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• W1967903062 abstract "Cardiovascular disease (CVD) is the most common cause of death in industrialized nations. Type 2 diabetes is a CVD risk factor that confers risk similar to a previous myocardial infarction in an individual who does not have diabetes. In addition, the most common cause of chronic kidney disease (CKD) is diabetes. Together, diabetes and hypertension account for more than two-thirds of CVD risk, and other risk factors such as dyslipidemia contribute to the remainder of CVD risk. CKD, particularly with presence of significant albuminuria, should be considered an additional cardiovascular risk factor. There is no consensus on how to assess and stratify risk for patients with kidney disease across subspecialties that commonly treat such patients. This paper summarizes the results of a consensus conference utilizing a patient case to discuss the integrated management of hypertension, kidney disease, dyslipidemia, diabetes, and heart failure across disciplines. Cardiovascular disease (CVD) is the most common cause of death in industrialized nations. Type 2 diabetes is a CVD risk factor that confers risk similar to a previous myocardial infarction in an individual who does not have diabetes. In addition, the most common cause of chronic kidney disease (CKD) is diabetes. Together, diabetes and hypertension account for more than two-thirds of CVD risk, and other risk factors such as dyslipidemia contribute to the remainder of CVD risk. CKD, particularly with presence of significant albuminuria, should be considered an additional cardiovascular risk factor. There is no consensus on how to assess and stratify risk for patients with kidney disease across subspecialties that commonly treat such patients. This paper summarizes the results of a consensus conference utilizing a patient case to discuss the integrated management of hypertension, kidney disease, dyslipidemia, diabetes, and heart failure across disciplines. This 58-year-old non-smoking obese man presents 1 week after hospital discharge for the treatment of heart failure. Hospital stay revealed left ventricular hypertrophy, diastolic dysfunction, with left ventricular systolic ejection fraction of 50% by echocardiogram, and no evidence of myocardial ischemia. He feels well. The past medical history includes type 2 diabetes, hypertension, and dyslipidemia treated with ramipril 5 mg, furosemide 40 mg, metoprolol XL 25 mg, metformin 1 g, and atorvastatin 20 mg (all daily). Physical exam: blood pressure (BP) 152/92 mm Hg, P 68/min and regular, and body mass index 33. Jugular venous pressure is not visible. Heart rate is regular with S1 and S2 and no gallop. Lung exam reveals bibasilar rales. There is +1 peripheral edema. Data are shown in Table 1. Screening results for anemia, and mineral and bone disorder are unremarkable (data not shown).Table 158-Year-old non-smoking obese man with heart failure in the setting of type 2 diabetes, hypertension with preserved left ventricular function, and dyslipidemiaVignette dataDischargeWeek 1Week 3Week 5Blood pressure138/88152/92138/86134/84eGFR (ml/min per 1.73 m2)45434034Fasting serum testCreatinine (mg/dl)1.61.61.72.0Potassium (mEq/l)3.85.03.84.1Cholesterol (mg/dl)188HDL (mg/dl)32LDL (mg/dl)112Triglycerides (mg/dl)220Glucose (mg/dl)188120136120Hemoglobin A1c (%)6.7Urinary testAlbumin–creatinine ratio (mg/g)480360300InterventionPrescribed treatmentRamipril 5 mg, furosemide 40 mg, metoprolol XL 25 mg, metformin XL 1 g, atorvastatin 20 mg (all once daily)Increase furosemide 40 mg twice dailyIncrease ramipril 10 mg, substitute glipizide 10 mg for metformin (all once daily)Add spironolactone 25 mg once dailyAbbreviations: eGFR, estimated glomerular filtration rate; HDL, high-density cholesterol; LDL, low-density cholesterol. Open table in a new tab Abbreviations: eGFR, estimated glomerular filtration rate; HDL, high-density cholesterol; LDL, low-density cholesterol. BP values >140/90 mm Hg are associated with higher risk for adverse kidney and cardiovascular outcomes.1.Chobanian A.V. Bakris G.L. Black H.R. et al.The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.JAMA. 2003; 289: 2560-2572Crossref PubMed Scopus (10827) Google Scholar The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI) hypertension guideline level of evidence is A: angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) for proteinuric individuals, B: target <130/80, and C: proteinuria attenuation as a goal of therapy.2.National Kidney Foundation KDOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease.Am J Kidney Dis. 2004; 43: S1-S290PubMed Google Scholar The optimal lower BP target is not clearly established as the trial evidence is limited by the failure of most studies to achieve <130/80 for patients with diabetes and/or CKD, as recommended by Joint National Committee 7,1.Chobanian A.V. Bakris G.L. Black H.R. et al.The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.JAMA. 2003; 289: 2560-2572Crossref PubMed Scopus (10827) Google Scholar American Diabetes Association,3.American Diabetes Association Standards of medical care in diabetes.Diabetes Care. 2010; 33: S1-S99PubMed Google Scholar and KDOQI guidelines,2.National Kidney Foundation KDOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease.Am J Kidney Dis. 2004; 43: S1-S290PubMed Google Scholar for slowing the loss of kidney function and improving cardiovascular disease (CVD) outcomes. However, most of the studies showed that the achieved systolic BP (SBP) target predicts loss of kidney function. In addition, for patients over the age of 50, the SBP is the best predictor of myocardial infarction, heart failure, and stroke. Lastly, the target of <130/80 does not address the risks of overtreatment. A meta-analysis of 61 observational studies, including one million adults with no pre-existing CVD, did demonstrate that risk for cardiovascular events doubles for every systolic/diastolic 20/10 above a BP of 115/75.4.Lewington S. Clarke R. Qizilbash N. et al.Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.Lancet. 2002; 360: 1903-1913Abstract Full Text Full Text PDF PubMed Scopus (4354) Google Scholar However, in two prospective studies that randomized subjects without diabetes to different levels of BP reduction, the African American Study of Kidney Disease (AASK)5.Wright Jr, J.T. Bakris G. Greene T. African American Study of Kidney Disease and Hypertension Study Group et al.Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial.JAMA. 2002; 288: 2421-2431Crossref PubMed Scopus (1104) Google Scholar and the Ramipril Efficacy in Nephropathy-2 (REIN-2) study,6.Ruggenenti P. Perna A. Loriga G. et al.Blood-pressure control for renoprotection in patients with non-diabetic chronic renal disease (REIN-2): multicentre, randomised controlled trial.Lancet. 2005; 365: 939-946Abstract Full Text Full Text PDF PubMed Scopus (318) Google Scholar neither kidney disease progression nor CVD risk was reduced at the lower target (mean arterial pressure ≤92 in AASK and <130/80 in REIN-2). The Action to Control Cardiovascular Risk in Diabetes (ACCORD) study showed no effect of an intensive target SBP <120 versus SBP <140 on CVD outcomes.7.ACCORD Study GroupCushman WCEvans G.W. Byington R.P. et al.Effects of intensive blood-pressure control in type 2 diabetes mellitus.N Engl J Med. 2010; 362: 1575-1585Crossref PubMed Scopus (0) Google Scholar A practical approach targets a sitting SBP of 130 or less if tolerated, including assessment of symptoms of orthostatic hypotension. In addition, current evidence supporting albuminuria as a therapeutic target is reviewed in detail elsewhere.8.Levey A.S. Cattran D. Friedman A. et al.Proteinuria as a surrogate outcome in CKD: report of a scientific workshop sponsored by the National Kidney Foundation and the US Food and Drug Administration.Am J Kidney Dis. 2009; 54: 205-226Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar Methods of monitoring BP are described in Table 2.9.Pickering T.G. White W.B. Giles T.D. et al.When and how to use self (home) and ambulatory blood pressure monitoring.J Am Soc Hypertens. 2010; 4: 56-61Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar, 10.Agarwal R. Home BP for assessing haemodialysis hypertension.Nephrol Dial Transplant. 2007; 22: 3089-3090Crossref PubMed Scopus (1) Google Scholar, 11.Bangash F. Agarwal R. Masked hypertension and white-coat hypertension in chronic kidney disease: a meta-analysis.Clin J Am Soc Nephrol. 2009; 4: 656-664Crossref PubMed Scopus (47) Google Scholar, 12.Agarwal R. Andersen M.J. Blood pressure recordings within and outside the clinic and cardiovascular events in chronic kidney disease.Am J Nephrol. 2006; 26: 503-510Crossref PubMed Scopus (52) , 13.Agarwal R. Andersen M.J. Prognostic importance of clinic and home blood pressure recordings in patients with chronic kidney disease.Kidney Int. 2006; 69: 406-411Abstract Full Text Full Text PDF PubMed Scopus (99) Google ScholarTable 2Methods of blood pressure measurementMethodAdvantagesDisadvantagesOffice/clinical blood pressure measurementMost commonly used in RCTs and long-term outcome trialsHighly variable, observer bias, white-coat HTNHBPMImproves patient compliance and hypertension control ratesRequires training and device calibrationDetection of white-coat and masked HTNWide availability and low costABPMOnly way to assess non-dipping (common in CKD)Not commonly reimbursed by all health insurersDetection of white-coat and masked HTNAvailabilityAbbreviations: ABPM, ambulatory blood pressure monitoring; CKD, chronic kidney disease; HBPM, self-home blood pressure monitoring; HTN, hypertension; RCTs, randomized controlled trials. Open table in a new tab Abbreviations: ABPM, ambulatory blood pressure monitoring; CKD, chronic kidney disease; HBPM, self-home blood pressure monitoring; HTN, hypertension; RCTs, randomized controlled trials. The diagnosis of CKD should influence the selection and sequence of antihypertensive agent use.1.Chobanian A.V. Bakris G.L. Black H.R. et al.The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.JAMA. 2003; 289: 2560-2572Crossref PubMed Scopus (10827) Google Scholar, 2.National Kidney Foundation KDOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease.Am J Kidney Dis. 2004; 43: S1-S290PubMed Google Scholar By the time individuals develop impaired kidney function, three or more drugs are generally needed to achieve BP targets. Overall, attaining BP targets receives less attention in the literature and is arguably more important than selection of individual agents. Studies in diabetic nephropathy demonstrate that the greater the initial decrease of kidney function with RAAS blockade, the greater the long-term preservation of kidney function.14.Bakris G.L. Williams M. Dworkin L. et al.Preserving renal function in adults with hypertension and diabetes: a consensus approach. National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group.Am J Kidney Dis. 2000; 36: 646-661Abstract Full Text Full Text PDF PubMed Google Scholar Consequently, an initial limited loss of estimated glomerular filtration rate (eGFR) following the initiation of RAAS blockade is not a concern unless it exceeds 30–50%, in which case states predisposing to excessive eGFR responses to RAAS blockade such as diuretic-induced hypovolemia or renal artery stenosis should be considered.2.National Kidney Foundation KDOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease.Am J Kidney Dis. 2004; 43: S1-S290PubMed Google Scholar, 15.Bakris G.L. Weir M.R. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern?.Arch Intern Med. 2000; 160: 685-693Crossref PubMed Google Scholar, 16.Mangrum A.J. Bakris G.L. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in chronic renal disease: safety issues.Semin Nephrol. 2004; 24: 168-175Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar If these conditions are not present, RAAS blockade should be continued. In addition to concern about the initial decrease of eGFR after RAAS blockade, another common misconception is the notion that RAAS blockade should be avoided if kidney function is impaired. Nevertheless, when initiating RAAS blockade, the clinician and the patient should be aware of potential side effects associated with this therapy, e.g., hyperkalemia, cough, angioedema, and anemia. Because of the association between increases in albuminuria and CKD progression,17.Ruggenenti P. Perna A. Remuzzi G. GISEN Group Investigators Retarding progression of chronic renal disease: the neglected issue of residual proteinuria.Kidney Int. 2003; 63: 2254-2261Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar it is important to monitor albuminuria before and after onset of RAAS blockade to achieve optimal attenuation. High-sodium intake further exacerbates pre-existing albuminuria and increases CKD progression.18.Jones-Burton C. Mishra S.I. Fink J.C. et al.An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease.Am J Nephrol. 2006; 26: 268-275Crossref PubMed Scopus (52) Google Scholar If urinary albumin–creatinine ratio is not decreased by at least >30% below initial levels where treatment was initiated or to <300 mg/g, in spite of BP levels <130/80 on a low-sodium diet, consideration should be given to addition of either a different class of RAAS blocker or possibly diltiazem.19.Kalaitzidis R.G. Bakris G.L. Should proteinuria reduction be the criterion for antihypertensive drug selection for patients with kidney disease?.Curr Opin Nephrol Hypertens. 2009; 18: 386-391Crossref PubMed Scopus (0) Google Scholar, 20.Lea J. Greene T. Hebert L. et al.The relationship between magnitude of proteinuria reduction and risk of end-stage renal disease: results of the African American study of kidney disease and hypertension.Arch Intern Med. 2005; 165: 947-953Crossref PubMed Scopus (185) Google Scholar, 21.Bakris G.L. Weir M.R. Secic M. et al.Differential effects of calcium antagonist subclasses on markers of nephropathy progression.Kidney Int. 2004; 65: 1991-2002Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar The evidence for the combination RAAS blocking therapy for proteinuria reduction is currently limited to a meta-analysis of 49 small, variable quality studies wherein proteinuria reduction was assessed against a dihydropyridine calcium channel blocker, thus, favoring the ACEi and ARB.22.Kunz R. Friedrich C. Wolbers M. et al.Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease.Ann Intern Med. 2008; 148: 30-48Crossref PubMed Google Scholar The renal outcomes with telmisartan, ramipril, or both in people at high vascular risk (ONTARGET) study demonstrated no benefit of the ACEi/ARB combination arm versus either the ramipril 10 mg daily or telmisartan 80 mg daily groups on initiation of chronic dialysis.23.Mann J.F. Schmieder R.E. McQueen M. et al.Renal outcomes with telmisartan, ramipril, or both, in people at high vascular risk (the ONTARGET study): a multicentre, randomised, double-blind, controlled trial.Lancet. 2008; 372: 547-553Abstract Full Text Full Text PDF PubMed Scopus (933) Google Scholar In contrast, the combination did significantly lower proteinuria versus either form of monotherapy. An important caveat is that the majority of the patients enrolled in the trial did not have albumin–creatinine ratio ≥300 mg/g.24.Sarafidis P.A. Bakris G.L. Renin-angiotensin blockade and kidney disease.Lancet. 2008; 372: 511-512Abstract Full Text Full Text PDF PubMed Scopus (41) Google Scholar Although the potassium sparing diuretics, spironolactone, and epleronone have been shown to reduce proteinuria, there are no kidney outcome data,25.Bomback A.S. Kshirsagar A.V. Amamoo M.A. et al.Change in proteinuria after adding aldosterone blockers to ACE inhibitors or angiotensin receptor blockers in CKD: a systematic review.Am J Kidney Dis. 2008; 51: 199-211Abstract Full Text Full Text PDF PubMed Scopus (114) Google Scholar and their addition to ACEi or ARB increases the risk of hyperkalemia. This hyperkalemia risk is predominantly seen, however, among those with an eGFR <45 ml/min per 1.73 m2 along with a baseline potassium of >4.5 mEq/l when already on an appropriate diuretic and maximal dose RAAS blocker.26.Khosla N. Kalaitzidis R. Bakris G.L. Predictors of hyperkalemia risk following hypertension control with aldosterone blockade.Am J Nephrol. 2009; 30: 418-424Crossref PubMed Scopus (72) Google Scholar Thus, the role of these agents is not established. In addition, the direct renin inhibitor, aliskiren, reduced proteinuria in one recent trial when added to an ARB.27.Parving H.H. Persson F. Lewis J.B. et al.Aliskiren combined with losartan in type 2 diabetes and nephropathy.N Engl J Med. 2008; 358: 2433-2446Crossref PubMed Scopus (811) Google Scholar Similarly, its role is not established. In non-proteinuric patients, there is little definite evidence for the superiority of the RAAS blockade over other antihypertensive medications, except in the AASK trial, and in light of the ONTARGET trial, combination ACEi/ARB therapy should be avoided in patients with albumin–creatinine ratio <300 mg/g. If BP remains uncontrolled on three or more drugs given in maximally effective and tolerated doses, the patient should be referred to a hypertension specialist or nephrologist. The main causes are insufficient diuretic treatment or failure to restrict excessive sodium intake, non-adherence to medications, or other medications such as nonsteroidal anti-inflammatory drugs-induced sodium retention, and obstructive sleep apnea.1.Chobanian A.V. Bakris G.L. Black H.R. et al.The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.JAMA. 2003; 289: 2560-2572Crossref PubMed Scopus (10827) Google ScholarTable 1 describes the patient's course and drug interventions received." @default.
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• W1967903062 date "2010-10-01" @default.
• W1967903062 modified "2023-10-03" @default.
• W1967903062 title "National Kidney Foundation consensus conference on cardiovascular and kidney diseases and diabetes risk: an integrated therapeutic approach to reduce events" @default.
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