Overview of diagnosis of heart disease in patients on dialysis

INTRODUCTION — 

Cardiovascular disease is an important cause of morbidity and mortality in patients undergoing maintenance dialysis.

This topic provides an overview of diagnosis of heart disease in patients on dialysis and includes discussion of the diagnosis of heart failure (HF) and asymptomatic left ventricular (LV) dysfunction in this patient population.

The management of heart disease in patients receiving maintenance dialysis is discussed separately:

●HF. (See "Management of heart failure in patients on dialysis".)

●Atrial fibrillation. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" and "Atrial fibrillation in adults: Selection of candidates for anticoagulation", section on 'Chronic kidney disease'.)

PATHOPHYSIOLOGY — 

Patients with end-stage kidney disease (ESKD) have a greater burden of traditional cardiovascular disease factors (older age, diabetes, hypertension) compared with the general population. In addition, kidney-specific factors such as anemia, volume overload, inflammation, and altered mineral metabolism, among others, are associated with increased cardiovascular risk. Ventricular-vascular remodeling and stiffening contribute to cardiovascular disease in patients on dialysis. Cardiac findings that are common in patients with ESKD on dialysis include LV hypertrophy (LVH), diffuse myocardial fibrosis, and hemodialysis-induced myocardial stunning [1].

●Left ventricular hypertrophy – LVH is common among patients with ESKD with a reported prevalence of up to 75 percent [2-4]. LVH is a major risk factor for cardiovascular morbidity and mortality in patients with ESKD [5]. Among those who have LVH, two-thirds die from HF or sudden death, while one-third die from a noncardiovascular event. Worsening of LVH is a strong predictor of sudden death [6]. LVH is associated with increased QT interval and dispersal [2]. Both concentric and eccentric patterns of LVH (figure 1) are associated with risk of all-cause mortality among patients on dialysis [7,8]. Patients with eccentric LVH may be at higher risk of sudden death than patients with concentric LVH [9,10]. LVH is also associated with LV diastolic dysfunction, and diastolic dysfunction is also observed in some patients on dialysis without LVH [7]. LV systolic dysfunction is less common than LV diastolic dysfunction. Right ventricular (RV) dysfunction has also been observed in patients on dialysis [11,12]. LV diastolic or systolic dysfunction may progress to cause HF [13]. Ventricular stiffening related to LVH can also make the patient more vulnerable to episodes of hypotension during dialysis.

Among patients on dialysis, the major risk factors for LVH are hypertension (particularly systolic blood pressure) and increasing age [14,15]. Chronic volume overload, anemia, Klotho deficiency, increased arterial stiffness with associated loss of aortic distensibility, and possibly an increase in cardiac index induced by the arteriovenous fistula created for hemodialysis access may also contribute to development of LVH. Elevated levels of fibroblast growth factor (FGF) 23 seen with decreased phosphorus renal clearance may contribute to an increase in LV mass independent of hypertension [16]. (See "Cardiovascular and renal effects of anemia in chronic kidney disease" and "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

●Myocardial fibrosis – Cardiovascular magnetic resonance (CMR) imaging studies have suggested that diffuse myocardial fibrosis is common among patients with ESKD, even in the presence of a normal LV ejection fraction (LVEF), and is associated with LVH [17-19]. A pattern consistent with diffuse fibrosis or infiltration is distinct from a pattern of focal subendocardial fibrosis (likely caused by myocardial infarction [MI]) and a pattern of midwall fibrosis or infiltration [19]. Extensive fibrosis has also been identified on biopsy. As an example, endocardial biopsies were performed in a study of 40 patients with ESKD with dilated cardiomyopathy without coronary artery disease and in a control group of 50 patients not on dialysis with idiopathic dilated cardiomyopathy [20]. Severe myocyte hypertrophy and extensive fibrosis were characteristic of the dialysis group. Patients not on dialysis had a similar proportion of fibrosis but, overall, a much smaller proportion of severely hypertrophic myocytes (8 versus 45 percent in patients on dialysis). In the patients on dialysis, increasing fibrosis correlated with a decreased survival rate. CMR spectroscopy in patients with ESKD has identified altered myocardial metabolism with less efficient use of high-energy phosphates [17,21]. (See "Definition and classification of the cardiomyopathies" and "Causes of dilated cardiomyopathy".)

●Myocardial stunning due to hemodialysis – Hemodialysis-induced myocardial stunning is common (eg, prevalence of 27 and 64 percent [22,23]) and is associated with reduced survival rates [22,23]. Hemodialysis-induced myocardial stunning is defined as hemodialysis-induced segmental LV dysfunction in the absence of known heart disease; however, the presence of coronary artery disease has not been excluded in studies of this condition. In support of an ischemic mechanism unrelated to coronary artery disease are observations of similar intradialytic cardiac stunning in 11 of 12 participants in a pediatric population (ages 2 to 17 years) [24]. At one-year follow-up, hemodialysis-induced myocardial stunning was associated with worse LV systolic function with fixed (persistent) regional wall motion abnormalities [22,25]. Intradialytic hypotension is one of the strongest risk factors for myocardial stunning.

●Uremic toxins – The retention of a wide variety of solutes in patients with impaired kidney function may adversely affect cardiac structure and function [1]. For example, high phosphate levels can directly damage endothelial cells and are associated with cardiovascular disease among patients on dialysis [26,27]. Compounds such as indoxyl sulfate and asymmetric dimethylarginine (ADMA) induce oxidative stress in vivo [28-30] and are associated with increased mortality and adverse cardiovascular events among patients with advanced chronic kidney disease [31-33]. Uremic retention solutes are discussed in detail elsewhere. (See "Uremic toxins".)

EPIDEMIOLOGY AND PROGNOSIS

Overview — Cardiovascular events account for over 40 percent of deaths of known etiology in end-stage kidney disease (ESKD) patients (figure 2) [34]. In general, patients with even mild chronic kidney disease have a greater burden of incident cardiovascular disease compared with similar age controls [35,36]. The specific causes of cardiovascular death include coronary heart disease, heart failure, and arrhythmias; with declining kidney function there is a progressive shift from ischemic to nonischemic etiologies of cardiac death (figure 3), particularly sudden death in the absence of evidence of an acute MI. According to the 2022 United States Renal Data System (USRDS), sudden cardiac death and arrythmias account for 43 percent of deaths among dialysis patients. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

Cardiovascular disease is also an important source of morbidity as the annual probability of hospital admission for HF and/or acute MI for ESKD patients is greater than 20 percent, with a three- to fivefold greater probability of an admission for HF versus an acute MI (figure 4 and figure 5) [34]. (See "Patient survival and maintenance dialysis".)

There are differences in the risk of HF and sudden death between patient groups treated with differing dialysis modalities, with a 34 percent lower rate of HF in patients on peritoneal versus hemodialysis. Furthermore, patients who receive peritoneal dialysis have a markedly lower sudden death rate than patients who receive hemodialysis (2 versus 7 percent) in the 12 months following the initiation of dialysis. This is counterbalanced by a higher unadjusted death rate in patients who receive peritoneal dialysis once diagnosed with HF or an MI [34].

Heart failure — In contrast to individuals without ESKD, HF is common among patients on dialysis. For patients on dialysis with HF, HF with preserved ejection fraction is more common than HF with reduced ejection fraction [37,38].

Risk factors for new-onset HF in patients with ESKD are similar to the general population and include hypertension, older age, anemia, ischemic heart disease, and baseline systolic dysfunction, but also include unique factors related to bone and mineral metabolism, volume overload, and inflammation [13,39]. The prevalence of atheromatous disease in ESKD is high, and this may, in part, be due to the clustering of risk factors and the direct result of kidney function impairment. (See "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)" and "Hypertension in patients on dialysis".)

HF in the patient on dialysis may be caused by fluid overload, LV diastolic dysfunction, LV systolic dysfunction (ischemic and nonischemic etiologies), valvular heart disease (eg, aortic stenosis), and atrial fibrillation. A high-output state caused by shunting through hemodialysis arteriovenous access also may precipitate HF, particularly in patients with underlying ventricular dysfunction [40]. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access" and "Clinical manifestations, diagnosis, and management of high-output heart failure".)

The presence of HF independently predicts early mortality in patients on dialysis, as it does in other patients [39,41-44]. In an analysis of data from the USRDS database, long-term survival was evaluated among 310,456 patients on hemodialysis with a first hospital admission for HF, fluid overload, or pulmonary edema [44]. Five-year survival was only 12.5, 20.2, and 21.3 percent for these three groups, respectively. Increasing clinical severity of HF, as determined by the New York Heart Association (NYHA) classification, is also associated with increased mortality in patients with ESKD [43]. (See "Prognosis of heart failure".)

The pathophysiology of heart disease in patients on dialysis is discussed above. (See 'Pathophysiology' above.)

Coronary heart disease — The prevalence of coronary heart disease in patients on dialysis is discussed separately. (See "Risk factors and epidemiology of coronary heart disease in end-stage kidney disease (dialysis)".)

Valvular heart disease — The prevalence of valvular heart disease in patients on dialysis is discussed separately. (See "Valvular heart disease in patients with end-stage kidney disease".)

Arrhythmias — The prevalence of atrial fibrillation and risk of sudden cardiac arrest in patients on dialysis is discussed separately. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis" and "Atrial fibrillation in adults: Selection of candidates for anticoagulation", section on 'Chronic kidney disease'.)

DIAGNOSIS OF HEART DISEASE

Approach to diagnosis — As described above, heart disease is highly prevalent among patients on dialysis, and cardiac disease impacts prognosis and management (including dialysis therapies). Thus, as recommended in the 2005 Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for cardiovascular disease in patients on dialysis, we suggest that patients receiving dialysis undergo evaluation for heart disease risk factors. In the absence of symptoms of coronary artery disease (CAD), diagnostic testing for CAD is not required unless the patient is under evaluation for kidney transplant (see "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient"), which is consistent with Kidney Disease Improving Global Outcomes (KDIGO) and American Heart Association recommendations [45-48]. In each patient on dialysis, a clinical evaluation is performed to determine the need for additional testing for coronary heart disease, valvular heart disease, ventricular dysfunction, and arrhythmia.

Clinical evaluation includes the following components [45]:

●Assessment for any symptoms or signs of heart disease. (See 'Clinical manifestations' below.)

●Evaluation for traditional cardiovascular and uremia-related cardiovascular risk factors including diabetes, hypertension, dyslipidemia, smoking, physical activity, anemia, albuminuria, arterial stiffness/vascular calcification, serum phosphorus/parathyroid hormone level, inflammation (C-reactive protein [CRP]), and intradialytic hypotension. Of note, limited data are available on the effects of correction of modifiable traditional risk factors in patients with stage IV or greater chronic kidney disease, making specific recommendations challenging [49].

●If there are symptoms of coronary heart disease, we obtain a 12-lead electrocardiogram (ECG).

●If the patient has signs or symptoms of HF at dry weight, we obtain a Doppler transthoracic echocardiogram.

The following are key echocardiographic features in patients with end-stage kidney disease (ESKD):

•LV dimensions and wall thickness (to assess LV hypertrophy [LVH] and geometry) (figure 1).

•LV systolic function (LVEF) (see "Tests to evaluate left ventricular systolic function", section on 'Echocardiography'), which has implications for risk of coronary heart disease as well as risk of HF. (See 'Coronary artery disease' below and 'Ventricular dysfunction' below.)

•LV diastolic function. Unlike a reduced LVEF, the presence of diastolic dysfunction on echocardiography, which is present in the majority of dialysis patients, may not be associated with a poor prognosis [12]. (See "Echocardiographic evaluation of left ventricular diastolic function in adults" and 'Ventricular dysfunction' below.)

•Assessment of valve appearance and function. (See 'Valvular heart disease' below and "Valvular heart disease in patients with end-stage kidney disease".)

•Assessment of right ventricular systolic dysfunction.

•Estimation of right atrial pressure and pulmonary artery systolic pressure, when possible. (See "Echocardiographic assessment of the right heart", section on 'Hemodynamics'.)

A referral to a cardiologist is suggested in the following settings: suspected HF, suspected coronary heart disease, suspected moderate or greater valve stenosis or regurgitation, new or unexplained pulmonary hypertension (pulmonary artery systolic pressure >35 mmHg), or new-onset arrhythmias (eg, incident atrial fibrillation, marked bradycardia, or ventricular tachycardia).

Coronary artery disease — Additional testing to evaluate for coronary artery disease may be performed in select patients on dialysis, including those with LVEF <40 percent as well as in selected potential kidney transplant recipients [47,48]. Additional criteria for stress testing and considerations in choosing a diagnostic test are discussed separately. (See "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Coronary artery disease' and "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation at dialysis initiation'.)

Diagnostic evaluation is performed for patients who develop symptoms of coronary artery disease, and monitoring is performed for patients with known coronary artery disease who have undergone coronary artery bypass graft surgery. Patients on dialysis with an acute MI are less likely to present with chest pain and more often have anginal equivalents such as fatigue and shortness of breath compared with nondialysis patients [50]. (See "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation of symptomatic patients'.)

The use of cardiac troponin I or T to diagnosis acute MI in patients with chronic kidney disease is discussed separately. (See "Cardiac troponins in patients with kidney disease".)

Valvular heart disease — Valvular heart disease should be assessed if there are signs and/or symptoms of such disease. Clinical manifestations and diagnosis of valve disease in patients with ESKD are discussed separately. On routine screening, potentially life-threatening valve abnormalities, such as moderate to severe aortic stenosis, are uncommon (3 to 3.3 percent) [12,51]. (See "Valvular heart disease in patients with end-stage kidney disease", section on 'Evaluation'.)

For patients on dialysis found to have valvular heart disease, recommendations for monitoring are similar to those for the general population except for greater frequency of follow-up for aortic stenosis [52,53]. Cardiac calcification, including aortic valve calcification, occurs at an accelerated rate in patients on dialysis, and the rate of aortic stenosis progression is greater than that observed in the general population. (See "Medical management of asymptomatic aortic stenosis in adults", section on 'Serial evaluation' and "Valvular heart disease in patients with end-stage kidney disease", section on 'Aortic stenosis'.)

Ventricular dysfunction — Ventricular dysfunction (eg, LV diastolic and/or systolic dysfunction) and LV remodeling (eg, LVH) can be assessed by echocardiography performed at clinically determined dry weight [45]. Most patients are volume overloaded at the time of initiation of dialysis, and it can take weeks to achieve relative euvolemia.

Echocardiography is the test of choice to assess ventricular systolic and diastolic dysfunction and LVH as it is widely available, noninvasive, and provides information on atrial and ventricular volumes, LV mass, biventricular systolic and diastolic function, valve function, and pulmonary pressures. LVH is defined as an LV mass index ≥130 and ≥110 g/m² body surface area in males and females, respectively [54].

If LV systolic function cannot be adequately assessed by echocardiography, alternative methods include radionuclide ventriculography, CMR imaging (for which no exogenous contrast is required for assessment of LV structure and function), cardiac computed tomography (which requires iodinated contrast), and invasive ventriculography (generally performed only if there is a concurrent indication for cardiac catheterization such as an indication for coronary angiography). (See "Tests to evaluate left ventricular systolic function".)

Arrhythmias — Patients with symptoms and signs of arrhythmias should undergo evaluation, as discussed separately. Studies in which implantable loop recorders have been implanted in dialysis patients suggest that the rates of arrythmias may be significantly higher than what is recognized clinically [55]. (See "Arrhythmia management for the primary care clinician" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Wide QRS complex tachycardias: Approach to the diagnosis".)

Atrial fibrillation — The clinical manifestations and diagnosis of atrial fibrillation are discussed separately. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

Ventricular arrhythmias — The clinical manifestations and diagnosis of ventricular arrhythmias and the risk of sudden cardiac arrest in patients with ESKD are discussed separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

CHALLENGES OF HEART FAILURE DIAGNOSIS — 

The signs and symptoms of HF often overlap with those related to ESKD, so it may be challenging to diagnose HF. In addition, echocardiographic, ECG, and biomarker findings will be less specific compared with patients without kidney disease. However, given the high risk in this population, there should be a relatively low threshold to evaluate for HF.

Clinical manifestations — Because many clinical manifestations of HF in patients with ESKD (eg, dyspnea, fatigue, and weakness) are the same as those observed generally in much of this population, it can be difficult to identify HF. Signs of HF include elevated jugular venous pressure, an S3 gallop, rales, and peripheral edema. ECG findings (such as LV hypertrophy [LVH] and changes consistent with myocardial infarction or ischemia) are not specific for HF but may suggest a cause of HF. The chest radiograph findings of cardiomegaly, cephalization of pulmonary vessels, Kerley B-lines, and alveolar edema strongly suggest HF but have limited sensitivity. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Diagnosis — The HF evaluation for patients with ESKD is generally the same as that for the general population except that we do not use natriuretic peptide levels (B-type natriuretic peptide [BNP] or N-terminal pro-BNP [NT-proBNP]), as they are typically elevated despite the absence of symptomatic HF (ie, poor specificity for the diagnosis of HF) [56]. Similar to the general population, there is a high incidence of HF with preserved ejection fraction (HFpEF). (See 'Approach to diagnosis' above and "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Evaluation'.)

Since HF is a clinical diagnosis, echocardiography is not used to exclude HF but to identify findings consistent with HF and potential causes of HF (eg, LV systolic dysfunction, LV diastolic dysfunction, and valve dysfunction). Cardiac catheterization is not generally required to diagnose HF, but right heart catheterization may be helpful in selected cases to assess intracardiac pressures and volume status, which may be challenging to assess noninvasively in patients on dialysis.

Identification of the type of heart failure — Most patients with ESKD have HF (whether HF with reduced ejection fraction [HFrEF], LVEF ≤40 percent; HFpEF, LVEF ≥50 percent; or HF with mildly reduced ejection fraction [HFmrEF], LVEF 41 to 49 percent) with low or normal cardiac output accompanied by elevated systemic vascular resistance. HFpEF is likely the more common HF type.

A minority of patients with HF present with a high-output state with low systemic vascular resistance. High-output HF should be suspected in patients with predisposing conditions, particularly patients with arteriovenous access for hemodialysis. Patients with high-output HF frequently have concurrent cardiac disease with impaired systolic and/or diastolic function. Diagnosis of high-output HF is discussed separately. (See "Clinical manifestations, diagnosis, and management of high-output heart failure" and "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

Limited utility of natriuretic peptides — Neither BNP nor NT-proBNP is sufficiently accurate for diagnosing HF in patients with ESKD. Plasma BNP and NT-proBNP concentrations are elevated in patients with renal failure due to reduced clearance as well as chronically increased volume, so thresholds for diagnosis of HF in patients on dialysis have not been established. (See "Natriuretic peptide measurement in heart failure".)

This contrasts with the utility of BNP and NT-proBNP in identifying patients with asymptomatic or symptomatic LV dysfunction among patients with normal kidney function or mild to moderate chronic kidney disease (defined as an estimated glomerular filtration rate [eGFR] >30 mL/min/1.73 m²). (See "Natriuretic peptide measurement in heart failure", section on 'Renal failure'.)

Both BNP and NT-proBNP can provide prognostic information with respect to all-cause mortality, cardiovascular mortality, and cardiovascular events in patients with ESKD, although we generally do not use either for this purpose. In a meta-analysis combining 23 studies and nearly 8000 ESKD patients, an elevated natriuretic peptide level was associated with a 3.85 higher odds ratio for all-cause mortality (95% CI 3.11-4.75) [57]. The odds ratio for cardiovascular death was 4.05 (95% CI 2.53-6.84), but with high heterogeneity, when evaluating 10 studies with 6396 ESKD subjects.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)

SUMMARY AND RECOMMENDATIONS

●Prevalence and prognosis – Cardiovascular disease is an important cause of morbidity and mortality in patients with end-stage kidney disease (ESKD). With declining kidney function, there is a progressive shift from ischemic to nonischemic etiologies of cardiac death, particularly sudden death in the absence of evidence of an acute myocardial infarction (MI). (See 'Epidemiology and prognosis' above.)

●Pathophysiology – Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality in patients on dialysis. Major risk factors for LVH include hypertension (particularly systolic blood pressure) and increasing age; chronic volume overload, anemia, and increased cardiac index may be contributing factors. (See 'Pathophysiology' above.)

●Epidemiology – Heart failure (HF) is common among patients on dialysis and predicts early mortality. Risk factors for HF include hypertension, older age, anemia, ischemic heart disease, and baseline systolic dysfunction. (See 'Pathophysiology' above and 'Epidemiology and prognosis' above.)

●Approach to diagnosis – In the presence of suggestive signs or symptoms of cardiovascular disease among patients receiving maintenance dialysis, we use a low threshold for cardiovascular diagnostic testing, including a 12-lead ECG and echocardiogram. (See 'Approach to diagnosis' above.)

•Coronary artery disease – Additional testing to evaluate for coronary artery disease is performed in selected patients on dialysis including those with LV ejection fraction (LVEF) <40 percent as well as in selected potential kidney transplant recipients. Evaluation may be performed by noninvasive stress imaging (nuclear or echocardiographic) and/or coronary angiography. Additional criteria for stress testing and considerations in choosing a diagnostic test are discussed separately. (See 'Coronary artery disease' above and "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Coronary artery disease' and "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation at dialysis initiation'.)

•Valve disease – Valvular heart disease should be assessed by Doppler echocardiography in the presence of symptoms. For patients on dialysis found to have valvular heart disease, recommendations for monitoring are similar to those for the general population except for greater frequency of follow-up for aortic stenosis. (See 'Valvular heart disease' above and "Valvular heart disease in patients with end-stage kidney disease" and "Medical management of asymptomatic aortic stenosis in adults", section on 'Serial evaluation'.)

•Ventricular dysfunction – Ventricular dysfunction (eg, LV diastolic and/or systolic dysfunction) and LV remodeling (eg, LVH) should be evaluated by echocardiography if there is a clinical suspicion for HF. (See 'Ventricular dysfunction' above and "Tests to evaluate left ventricular systolic function" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Echocardiographic evaluation of left ventricular diastolic function in adults".)

•Arrhythmias – Evaluation for atrial and ventricular arrhythmias in patients on dialysis should include a 12-lead ECG. (See "Arrhythmia management for the primary care clinician" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Wide QRS complex tachycardias: Approach to the diagnosis".)

●Challenges of heart failure diagnosis – The clinical syndrome of HF is diagnosed in patients with ESKD based upon identification of a combination of symptoms, signs, and test findings. This diagnosis may be challenging in patients with ESKD, as it is difficult to distinguish between volume overload versus HF. However, there should be a low threshold to evaluate for HF given the high incidence and prevalence rates in this population. The evaluation is the same as that for HF generally except that we do not use natriuretic peptides to diagnose HF in patients with ESKD; however, natriuretic peptides may be helpful for prognostication. (See 'Challenges of heart failure diagnosis' above and "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Evaluation' and "Natriuretic peptide measurement in heart failure", section on 'Renal failure'.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges William L Henrich, MD, MACP, who contributed to earlier versions of this topic review.