Function in General Population.\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EReproduced with permission from D. De Zeeuw, MD, PhD.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-6\u0022\u003EIn a post hoc analysis of the data from the Captopril and Thrombolysis Study (CATS), a significant decline in the estimated glomerular filtration rate (eGFR) was observed, beginning 3 days after an MI in patients with and without CHF (5.5 ml\/min\/yr vs 12 ml\/min\/yr, respectively) [Hillege HI et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2003].\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ERenal Biomarkers for CV\u003C\/h2\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EThere are two types of renal biomarkers that are associated with CV dysfunction. The first type includes markers, such as creatinine and cystatin C, that allow estimation of the filtration capacity of the kidney (GFR). Measurement of urine albumin represents a different type of renal biomarker, as it identifies impaired handling of proteins by the kidney that can be detected at an early stage of kidney dysfunction, particularly when microalbuminuria is assessed using sensitive assays.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003ENumerous studies have reported the value of serum creatinine or eGFR (estimated from serum creatinine or serum cystatin-C levels) as markers for CVD risk or all-cause mortality. In a seminal paper, Go et al. showed that an above mean GFR of 3 years in duration was strongly associated with all-cause mortality, with the risk of death increasing as GFR decreased below 60 ml\/min\/1.73 m\u003Csup\u003E2\u003C\/sup\u003E. The adjusted hazard ratio for death was 5.9, with an estimated GFR of less than 15 ml\/min\/1.73 m\u003Csup\u003E2\u003C\/sup\u003E (95% CI, 5.4 to 6.5). A similar increase in the risk for CV events and hospitalization was also associated with declining GFR [Go AS et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2004].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EGibson et al. analyzed data from the Thrombolysis In Myocardial Infarction (TIMI)-10, TIMI-14, and Intravenous nPA for the Treatment of Infarcting Myocardium Early (InTIME-II) trials, finding that 30-day mortality increased within each TIMI risk score for ST-elevation myocardial infarction (STEMI) as renal function declined. The odds ratio for 30-day mortality in patients with severe impairment (defined as a creatinine clearance \u0026lt;30 ml\/min) was 3.73 (95% CI, 2.55 to 5.45; p\u0026lt;0.001) [Gibson CM et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2003].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003ECooper et al. found that renal function was associated with the risk of postoperative complications after coronary artery bypass surgery, with the mortality rate increasing from 1.3% for those with normal renal function to 9.3% for those with severe renal dysfunction who were not on dialysis and 9.0% for those who were on dialysis. The most powerful predictor of postoperative mortality and morbidity was preoperative GFR [Cooper WA et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2006].\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EAn analysis of the Valsartan in Acute Myocardial Infarction Trial (VALIANT) found that the risk of death or the composite endpoint (death from CV causes, reinfarction, CHF, stroke, or resuscitation after cardiac arrest) increased with declining eGFR. Each 10-unit reduction in patients with GFR \u0026lt;81.0 ml\/min\/1.73 m\u003Csup\u003E2\u003C\/sup\u003E was associated with a hazard ratio for death and nonfatal CV outcomes of 1.10 (95% CI, 1.08 to 1.12), regardless of treatment [Anavekar NS et al. \u003Cem\u003EN Eng J Med\u003C\/em\u003E 2004].\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EMultiple studies have shown that albuminuria is related to CV outcome. This is true in the general population but also in several different disease populations, including hypertension, diabetes, and heart failure [Wachtell et al. \u003Cem\u003EAnnals Int Med\u003C\/em\u003E 2003; Yuyun et al. \u003Cem\u003EDiabetes Med\u003C\/em\u003E 2003; Gerstein et al. \u003Cem\u003EJAMA\u003C\/em\u003E 2001; de Zeeuw D et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2004].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETreatment?\u003C\/h2\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EMore evidence for the relationship between kidney function and CVD comes from examining the benefits of treating parameters that are related to kidney function or to cardiac function and the impact of long-term renal and CV outcomes.\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EIt is hard to treat GFR\u2014the only way to do so is to transplant extra kidney tissue and see what the impact on CV morbidity and mortality is. Thus, the goal of therapy is to reduce further progression of disease and loss of kidney function with improvements in surrogate markers that are associated with outcomes, such as urine albumin.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EThe PREVEND Intervention (PREVEND-IT) trial found that treatment with the angiotensin-converting enzyme (ACE) inhibitor fosinopril significantly reduced mean urinary albumin excretion by 26% (p\u0026lt;0.001), simultaneously providing a 40% RRR in CV mortality and morbidity. Although the latter finding was not statistically significant, the study suggested that the mere treatment of patients (lowering their albuminuria) who have only slightly increased albuminuria is associated with better CV outcome (HR, 0.60; 95% CI, 0.33 to 1.10; p=0.098, log-rank) [Asselbergs FW et al. Circulation 2004]. Other trials found cardioprotective effects from lowering urinary albumin with losartan in patients with hypertension and left ventricular hypertrophy, normotensive type 2 diabetes, and advanced nephropathy and type 2 diabetes [Ibsen H et al. \u003Cem\u003EHypertension\u003C\/em\u003E 2005; Zandbergen AA et al. \u003Cem\u003EDiabetes Care\u003C\/em\u003E 2007; de Zeeuw D et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2004].\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EIntriguingly, when the ACE inhibitor captopril was administered to prevent heart failure post-MI, the additional benefit of protecting the kidney, regardless of renal function, was observed, thus giving two compelling reasons to administer ACE inhibitors in these patients [Hillege HL et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2003].\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EHow exactly albuminuria reduction is related to CV protection is still not fully understood. But, recent data on the glycocalyx layer that is present in all small capillaries is quite interesting, as changes in glycocalyx function may explain why the kidney leaks albumin and why other vascular beds are also compromised. Thus, increased albuminuria may well reflect general vascular endothelial dysfunction [Haraldsson B et al. \u003Cem\u003EPhysiol Rev\u003C\/em\u003E 2008].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EDefining the Cardiorenal Syndrome\u003C\/h2\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EClaudio Ronco, MD, St. Bortolo Hospital, Vicenza, Italy, discussed controversies in defining the cardiorenal syndrome (CRS), for which there has been no commonly accepted definition. Instead, the term has been borrowed from other areas, with the supposition that improving CV function would also improve renal function. The condition, however, is bidirectional. \u003Ca id=\u0022xref-fig-2-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F2\u0022\u003EFigure 2\u003C\/a\u003E depicts the bidirectionality of cardiorenal interactions.\u003C\/p\u003E\n         \u003Cdiv id=\u0022F2\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F2.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Cardio-Renal Interactions.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-961739237\u0022 data-figure-caption=\u0022Cardio-Renal Interactions.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 2.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F2.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F2.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 2.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/10\/10\/30\/F2.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/11417\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 2.\u003C\/span\u003E \n               \u003Cp id=\u0022p-19\u0022 class=\u0022first-child\u0022\u003ECardio-Renal Interactions.\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003EReproduced with permission from C. Ronco, MD.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-20\u0022\u003EThe Acute Dialysis Quality Initiative (ADQI) was developed to provide an objective, dispassionate distillation of the literature and a description of the current state of practice to form a consensus of opinion\u2014evidence-based when possible\u2014on the best practices in acute renal failure and to articulate a research agenda to focus on important unanswered questions. It has held numerous conferences and has published extensively.\u003C\/p\u003E\n         \u003Cp id=\u0022p-21\u0022\u003EIn 2006, the ADQI developed the RIFLE consensus classification for acute kidney injury, defining three grades of increasing severity based on changes in serum creatinine or urine output from baseline\u2014risk (class R), injury (class I), and failure (class F)\u2014and two outcome classes (loss and ESRD) [Bellomo R et al. \u003Cem\u003ECrit Care\u003C\/em\u003E 2004]. The classification scheme can predict hospital mortality and resource use among patients in the intensive care unit [Hoste EA et al. \u003Cem\u003ECrit Care\u003C\/em\u003E 2004]. A meta-analysis of 13 studies on patient mortality also suggested that even mild degrees of kidney dysfunction could increase the risk of death [Ricci Z et al. \u003Cem\u003ECrit Care\u003C\/em\u003E 2006].\u003C\/p\u003E\n         \u003Cp id=\u0022p-22\u0022\u003EIn 2008, the ADQI developed a definition of the CRS, defining it as a \u201cpathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other.\u201d The group also identified five subtypes of CRS [Ronco C et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2008] based on pathophysiology, time frame, and nature of concomitant cardiac and renal dysfunction:\u003C\/p\u003E\n         \u003Cul class=\u0022list-unord \u0022 id=\u0022list-1\u0022\u003E\u003Cli id=\u0022list-item-1\u0022\u003E\n               \u003Cp id=\u0022p-23\u0022\u003EType 1: An abrupt worsening of cardiac function (eg, acute cardiogenic shock or decompensated CHF), leading to acute kidney injury\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-2\u0022\u003E\n               \u003Cp id=\u0022p-24\u0022\u003EType 2 : Chronic abnormalities in cardiac function (eg, chronic CHF) that cause progressive CKD\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-3\u0022\u003E\n               \u003Cp id=\u0022p-25\u0022\u003EType 3: An abrupt worsening of renal function (eg, acute kidney ischemia or glomerulonephritis) that causes acute cardiac dysfunction (eg, heart failure, arrhythmia, ischemia)\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-4\u0022\u003E\n               \u003Cp id=\u0022p-26\u0022\u003EType 4: A state of CKD (eg, chronic glomerular disease) that contributes to decreased cardiac function, cardiac hypertrophy, and\/or increased risk of adverse CV events\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-5\u0022\u003E\n               \u003Cp id=\u0022p-27\u0022\u003EType 5: A systemic condition (eg, sepsis) that causes both cardiac and renal dysfunction\u003C\/p\u003E\n            \u003C\/li\u003E\u003C\/ul\u003E\n         \u003Cp id=\u0022p-28\u0022\u003EWhile numerous biomarkers are available that can lead to an early diagnosis of CRS and therapeutic interventions that could reduce the risk of or prevent progression, clinicians remain unaware of the possibility of prevention through early intervention; the importance of monitoring biomarkers, like creatinine levels and GFR; and the implications of outcomes in this condition.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2010 MD Conference Express\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/10\/10\/30.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzmnm3\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzmnm3\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}