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(HR 0.75 [95% CI 0.65 –0.86]; P<0.001)\nand fewer total hospitalizations for heart\nfailure (HR 0.70 [95% CI 0.58 –0.85]; P<\n0.001). The effect of empagli flozin on the\nprimary outcome was consistent irrespec-tive of diabetes diagnosis at baseline. Therisk of a prespeci fied renal composite\noutcome (chronic dialysis, ... | [
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outcome (chronic dialysis, renal trans-\nplantation, or a sustained reduction in\neGFR) was lower in the empagli flozin\ng r o u pt h a ni nt h ep l a c e b og r o u p( 1 . 6 %i nthe empagli flozin group vs. 3.1% in the pla-\ncebo group; HR 0.50 [95% CI 0.32– 0.77]).\nEMPEROR-Preserved, a randomized | [
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EMPEROR-Preserved, a randomized\ndouble-blinded placebo-controlled trialof 5,988 adults with NYHA functionalclass I –IV chronic HFpEF (LVEF >40%),\nevaluated the ef ficacy of empagli flozin\n10 mg daily versus placebo on top ofstandard of care on the primary out-come of composite cardiovascular death\nor hospitalization ... | [
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or hospitalization for heart failure (242).\nApproximately 50% of subjects had type 2diabetes at baseline. Over a median of26.2 months, there was a 21% reduction(HR 0.79 [95% CI 0.69 –0.90]; P<0.001)\nof the primary outcome. The effects ofempagli flozin were consistent in people\nwith or without diabetes (242).\nIn the ... | [
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In the DELIVER trial, 6,263 individuals\nwith heart failure and an ejection frac-\ntion>40% were randomized to receive\neither dapagli flozin or placebo (252).\nThe primary outcome of a composite\nof worsening heart failure, de fined as | [
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of worsening heart failure, de fined as\nhospitalization or urgent visit for heartfailure, or cardiovascular death was re-duced by 18% in individuals treatedwith dapagli flozin compared with pla-\ncebo (HR 0.82 [95% CI 0.73 –0.92]; P<\n0.001). Approximately 44% of individu-als randomized to either dapagli flozin or | [
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placebo had type 2 diabetes, and results\nwere consistent regardless of the pres-\nence of type 2 diabetes.\nA large recent meta-analysis (293) of\ndata from EMPEROR-Reduced, EMPEROR-Preserved, DAPA-HF, DELIVER, and the\nEffect of Sotagli flozin on Cardiovascular\nEvents in Patients With Type 2 Diabetes | [
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Events in Patients With Type 2 Diabetes\nPost Worsening Heart Failure (SOLOIST-WHF) trial included 21,947 individualsand demonstrated reduced risk for the\ncomposite of cardiovascular death or hos-\npitalization for heart failure, cardiovasculardeath, first hospitalization for heart failure,\nand all-cause mortality. Th... | [
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and all-cause mortality. The findings on\nthe studied end points were consistent inboth trials of heart failure with mildly re-duced or preserved ejection fraction and\nin all five trials combined. Collectively,\nthese studies indicate that SGLT2 inhibi-\ntors reduce the risk for heart failure hospi-talization and cardio... | [
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wide range of people with heart failure.\nIn addition to the hospitalization and\nmortality bene fit in people with heart\nfailure, several recent analyses have\naddressed whether SGLT2 inhibitor treat-\nment improves clinical stability and func- | [
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ment improves clinical stability and func-\ntional status in individuals with heartfailure. In 3,730 individuals with NYHAclass II –IV heart failure with an ejection\nfraction of #40%, treatment with empa-\ngliflozin reduced the combined risk of | [
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gliflozin reduced the combined risk of\ndeath, hospitalization for heart failure, oran emergent/urgent heart failure visitrequiring intravenous treatment and re-\nduced the total number of hospitalizations\nfor heart failure requiring intensive care, avasopressor or positive inotropic drug, ormechanical or surgical inte... | [
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In addition, individuals treated with empa-\ngliflozin were more likely to experience\nan improvement in NYHA functional class(294). In people hospitalized for acute de\nnovo or decompensated chronic heart fail-\nure, initiation of empagli flozin treatment | [
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ure, initiation of empagli flozin treatment\nduring hospitalization reduced the primaryoutcome of a composite of death fromany cause, number of heart failure events\nand time to first heart failure event, or a\n5-point or greater difference in change\nfrom baseline in the Kansas City Cardio-myopathy Questionnaire Total S... | [
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Score (295). Furthermore, PRESERVED-\nHF, a multicenter study (26 sites in theU.S.), showed that dapagli flozin treat-\nment leads to signifi cant improvement in | [
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ment leads to signifi cant improvement in\nboth symptoms and physical limitation aswell as objective measures of exercisefunction in people with chronic HFpEF,regardless of diabetes status (251). Fi-nally, canaglifl ozin improved heart failure | [
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symptoms assessed using the KansasCity Cardiomyopathy Questionnaire To-tal Symptom Score, irrespective of LVEFor the presence of diabetes (296).\nTherefore, in people with type 2 diabe-\ntes and established HFpEF or HFrEF, anSGLT2 inhibitor with proven bene fiti n\nthis patient population is recommended\nto reduce the r... | [
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to reduce the risk of worsening heart fail-\nure and cardiovascular death. In addition,an SGLT2 inhibitor is recommended indiabetesjournals.org/care Cardiovascular Disease and Risk Management S207\n©AmericanDiabetesAssociation | [
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this patient population to improve symp-\ntoms, physical limitations, and quality oflife. The bene fits seen in this patient pop-\nulation likely represent a class effect, andthey appear unrelated to glucose lower-\ning, given comparable outcomes in peo-\nple with heart failure with and withoutdiabetes.\nSotagliflozin | [
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ple with heart failure with and withoutdiabetes.\nSotagliflozin\nSotagli flozin, a dual SGLT1 and SGLT2 in-\nhibitor, was recently approved by theFDA in the U.S. to reduce the risk ofcardiovascular death, hospitalization forheart failure, and urgent heart failure\nin people with heart failure or type 2 | [
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in people with heart failure or type 2\ndiabetes, CKD, and other cardiovascularrisk factors. This drug is distinct fromother SGLT inhibitors, as it lowers glu-\ncose via delayed glucose absorption in\nthe gut via inhibition of the cotrans-porter SGLT1 in addition to increasingurinary glucose excretion; however, it is | [
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not currently approved by the FDA for\nglycemic management of type 1 ortype 2 diabetes. Sotagli flozin was evalu-\nated in the SCORED trial (281) andSOLOIST-WHF trial (297). A total of\n10,584 people with type 2 diabetes,\nCKD, and additional cardiovascular riskwere enrolled in SCORED and random-ized to sotagli flo z i n... | [
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(uptitrated to 400 mg once daily if toler-ated) or placebo. SCORED ended earlydue to a lack of funding; thus, changesto the prespeci fied primary end points\nwere made prior to unblinding to accom-modate a lower-than-anticipated numberof end point events. The primary endpoint of the trial was the total number of | [
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deaths from cardiovascular causes, hospi-\ntalizations for heart failure, and urgentvisits for heart failure. After a median of16 months of follow-up, the rate of pri-mary end point events was reduced with\nsotagli flozin (5.6 events per 100 patient-\nyears in the sotagli flozin group and 7.5\nevents per 100 patient-year... | [
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events per 100 patient-years in the pla-\ncebo group [HR 0.74; [95% CI 0.63– 0.88];\nP<0.001]). Sotagli flozin also reduced\nthe risk of the secondary end point of to-tal number of hospitalizations for heartfailure and urgent visits for heart failure\n(3.5% in the sotagli flozin group and 5.1%\nin the placebo group [HR 0... | [
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in the placebo group [HR 0.67 [95% CI\n0.55–0.82]; P<0.001]) but not the sec-\nondary end point of deaths from cardio-vascular causes. No signi ficant between-\ngroup differences were found for theoutcome of all-cause mortality or for acomposite renal outcome comprising thefirst occurrence of long-term dialysis, re- | [
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nal transplantation, or a sustained reduc-tion in eGFR. In general, the adverseeffects of sotaglifl ozin were similar to\nt h o s es e e nw i t hu s eo fS G L T 2i n h i b i t o r s ,but they also included an increased rateof diarrhea potentially related to the in-hibition of SGLT1. In general, the adverse\neffects of s... | [
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effects of sotagli flozin were similar to\nt h o s es e e nw i t hu s eo fS G L T 2i n h i b i t o r s ,\nbut they also included an increased rateof diarrhea potentially related to the in-\nhibition of SGLT1.\nIn SOLOIST-WHF, 1,222 people with\ntype 2 diabetes who were recently hos- | [
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type 2 diabetes who were recently hos-\npitalized for worsening heart failurewere randomized to sotaglifl ozin 200 mg\nonce daily (with uptitration to 400 mgonce daily if tolerated) or placebo eitherbefore or within 3 days after hospitaldischarge. Individuals were eligible ifhospitalized for signs and symptoms of | [
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heart failure (including elevated natri-\nuretic peptide levels) requiring treatmentwith intravenous diuretic therapy. Exclu-sion criteria included end-stage heart fail-\nure, recent acute coronary syndrome or\nintervention, or an eGFR <30 mL/min/\n1.73 m\n2. Individuals were required to be\nclinically stable prior to ... | [
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clinically stable prior to randomization,\nwhich was de fined as no use of supple-\nmental oxygen, systolic blood pressure\n$100 mmHg, and no need for intrave-nous inotropic or vasodilator therapyother than nitrates. Similar to SCORED,\nSOLOIST-WHF ended early due to a lack\nof funding, resulting in a change to thepresp... | [
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unblinding to accommodate a lower-than-\nanticipated number of end point events. At\na median follow-up of 9 months, the rateof primary end point events (the totalnumber of cardiovascular deaths and hos-\npitalizations and urgent visits for heart\nfailure) was lower in the sotagli flozin | [
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failure) was lower in the sotagli flozin\ngroup than in the placebo group (51.0 vs.76.3; HR 0.67 [95% CI 0.52– 0.85]; P<\n0.001). No signi ficant between-group dif-\nferences were found in the rates of car-diovascular death or all-cause mortality.Both diarrhea (6.1% vs. 3.4%) and severehypoglycemia (1.5% vs. 0.3%) were m... | [
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common with sotaglifl ozin than with pla-\ncebo. The trial was originally also intended\nto evaluate the effects of SGLT inhibitionin people with HFpEF, and ultimately no\nevidence of heterogeneity of treatment\neffect by ejection fraction was noted.However, the relatively small percentageof such individuals enrolled (o... | [
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participants had ejection fraction >50%)\nand the early termination of the trial lim-\nited the ability to determine the effectsof sotagli flozin in HFpEF speci fically (297).\nOne concern with expanded use of\nSGLT inhibition is the infrequent but se-\nrious risk of diabetic ketoacidosis, in- | [
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rious risk of diabetic ketoacidosis, in-\ncluding the atypical presentation ofeuglycemic ketoacidosis. There are mul-tiple proposed pathways through which\nSGLT inhibition results in ketosis (in-\ncreased b-hydroxybutyrate and acetoa-\ncetate), such as increased productiondue to reduction in insulin doses, in-\ncreases... | [
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creases in glucagon levels leading to in-\ncreased lipolysis and ketone production,and decreased renal clearance of ke-tones (298,299). Thus, the use of SGLTinhibitors (whether for glycemic control\nor another indication) increases the sus- | [
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or another indication) increases the sus-\nceptibility to diabetic ketoacidosis, par-ticularly when other risk factors orsituations occur (including, but not lim-\nited to, insulin pump malfunctions, sig-\nnificant reduction in insulin doses, and | [
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nificant reduction in insulin doses, and\nnutritional intake plans with prolongedperiods of fasting or carbohydraterestriction). Although there were low\nrates of ketoacidosis in the cardiovascu-\nlar and heart failure outcomes trialsevaluating SGLT inhibition, these studiesexcluded individuals with type 1 diabe- | [
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tes and/or recent history of diabetic ke-\ntoacidosis (297,300). To decrease therisk of ketoacidosis when using SGLT in-hibition in people with type 1 diabetes,it is recommended that clinicians assess\nthe underlying susceptibility; provide\neducation regarding the risks, symp-toms, and prevention strategies; andprescr... | [
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forb-hydroxybutyrate (299,301). Use\nof these processes may have contrib-\nuted to the lower rates of ketoacidosisseen in some of the studies of theseagents for adjunctive glycemic man-\nagement in people with type 1 diabe-\ntes (302 –304) compared with those\nthat did not include preventative strate-gies (298,305). Re... | [
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ceptibility, education, and provision of\nmonitoring supplies should reoccurthroughout the duration of SGLT in-hibitor treatment, particularly as pre-\nventative strategies and monitoring | [
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ventative strategies and monitoring\ncan minimize, but not eliminate, therisk of ketoacidosis in those who aresusceptible (306,307).S208 Cardiovascular Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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Finerenone in People With Type 2 Diabetes\nand Chronic Kidney Disease\nAs discussed in detail in Section 11,\n“Chronic Kidney Disease and Risk Mana-\ngement, ”people with diabetes are at an | [
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gement, ”people with diabetes are at an\nincreased risk for CKD, which increasescardiovascular risk (308). Finerenone, aselective nonsteroidal MRA, has beens h o w ni nt h eF I D E L I O - D K Dt r i a lt oi m -\nprove CKD outcomes in people with | [
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prove CKD outcomes in people with\ntype 2 diabetes with stage 3 or 4 CKDand severe albuminuria (281). In theFIGARO-DKD trial, 7,437 individuals withUACR 30 –300 mg/g and eGFR 25 –90 mL/min/1.73 m\n2or UACR 300 –5,000 and\neGFR$60 mL/min/1.73 m2on maximum\ndose of renin-angiotensin system blockade\nwere randomized to re... | [
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... |
were randomized to receive finerenone\nor placebo (240). The HR of the primaryoutcome of cardiovascular death, nonfatalMI, nonfatal stroke, or hospitalizationfrom heart failure was reduced by 13% inindividuals treated with finerenone. A pre-\nspecified subgroup analysis from FIGARO-\nDKD further revealed that in individua... | [
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DKD further revealed that in individuals\nwithout symptomatic HFrEF, finerenone | [
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reduces the risk for new-onset heart fail-ure and improves heart failure outcomesin people with type 2 diabetes and CKD(239). Finally, in the pooled analysis of13,026 people with type 2 diabetes andCKD from both FIDELIO-DKD and FIGARO-DKD, the HR for the composite of cardio-vascular death, nonfatal MI, nonfatalstroke, ... | [
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death, nonfatal MI, nonfatalstroke, or hospitalization for heart failureas well as a composite of kidney failure, asustained $57% decrease in eGFR from | [
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baseline over $4 weeks, or renal death\nwere 0.86 and 0.77, respectively (241).These collective studies indicate that fi-\nnerenone improves cardiovascular andrenal outcomes in people with type 2\nFigure 10.3— Approach to risk reduction with sodium-glucose cotransporter 2 inhibitor or glucagon-like peptide 1 receptor ag... | [
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junction with other traditional, guideline-based preventive medical therapies for blood pressure, lipids, and glycemia and antiplatelet therapy. Re-\nprinted with permission from Das et al. (309).diabetesjournals.org/care Cardiovascular Disease and Risk Management S209\n©AmericanDiabetesAssociation | [
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... |
diabetes. Therefore, in people with type 2\ndiabetes and CKD with albuminuria\ntreated with maximum tolerated dosesof ACE inhibitor or ARB, addition of finer-\nenone should be considered to improvecardiovascular outcomes and reduce therisk of CKD progression.\nClinical Approach\nAs has been carefully outlined in Fig. 9.... | [
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Clinical Approach\nAs has been carefully outlined in Fig. 9.3\nin Section 9, “Pharmacologic Approaches\nto Glycemic Treatment, ”people with\ntype 2 diabetes with or at high risk forASCVD, heart failure, or CKD should be\ntreated with a cardioprotective SGLT2 in-\nhibitor and/or GLP-1 receptor agonist aspart of the comp... | [
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cardiovascular and kidney risk reduction.\nImportantly, these agents should be in-cluded in the plan of care irrespective of\nthe need for additional glucose lowering\nand irrespective of metformin use. Suchan approach has also been describedin the ADA-endorsed American College\nof Cardiology “2020 Expert Consensus\nDe... | [
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Decision Pathway on Novel Therapies\nfor Cardiovascular Risk Reduction in\nPatients With Type 2 Diabetes ”(309).\nFigure 10.3, reproduced from that deci-\nsion pathway, outlines the approach to\nrisk reduction with SGLT2 inhibitor or\nGLP-1 receptor agonist therapy in con-junction with other traditional, guideli-ne-bas... | [
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for blood pressure, lipids, and glycemia\nand antiplatelet therapy.\nAdoption of these agents should be\nreasonably straightforward in people\nwith established cardiovascular or kid-\nney disease who are later diagnosedwith diabetes, as the cardioprotectiveagents can be used from the outset of di-\nabetes management. O... | [
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0.01381351426243782,
0.045774053782224655,
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abetes management. On the other hand,\nincorporation of SGLT2 inhibitor or GLP-1receptor agonist therapy in the care of\nindividuals with more long-standing dia-\nbetes may be more challenging, particu-larly if individuals are using an already\ncomplex glucose-lowering plan. In such | [
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complex glucose-lowering plan. In such\nindividuals, SGLT2 inhibitor or GLP-1receptor agonist therapy may need toreplace some or all of their existing medi-\ncations to minimize risks of hypoglycemia\nand adverse side effects and potentiallyto minimize medication costs. Close col-\nlaboration between primary and specia... | [
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laboration between primary and specialty\ncare professionals can help to facilitatethese transitions in clinical care and, inturn, improve outcomes for high-risk\npeople with type 2 diabetes.\nReferences\n1. Parker ED, Lin J, Mahoney T, et al. Economic\ncosts of diabetes in the U.S. in 2022. Diabetes | [
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-0.035857681185007095,
0.03800695016980171,
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-0.03388045355677605,
-0.1183617040514946,
0.07052372395992279,
-0.14115367829799652,
0... |
costs of diabetes in the U.S. in 2022. Diabetes\nCare 1 November 2023 [Epub ahead of print].DOI: 10.2337/dci23-0085\n2. Gæde P , Oellgaard J, Carstensen B, et al. Years\nof life gained by multifactorial intervention in\npatients with type 2 diabetes mellitus and micro-\nalbuminuria: 21 years follow-up on the Steno-2 | [
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0.02874898910522461,
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-0.02886379137635231,
0.05339094623923302,
-0.02407027594745159,
-0.00762007012963295,
-0.034039564430713654,
0.016903046518564224,
-0.06224256381392479,
-0.044... |
albuminuria: 21 years follow-up on the Steno-2\nrandomised trial. Diabetologia 2016;59:2298 –\n2307\n3. Gaede P, Lund-Andersen H, Parving HH,\nPedersen O. Effect of a multifactorial inter-\nvention on mortality in type 2 diabetes. N Engl JMed 2008;358:580– 591\n4. Khunti K, Kosiborod M, Ray KK. Legacy\nbene fits of bloo... | [
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0.024482382461428642,
-0.053589604794979095,
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-0... |
bene fits of blood glucose, blood pressure and\nlipid control in individuals with diabetes and\ncardiovascular disease: time to overcome multi-\nfactorial therapeutic inertia? Diabetes Obes\nMetab 2018;20:1337– 1341\n5. Ali MK, Bullard KM, Saaddine JB, Cowie CC,\nImperatore G, Gregg EW. Achievement of goals in | [
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-0.041... |
Imperatore G, Gregg EW. Achievement of goals in\nU.S. diabetes care, 1999-2010. N Engl J Med2013;368:1613– 1624\n6. Buse JB, Ginsberg HN, Bakris GL, et al.;\nAmerican Heart Association; American Diabetes\nAssociation. Primary prevention of cardiovasculardiseases in people with diabetes mellitus: a\nscienti fic statement... | [
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-0.02820776030421257,
-0.0... |
scienti fic statement from the American Heart\nAssociation and the American Diabetes Associ-\nation. Diabetes Care 2007;30:162 –172\n7. Pop-Busui R, Januzzi JL, Bruemmer D, et al.Heart failure: An underappreciated complicationof diabetes. A consensus report of the american\ndiabetes association. Diabetes Care 2022;45:\n... | [
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diabetes association. Diabetes Care 2022;45:\n1670– 1690\n8. Cavender MA, Steg PG, Smith SC Jr, et al.;REACH Registry Investigators. Impact of diabetes\nmellitus on hospitalization for heart failure,\ncardiovascular events, and death: outcomes at4 years from the Reduction of Atherothrombosis\nfor Continued Health (REAC... | [
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for Continued Health (REACH) Registry. Cir-\nculation 2015;132:923– 931\n9. McAllister DA, Read SH, Kerssens J, et al.\nIncidence of hospitalization for heart failure and\ncase-fatality among 3.25 million people with andwithout diabetes mellitus. Circulation 2018;138:\n2774– 2786\n10. Lam CSP , Voors AA, de Boer RA, So... | [
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2774– 2786\n10. Lam CSP , Voors AA, de Boer RA, Solomon SD,\nvan Veldhuisen DJ. Heart failure with preservedejection fraction: from mechanisms to therapies.\nEur Heart J 2018;39:2780– 2792\n11. Zinman B, Wanner C, Lachin JM, et al.;\nEMPA-REG OUTCOME Investigators. Empagli-\nflozin, cardiovascular outcomes, and mortalit... | [
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flozin, cardiovascular outcomes, and mortality\nin type 2 diabetes. N Engl J Med 2015;373:\n2117– 2128\n12. Neal B, Perkovic V, Mahaffey KW, et al.;\nCANVAS Program Collaborative Group. Canagli-\nflozin and cardiovascular and renal events in type 2\ndiabetes. N Engl J Med 2017;377:644 –657\n13. Fitchett D, Butler J, van ... | [
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13. Fitchett D, Butler J, van de Borne P , et al.;\nEMPA-REG OUTCOME trial investigators. Effects\nof empagli flozin on risk for cardiovascular death\nand heart failure hospitalization across the\nspectrum of heart failure risk in the EMPA-REG\nOUTCOME trial. Eur Heart J 2018;39:363– 37014. McMurray JJV, Solomon SD, Inz... | [
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et al.; DAPA-HF Trial Committees and In-\nvestigators. Dapagli flozin in patients with heart\nfailure and reduced ejection fraction. N Engl JMed 2019;381:1995– 2008 | [
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15. Arnott C, Li Q, Kang A, et al. Sodium-glucosecotransporter 2 inhibition for the prevention ofcardiovascular events in patients with type 2diabetes mellitus: a systematic review and meta-\nanalysis. J Am Heart Assoc 2020;9:e014908\n16. Lloyd-Jones DM, Braun LT, Ndumele CE, | [
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16. Lloyd-Jones DM, Braun LT, Ndumele CE,\net al. Use of risk assessment tools to guidedecision-making in the primary prevention ofatherosclerotic cardiovascular disease: a special\nreport from the American Heart Association\nand American College of Cardiology. Circulation\n2019;139:e1162– e1177\n17. Whelton PK, Carey ... | [
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-0.... |
2019;139:e1162– e1177\n17. Whelton PK, Carey RM, Aronow WS, et al.\n2017 ACC/AH A/AAPA/ABC/ACPM/AGS/APhA/\nASH/ASPC/NMA/PCNA guideline for the pre-\nvention, detection, evaluation, and managementof high blood pressure in adults: a report of the\nAmerican College of Cardiology/American Heart | [
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0.057160139083862305,
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-0.008489752188324928,
-0.029994970187544823,
0.0337534137070179,
-0.036183036863803864,
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-0.04590018093585968,
-0.020867764949798584,
0.023512084037065506,
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-0.06033850088715553,
... |
American College of Cardiology/American Heart\nAssociation Task Force on Clinical PracticeGuidelines. J Am Coll Cardiol 2018;71:e127 –e248\n18. de Boer IH, Bangalore S, Benetos A, et al.Diabetes and hypertension: a position statement\nby the American Diabetes Association. Diabetes\nCare 2017;40:1273– 1284 | [
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-0.07626979798078537,
0.032634034752845764,
-0.02057785727083683,
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-0.03872658312320709,
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Care 2017;40:1273– 1284\n19. Unger T, Borghi C, Charchar F, et al. 2020International Society of Hypertension global\nhypertension practice guidelines. Hypertension\n2020;75:1334– 1357\n20. Williams B, Mancia G, Spiering W, et al.; ESCScienti fic Document Group. 2018 ESC/ESH\nguidelines for the management of arterial | [
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-0.052781879901885986,
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guidelines for the management of arterial\nhypertension. Eur Heart J 2018;39:3021– 3104\n21. Ishigami J, Charleston J, Miller ER 3rd,\nMatsushita K, Appel LJ, Brady TM. Effects of cuffsize on the accuracy of blood pressure readings:\nthe Cuff(SZ) randomized crossover trial. JAMA\nIntern Med 2023;183:1061– 1068 | [
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0.07934466004371643,
-0.05996474251151085,
-0.019818810746073723,
-0.05023656412959099,
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-0.08264856785535812,
0.017570899799466133,
-0.019023161381483078,
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Intern Med 2023;183:1061– 1068\n22. Bobrie G, Gen /C18es N, Vaur L, et al. Is “isolated\nhome ”hypertension as opposed to “isolated\noffice”hypertension a sign of greater cardio-\nvascular risk? Arch Intern Med 2001;161:\n2205– 2211 | [
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0.016679957509040833,
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-0.07009440660476685,
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-0.0... |
vascular risk? Arch Intern Med 2001;161:\n2205– 2211\n23. Sega R, Facchetti R, Bombelli M, et al.Prognostic value of ambulatory and home bloodpressures compared with of fice blood pressure in\nthe general population: follow-up results fromt h eP r e s s i o n iA r t e r i o s eM o n i t o r a t eeL o r oAssociazioni (PA... | [
-0.00011580716818571091,
0.06349898874759674,
-0.028826897963881493,
0.029311900958418846,
-0.029546041041612625,
0.004625947680324316,
-0.050922952592372894,
0.11590512096881866,
-0.029645131900906563,
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-0.020792540162801743,
-... |
111:1777– 1783\n24. Omboni S, Gazzola T, Carabelli G, Parati G.\nClinical usefulness and cost effectiveness ofhome blood pressure telemonitoring: meta-analysis of randomized controlled studies. J\nHypertens 2013;31:455– 467; discussion 467– 468\n25. Emdin CA, Rahimi K, Neal B, Callender T, | [
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0.07226766645908356,
-0.016361558809876442,
-0.026365306228399277,
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0.017649730667471886,
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-0.06... |
25. Emdin CA, Rahimi K, Neal B, Callender T,\nPerkovic V, Patel A. Blood pressure lowering intype 2 diabetes: a systematic review and meta-\nanalysis. JAMA 2015;313:603– 615\n26. Arguedas JA, Leiva V, Wright JM. Blood\npressure targets for hypertension in people withdiabetes mellitus. Cochrane Database Syst Rev2013;10:... | [
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0.0993741974234581,
-0.036661867052316666,
0.024578141048550606,
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27. Ettehad D, Emdin CA, Kiran A, et al. Blood\npressure lowering for prevention of cardio-\nvascular disease and death: a systematic reviewand meta-analysis. Lancet 2016;387:957– 967S210 Cardiovascular Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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-0.011318785138428211,
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0.04868973419070244,
-0.054919689893722534,
-0.0... |
11. Chronic Kidney Disease and\nRisk Management: Standards of\nCare in Diabetes— 2024\nDiabetes Care 2024;47(Suppl. 1):S219 –S230 |https://doi.org/10.2337/dc24-S011American Diabetes Association\nProfessional Practice Committee *\nThe American Diabetes Association (ADA) “Standards of Care in Diabetes ”includes | [
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-0.013038504868745804,
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-0.07193382829427719,
0.10711489617824554,
-0.07253695279359818,
-0... |
the ADA ’s current clinical practice recommendations and is intended to provide the\ncomponents of diabetes care, general treatment goals and guidelines, and tools to\nevaluate quality of care. Members of the ADA Professional Practice Committee, an\ninterprofessional expert committee, are responsible for updating the S... | [
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-0.06390462070703506,
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-0.1396506130695343,
0.016396852... |
Care annually, or more frequently as warranted. For a detailed description of ADAstandards, statements, and reports, as well as the evidence-grading system for ADA ’s | [
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-0.028547164052724838,
-0.0001817629236029461,
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-0.03224292770028114,
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... |
clinical practice recommendations and a full list of Professional Practice Committeemembers, please refer to Introduction and Methodology. Readers who wish to com-ment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.\nFor prevention and management of diabetes complications in children and... | [
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-0.0947912409901619,
0.03127... |
please refer to Section 14, “Children and Adolescents. ”\nCHRONIC KIDNEY DISEASE\nScreening\nRecommendations\n11.1a At least annually, urinary albumin (e.g., spot urinary albumin-to-creatinine\nratio [UACR]) and estimated glomerular filtration rate [eGFR] should be assessed\nin people with type 1 diabetes with duration ... | [
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0.03079981915652752,
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0.029324971139431,
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0.03949... |
type 2 diabetes regardless of treatment. B\n11.1b In people with established chronic kidney disease (CKD), urinary albu-\nmin (e.g., spot UACR) and eGFR should be monitored 1 –4 times per year de-\npending on the stage of the kidney disease ( Fig. 11.1 ).B\nTreatment\nRecommendations | [
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Treatment\nRecommendations\n11.2 Optimize glucose management to reduce the risk or slow the progression\nof CKD. A\n11.3 Optimize blood pressure control and reduce blood pressure variability to\nreduce the risk or slow the progression of CKD and reduce cardiovascular\nrisk. A\n11.4a In nonpregnant people with diabetes ... | [
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inhibitor or an angiotensin receptor blocker (ARB) is recommended for thosewith moderately increased albuminuria (UACR 30 –299 mg/g creatinine) Band is\nstrongly recommended for those with severely increased albuminuria (UACR$300 mg/g creatinine) and/or eGFR <60 mL/min/1.73 m\n2to prevent the pro- | [
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... |
2to prevent the pro-\ngression of kidney disease and reduce cardiovascular events. A*A complete list of members of the American\nDiabetes Association Professional Practice Committeecan be found at https://doi.org/10.2337/dc24-SINT.\nDuality of interest information for each author is\navailable at https://doi.org/10.233... | [
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available at https://doi.org/10.2337/dc24-SDIS.\nSuggested citation: American Diabetes Association\nProfessional Practice Committee. 11. Chronickidney disease and risk management: Standards\nof Care in Diabetes —2024. Diabetes Care 2024;\n47(Suppl. 1):S219 –S230 | [
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-0... |
47(Suppl. 1):S219 –S230\n© 2023 by the American Diabetes Association.Readers may use this article as long as thework is properly cited, the use is educationaland not for profi t, and the work is not altered. | [
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More information is available at https://www.diabetesjournals.org/journals/pages/license.11. CHRONIC KIDNEY DISEASE AND RISK MANAGEMENTDiabetes Care Volume 47, Supplement 1, January 2024 S219\n©AmericanDiabetesAssociation | [
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11.4b Periodically monitor for increased\nserum creatinine and potassium levels\nwhen ACE inhibitors, ARBs, and miner-\nalocorticoid receptor antagonists areused, or for hypokalemia when diu-retics are used. B\n11.4c An ACE inhibitor or an ARB is | [
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11.4c An ACE inhibitor or an ARB is\nnot recommended for the primary pre-vention of CKD in people with diabetesw h oh a v en o r m a lb l o o dp r e s s u r e ,n o r -mal UACR ( <30 mg/g creatinine), and\nnormal eGFR. A\n11.4d Do not discontinue renin-\nangiotensin system blockade for mildto moderate increases in serum... | [
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-0.09871275722980499,
-0.02... |
nine (#30%) in the absence of signs of\nextracellular fluid volume depletion. A\n11.5a For people with type 2 diabe-\ntes and CKD, use of a sodium –glucose\ncotransporter 2 (SGLT2) inhibitor isrecommended to reduce CKD pro-\ngression and cardiovascular events inindividuals with eGFR $20 mL/min/\n1.73 m\n2and urinary alb... | [
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0.024642126634716988,
-0.04535635560750961,
-0.025614939630031586,
... |
1.73 m\n2and urinary albumin $200 mg/g\ncreatinine. A11.5b For people with type 2 diabe-\ntes and CKD, use of an SGLT2 inhibi-\ntor is recommended to reduce CKD\nprogression and cardiovascular eventsin individuals with eGFR $20 mL/min/\n1.73 m\n2and urinary albumin rang-\ning from normal to 200 mg/g creati-nine. B\n11.... | [
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11.5c For cardiovascular risk reduc-\ntion in people with type 2 diabetesand CKD, consider use of an SGLT2inhibitor (if eGFR is $20 mL/min/\n1.73 m\n2), a glucagon-like peptide 1\nagonist, or a nonsteroidal mineralo-corticoid receptor antagonist (if eGFRis$25 mL/min/1.73 m\n2).A\n11.5d As people with CKD and albu- | [
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... |
2).A\n11.5d As people with CKD and albu-\nminuria are at increased risk forcardiovascular events and CKD pro-gression, a nonsteroidal mineralocor-ticoid receptor antagonist that has\nbeen shown to be effective in clinical\ntrials is recommended to reduce car-diovascular events and CKD progres-\nsion (if eGFR is $25 mL/... | [
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0.09211047738790512,
-0.05230336636304855,
-0.02507510408759117,
0.00... |
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