Management of heart failure in patients on dialysis

INTRODUCTION — Patients with end-stage kidney disease (ESKD) who require dialysis are at increased risk for the development of heart failure (HF). Patients with ESKD who have HF may benefit from modification to their dialysis regimen and specific therapy for HF.

This topic will discuss the approach to prevention and management of HF in patients who receive dialysis.

The diagnosis of HF in patients on dialysis and issues related to vascular access for dialysis in patients with HF are discussed separately:

●(See "Overview of screening and diagnosis of heart disease in patients on dialysis".)

●(See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

PREVENTION — All patients who receive dialysis who have one or more diseases that increase the risk of ventricular dysfunction should undergo appropriate treatment of such conditions. Common comorbid conditions in patients who receive dialysis include:

●Hypertension – Control of hypertension is a key intervention in preventing and managing HF in dialysis patients. The management of hypertension in dialysis patients includes achieving and maintaining euvolemia as much as possible during the interdialytic interval as well as treatment with antihypertensive agents appropriate for patients with advanced kidney disease. In addition, patients with HF and hypertension who receive dialysis should preferentially receive antihypertensive medications that are beneficial for the treatment of HF. (See "Hypertension in patients on dialysis" and 'Heart failure with reduced ejection fraction (HFrEF)' below and 'Heart failure with preserved ejection fraction (HFpEF)' below and 'Other types of HF' below.)

●Coronary artery disease – The treatment of coronary artery disease is aimed at relieving symptoms and improving outcomes. Management options include pharmacologic therapy (antithrombotic therapy, antianginal therapy, and treatment of anemia, hypertension, and other cardiovascular risk factors) and revascularization (percutaneous or surgical). In some cases, revascularization of obstructive coronary artery disease may improve systolic and diastolic ventricular function. Management of coronary heart disease in this group of patients is discussed separately. (See "Chronic kidney disease and coronary heart disease".)

●Valve disease – Patients with symptomatic valve disease should undergo optimization of volume status and appropriate anatomic correction of valve disease, as discussed separately. (See "Valvular heart disease in patients with end-stage kidney disease".)

●Diabetes – In patients who receive dialysis, diabetes is a common comorbidity. Optimal management of such patients is discussed separately. (See "Management of hyperglycemia in patients with type 2 diabetes and advanced chronic kidney disease or end-stage kidney disease".)

GENERAL MANAGEMENT

Monitoring — Patients with HF who receive dialysis should be monitored with a regular review of symptoms, physical examination, and a review of medications with a focus on any agents that require adjustment to avoid toxicity in the presence of decreased kidney function. The frequency of monitoring by clinicians is individualized based on factors such as clinical stability and duration of HF. Care should be taken to avoid drugs that may cause worsening HF. (See "Drugs that should be avoided or used with caution in patients with heart failure".)

Patients with worsening symptoms or signs of HF despite optimal dialysis should undergo prompt clinical evaluation for worsening left ventricular (LV) function with follow-up echocardiography. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".)

Self-management — Patients on dialysis with HF should be counseled on daily monitoring of weights (considering pre- and postdialysis fluctuations), edema, and symptoms; medication management; exercise as tolerated; and diet. Patients should also receive advice on smoking cessation and restriction of alcohol consumption and avoidance of illicit drug use. (See "Heart failure self-management".)

Management of salt restriction is essential in patients on dialysis with HF. Dietary recommendations for patients on dialysis with HF should follow recommendations for patients on dialysis, which are discussed in detail elsewhere. (See "Nutritional status and protein intake in patients on peritoneal dialysis" and "Assessment of nutritional status in patients on hemodialysis" and "Protein intake in patients on maintenance hemodialysis".)

Dialysis modality — The preferred dialysis modality is determined by patient preference and a variety of clinical and socioeconomic factors; the presence of HF does not require a specific dialysis modality. Patients with end-stage kidney disease and HF should be evaluated for each type of dialysis (ie, peritoneal dialysis [PD], in-center hemodialysis, home hemodialysis). (See "Dialysis modality and patient outcome", section on 'Selection of dialysis modality'.)

Advantages and disadvantages of each type of dialysis from the HF standpoint include the following:

●Peritoneal dialysis – PD avoids the risks of high-output HF associated with arteriovenous fistula and allows for slower rates but longer durations of fluid removal. Therefore, the desirable body fluid volume target can often be attained in patients at risk of hypotension. Except for patients who have lost their peritoneal ultrafiltration properties, PD does not have disadvantages from the HF management standpoint. The details of PD are discussed separately. (See "Dialysis modality and patient outcome", section on 'Selection of dialysis modality'.)

●In-center or home hemodialysis – In-center hemodialysis allows for frequent in-person monitoring by the health care team. However, this modality typically involves relatively short (3.5- to 4-hour) thrice weekly sessions during which volume is removed relatively quickly compared with other forms of dialysis. In patients with HF who receive medications with vasodilatory effects or beta blockers that inhibit compensatory tachycardia, this type of dialysis may increase the risk of hypotension. In this population, such hypotensive episodes can be difficult to manage and may result in interrupted sessions with incomplete dialysis.

Compared with conventional in-center dialysis, in-center nocturnal hemodialysis (six to eight hours thrice weekly) and home hemodialysis (four to six times per week) typically allow for slower rates of fluid removal due to increased dialysis time. As such, these modalities may lower the risk of intradialytic hypotension and permit greater fluid removal. (See "Outcomes associated with nocturnal hemodialysis" and "Short daily hemodialysis" and "Short daily home hemodialysis: The low dialysate volume approach".)

●Hemodialysis access – In patients with HF, there is also an increased risk with the surgery required to create a dialysis fistula, and high-flow shunting of blood through an arteriovenous fistula sometimes produces high-output HF. However, the infection risks of catheter-based dialysis are high. The approach to hemodialysis access in patients with HF is discussed separately. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access", section on 'Prevention'.)

The evidence on type of dialysis in patients with HF is inconclusive; the available studies are retrospective in nature and are likely influenced by significant selection bias:

●In a study that included 4401 patients with HF who began dialysis, the median survival time with PD was 20.4 months and with hemodialysis was 36.7 months (adjusted hazard ratio [HR] 1.5, 95% CI 1.3-1.7) [1].

●In a cohort of patients without HF who underwent dialysis, the incidence of HF was lower in patients who underwent PD compared with those who underwent hemodialysis (26 versus 20 events per 1000 patient-years; adjusted HR 1.5, 95% CI 1.2-1.7) [2].

Dialysis prescription — Achieving adequate volume control for patients on dialysis with HF requires accurate assessment of volume status and an optimal dialysis prescription.

●Assessment and maintenance of optimal volume status – In patients with HF with reduced ejection fraction (HFrEF) who receive dialysis, we rely on physical examination (eg, jugular venous pressure, peripheral edema, heart sounds, rales) and weight to establish and maintain volume status. In patients with HFrEF who receive dialysis, the ideal weight is likely to change over time due to multiple factors (eg, cardiac cachexia, changes in cardiac performance) and filling pressures are unlikely to be normal.

In patients in whom physical examination and weight are poor indicators of volume status (eg, difficult to assess, discrepant findings), echocardiography can help to determine volume status and identify changes in cardiac structure or function. If volume status remains uncertain after noninvasive assessment, we suggest referral to a cardiologist to evaluate the risks and benefits of invasive hemodynamic assessment. Although bioimpedance and bedside lung ultrasound are options for volume assessment, the clinical utility of these tests is uncertain. (See "Echocardiographic assessment of the right heart", section on 'RA pressure' and "Echocardiographic evaluation of left ventricular diastolic function in adults", section on 'Estimation of left atrial pressure'.)

●Hemodialysis regimen – In patients with HF, major barriers to achieving the optimal dry weight are symptoms of hypotension or intravascular hypovolemia such as intradialytic cramping, nausea, or vomiting. These adverse sequelae of fluid removal are ideally mitigated by slowing the rate of ultrafiltration by increasing hemodialysis duration and/or frequency. Additional measures to mitigate intradialytic hypotension, including use of cool dialysate, are detailed elsewhere. (See "Intradialytic hypotension in an otherwise stable patient", section on 'Prevention of recurrent episodes'.)

Compared with conventional thrice-weekly dialysis, longer duration and/or more frequent (eg, daily) hemodialysis is likely to provide better volume control and minimize intradialytic hypotension and interdialytic hypervolemia. However, most dialysis units have relatively little flexibility in their schedules for longer or more frequent hemodialysis sessions, the availability of in-center nocturnal dialysis is limited in many regions, and many patients are reluctant to accept recommendations for additional in-center treatment time. In these cases, home hemodialysis is often preferred. (See 'Dialysis modality' above.)

For patients on hemodialysis, our general approach to achieving and maintaining the optimal target weight, once established, is detailed elsewhere. (See "Prescribing and assessing adequate hemodialysis", section on 'Patient-specific parameters' and "Hypertension in patients on dialysis", section on 'How to reduce target dry weight'.)

Results from randomized trials of alternative hemodialysis schedules in the general maintenance hemodialysis population appear to be inconsistent:

•A randomized trial that included 245 patients without HF found that daily dialysis (nearly six sessions per week) reduced the risk of death compared with conventional dialysis (16 versus 28 percent; HR 0.54, 95% CI 0.31-0.93) [3].

•In apparent contrast, a randomized trial of 87 patients comparing six-session-weekly long-duration nocturnal hemodialysis with conventional dialysis did not demonstrate significant beneficial effects on the composite endpoint of mortality or LV mass [4]. However, this study was significantly underpowered.

These studies are discussed in detail separately. (See "Short daily hemodialysis", section on 'Frequent Hemodialysis Network (FHN) daily trial' and "Outcomes associated with nocturnal hemodialysis".)

●Peritoneal dialysis prescription – Our approach to optimizing volume control in patients on PD is discussed in detail elsewhere. (See "Management of hypervolemia in patients on peritoneal dialysis".)

Diuretic therapy — In dialysis patients with HF who have significant urine output, loop diuretic therapy is helpful to increase urine output and sodium excretion and decrease the need for volume removal with dialysis. Dialysis patients receiving high dose diuretics should be monitored for hearing loss. Diuretics should be stopped when urine output becomes negligible. (See "Residual kidney function in kidney failure", section on 'Diuretics' and "Management of hypervolemia in patients on peritoneal dialysis", section on 'Loop diuretics'.)

MANAGEMENT BY TYPE OF HEART FAILURE

Heart failure with reduced ejection fraction (HFrEF) — HF due to LV ejection fraction (LVEF) ≤40 percent is referred to as HF with reduced ejection fraction (HFrEF). The management of HFrEF includes:

Pharmacologic therapy — For patients with HFrEF on dialysis, we suggest therapy with a beta blocker and a renin-angiotensin-aldosterone system (RAAS) inhibitor (ie, angiotensin converting enzyme [ACE] inhibitor, angiotensin II receptor blocker [ARB], angiotensin receptor-neprilysin inhibitor [ARNI]) rather than no therapy or other pharmacologic regimens. In such patients, we suggest avoiding mineralocorticoid receptor antagonist (MRA) and/or sodium-glucose co-transporter 2 (SGLT2) inhibitor therapy.

We typically start beta blocker therapy with carvedilol, though metoprolol succinate is a reasonable alternative for patients in whom hypotension limits achievement of the target weight.

If beta blocker therapy is tolerated, we add a low-dose ACE inhibitor, ARB, or sacubitril-valsartan. For patients in whom hypotension limits achievement of the target weight, we prefer an ACE inhibitor or an ARB, since these agents usually have less of an effect on blood pressure than sacubitril-valsartan.

Thereafter, the beta blocker and RAAS inhibitor can be increased in a fashion that achieves the highest tolerated dose of both drugs while avoiding hypotension or hyperkalemia. After the first dose or an increase in dose of a RAAS inhibitor, we evaluate for hyperkalemia within one week.

Factors that typically limit the use of this regimen are intradialytic hypotension and hyperkalemia. Our approach to these complications is as follows:

●Patients with hypotension – In patients with hypotension attributable to pharmacologic therapy for HFrEF, the usual approach to management is similar to that in patients with HFrEF who do not receive dialysis, which is discussed separately. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Management of adverse drug effects'.)

If interventions such as dose reduction are not effective and hypotension occurs during or immediately following dialysis, another option is to modify the dosing schedule to avoid peridialytic hypotension (eg, holding doses of vasoactive agents immediately before dialysis). (See "Intradialytic hypotension in an otherwise stable patient", section on 'First-line approach'.)

●Patients with hyperkalemia – The management of patients with persistent hyperkalemia (eg, predialysis serum potassium concentration of 5.5 mEq/L or higher) despite usual modifications of the dialysis prescription and dietary potassium restriction includes dose reduction or discontinuation of RAAS inhibitor therapy. The use of cation exchangers (eg, patiromer, sodium zirconium cyclosilicate) to allow for ongoing RAAS inhibitor therapy is controversial. While some contributors to this topic favor a strategy of RAAS inhibitor discontinuation in patients who are hyperkalemic, other contributors may treat hyperkalemia to allow for continuation of a RAAS inhibitor if the benefit of RAAS inhibitor therapy is judged to exceed the risks. There are no high-quality studies to guide the approach to therapy in this population.

Management of hyperkalemia is discussed separately. (See "Treatment and prevention of hyperkalemia in adults", section on 'Gastrointestinal cation exchangers'.)

Our approach is broadly consistent with the 2005 Kidney Disease Outcomes Quality Initiative clinical practice guidelines [5].

Our rationale for the use of RAAS inhibitors and beta blockers in patients with HFrEF who receive dialysis is primarily based on indirect evidence and our experience with the safety of these agents in this population. The indirect evidence of efficacy is from patients with HFrEF who do not receive dialysis; patients with HFrEF who receive dialysis are routinely excluded from trials of HFrEF pharmacotherapy.

Though there is indirect evidence to suggest that patients with HFrEF who receive dialysis may benefit from MRA or SGLT2 inhibitor therapy, we do not add MRA therapy to existing RAAS inhibitor therapy due to the higher risk of hyperkalemia, and we do not add SGLT2 inhibitor therapy due to unproven safety in this population. The evidence on the efficacy of these agents in patients with HFrEF who do not receive dialysis is discussed separately. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Management of specific agents'.)

The direct evidence for and against specific agents in patients who receive dialysis is limited and includes the following:

●Beta blockers – The benefit of beta blockers in patients with HFrEF who receive dialysis has not been established. In a small trial that included 114 patients with HFrEF who received hemodialysis, patients randomly assigned to carvedilol had a lower rate of mortality compared with patients randomly assigned to placebo (52 versus 73 percent) [6]. The rates of cardiovascular death (29 versus 68 percent) and hospital admissions (35 versus 59 percent) were also lower. However, there are concerns that the magnitude of benefit described in this trial was unusually high (eg, higher than the effect of beta blockers in patients with HFrEF who do not receive dialysis).

●RAAS inhibitors – The efficacy of ACE inhibitors, ARBs, and sacubitril-valsartan in patients with HFrEF who receive dialysis is uncertain due to the lack of high-quality trials and studies [7-9].

We do not use dual therapy with an ACE inhibitor and ARB in this population because of the higher risk of hyperkalemia and hypotension. Although one trial showed a large mortality benefit with dual therapy (35 versus 54 percent with placebo), effects this large are rarely observed in trials of cardiovascular agents, these results have not been replicated, and observational studies show conflicting results [10,11].

●Mineralocorticoid receptor antagonists – In patients with HFrEF who receive dialysis, there are no high-quality trials or analyses that directly address the efficacy or safety of MRA therapy. MRA use among patients on dialysis is associated with hyperkalemia [12-14], a risk that may be potentiated by concomitant RAAS inhibition.

The largest trials of MRA use in patients on dialysis included few patients with HF and most patients were not treated with a concomitant ACE inhibitor or ARB [12,13]. In two small (combined n = 44) trials of patients with HFrEF who received dialysis, MRAs improved surrogate markers of LV systolic function and rates of significant hyperkalemia were similar between groups [15,16].

●SGLT2 inhibitors – The experience with SGLT2 inhibitors in patients with dialysis is limited, and large clinical outcome trials routinely exclude patients with estimated glomerular filtration rates less than 20 mL/min per 1.73 m² and those who receive dialysis. Since the primary mechanism of action of these agents requires kidney function, it is unclear if these agents have similar efficacy in patients on dialysis. Thus, the safety and efficacy of these agents in this group of patients is unknown.

Devices for rhythm management — In patients with HFrEF who receive dialysis, the approach to cardiac resynchronization therapy (CRT) is similar to that in patients with HFrEF who do not receive dialysis:

●Cardiac resynchronization therapy – Indications for CRT are discussed separately. The risk for device infection is increased among patients receiving dialysis through chronic indwelling catheters because of the risk for intermittent bacteremia. There is insufficient evidence regarding the use of CRT in dialysis patients with HF to support its routine use, and decisions are made on a case-by-case basis [17,18]. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system".)

●Implantable cardioverter-defibrillators – Dialysis patients with and without HF are at risk for ventricular arrhythmias and sudden cardiac death. Indications for implantable cardioverter-defibrillator (ICD) therapy for primary or secondary prevention of sudden cardiac arrest are discussed separately. Subcutaneous ICDs are one strategy to reduce the rate of (lead-related) ICD infections in dialysis patients. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

Therapy for anemia — In patients with HFrEF who receive dialysis, the primary approach to treating anemia consists of prevention and management of iron deficiency using the same strategy as that for all patients who receive dialysis. (See "Treatment of anemia in patients on dialysis" and "Treatment of iron deficiency in patients on dialysis".)

In patients with HFrEF who receive dialysis and have severe anemia, erythropoiesis-stimulating agents (ESAs) or hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF PHIs) are typically needed to prevent dependence on red blood cell transfusions. Similar to patients without HFrEF, the doses of these agents should be minimized as much as possible to reduce the risk of adverse effects. (See "Treatment of anemia in patients on dialysis" and "Treatment of iron deficiency in patients on dialysis".)

Heart failure with preserved ejection fraction (HFpEF) — Patients with HFpEF on dialysis should receive monitoring and optimization of volume status and should receive treatment for conditions commonly associated with HFpEF (eg, hypertension, obesity), as described elsewhere. (See 'General management' above and "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Management of associated conditions'.)

There is no specific pharmacologic regimen to treat HFpEF in patient on dialysis. In patients with HFpEF who receive dialysis, we suggest not treating with an MRA or an SGLT2 inhibitor.

Agents typically used to treat patients with HFpEF (eg, MRAs, SGLT2 inhibitors) are potentially unsafe for use in patients on dialysis. The evidence that describes the efficacy of specific treatments for HFpEF in patients with dialysis is composed of retrospective studies prone to bias [19,20]. Further details on the safety of MRAs and SGLT2 inhibitors in this population are discussed elsewhere in this topic. (See 'Pharmacologic therapy' above.)

Other types of HF — In patients on dialysis who have HF with mid-range ejection fraction (HFmrEF; LVEF 41 to 49 percent) or asymptomatic LV systolic dysfunction, the management is the same as that for patients on dialysis with HFrEF. (See 'Heart failure with reduced ejection fraction (HFrEF)' above.)

REFRACTORY HEART FAILURE

Avoid digoxin — We avoid digoxin use in patients with HF with reduced ejection fraction (HFrEF) who receive dialysis. In dialysis patients, we reserve use of digoxin for selected patients with atrial fibrillation who do not achieve adequate rate control by optimum doses of beta blocker and who can be closely followed to maintain a digoxin level <1.0 ng/mL. When digoxin is administered to a dialysis patient, dosing of digoxin should be adjusted for renal failure and close monitoring is required. (See "Treatment with digoxin: Initial dosing, monitoring, and dose modification".)

Among dialysis patients, a retrospective cohort study also found that higher digoxin levels were associated with increased risk of death, particularly with lower serum potassium levels; the risk of mortality was significantly increased with a digoxin level ≥1.0 if predialysis levels of serum potassium were less than 4.3 mEq/dL [21].

Role of transplantation — Patients with severe refractory HF symptoms despite optimal management who are expected to receive long-term dialysis may be candidates for combined heart-kidney transplantation. In such patients, every effort should be made to exclude and treat any reversible causes of cardiac or renal dysfunction. The evaluation for kidney and heart transplantation are discussed separately. (See "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient" and "Heart transplantation in adults: Indications and contraindications".)

In practice, most patients with refractory HF who receive dialysis appropriately undergo combined heart-kidney transplantation to mitigate the risks of kidney allograft loss in patients with HFrEF and to mitigate the risks of ongoing end-stage kidney disease (ESKD) in patients who undergo isolated heart transplantation. However, in highly selected patients, isolated kidney transplantation may result in improved LV systolic function and improved survival. The broad use of isolated kidney transplantation in patients with HFrEF is limited by the absence of criteria that reliably predict a favorable outcome. Studies that describe this approach are older and included relatively few patients:

●This was illustrated by a study of over 100 dialysis patients with HFrEF who underwent kidney transplantation between 1998 and 2002 [22]. In this cohort of patients, there were no perioperative deaths, mean LVEF increased from 32 to 52 percent at 12 months, and more than two-thirds of patients achieved an LVEF of greater than 50 percent. Patients with normalized LVEF had significantly improved New York Heart Association class and lower risk of death or hospitalization for HF. However, patients with ejection fractions less than 30 percent did not typically normalize.

●Kidney transplantation may also have a beneficial effect on cardiac remodeling as it is associated with regression of LV hypertrophy (LVH) [23-25]. As an example, one prospective study of 24 dialysis patients evaluated changes in LV mass by echocardiography at 3, 6, and 12 months posttransplantation [23]. There was a significant decrease in blood pressure at 12 months, and the incidence of LVH decreased from 75 to 52 percent. There was also a significant decrease in LV dilation, and systolic dysfunction normalized in all patients after 12 months. It is unclear if removing the uremic milieu, improving blood pressure, or both were significant factors underlying these changes.

Palliative care — In patients with refractory HF symptoms who receive dialysis, palliative care appropriate for HF and dialysis should be implemented. These issues are discussed in detail separately. (See "Kidney palliative care: Principles, benefits, and core components" and "Palliative care for patients with advanced heart failure: Indications and systems of care".)

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: Heart failure in adults" and "Society guideline links: Dialysis".)

SUMMARY AND RECOMMENDATIONS

●Prevention – Management of risk factors for ventricular dysfunction and the choice of dialysis modality may reduce the likelihood of heart failure (HF) in patients who receive dialysis. (See 'Prevention' above.)

●General management – General management of patients with HF who receive dialysis includes monitoring and self-management appropriate for both HF and end-stage kidney disease (ESKD), such as restriction of salt intake. HF management specific to dialysis includes the following:

•Dialysis modality – We generally do not select a dialysis modality based solely on the presence or absence of HF. Each modality (ie, peritoneal dialysis [PD], in-center hemodialysis, home hemodialysis) has advantages and disadvantages from the HF standpoint. (See 'Dialysis modality' above.)

•Dialysis prescription – Achieving adequate volume control for patients on dialysis with HF requires accurate assessment of volume status and an optimal dialysis prescription. For patients on hemodialysis with HF, a major barrier to achieving the target dry weight is intradialytic hypotension. This may be mitigated by minimizing interdialytic fluid accumulation and by slowing the rate of ultrafiltration by increasing dialysis duration and/or frequency. (See 'Dialysis prescription' above.)

•Diuretic therapy – In dialysis patients with HF who have significant urine output, loop diuretic therapy is helpful to increase urine output and sodium excretion and decrease the need for volume removal with dialysis. (See "Residual kidney function in kidney failure", section on 'Diuretics' and "Management of hypervolemia in patients on peritoneal dialysis", section on 'Loop diuretics'.)

●Heart failure with reduced ejection fraction (HFrEF)

•Pharmacologic therapy – For patients with HFrEF on dialysis, we suggest therapy with a beta blocker and a renin-angiotensin-aldosterone system (RAAS) inhibitor (ie, angiotensin converting enzyme [ACE] inhibitor, angiotensin II receptor blocker [ARB], angiotensin receptor-neprilysin inhibitor [ARNI]) rather than no therapy or other pharmacologic regimens (Grade 2C).

In such patients, we suggest avoiding mineralocorticoid receptor antagonist (MRA) and/or sodium-glucose co-transporter 2 (SGLT2) inhibitor therapy (Grade 2C). We do not add MRA therapy to existing RAAS therapy due to the higher risk of hyperkalemia, and we do not add SGLT2 inhibitor therapy due to unproven safety in this population. (See 'Pharmacologic therapy' above.)

•Other therapies for HFrEF – In patients with HFrEF who receive dialysis, other therapies may include:

-Cardiac resynchronization therapy – The indications for cardiac resynchronization therapy (CRT) in patients with ESKD are similar to those in patients without ESKD, though in patients with an indwelling hemodialysis catheter, the higher risk of infection may influence the decision to place a CRT device. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system".)

-Implantable cardioverter-defibrillators – Indications for implantable cardioverter-defibrillator (ICD) therapy for primary or secondary prevention of sudden cardiac arrest are discussed separately. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

-Therapies for anemia – In patients with HFrEF who receive dialysis, the primary approach to treating anemia consists of prevention and management of iron deficiency using the same strategy as that for all patients who receive dialysis.

In patients with HFrEF who receive dialysis and have severe anemia, erythropoiesis-stimulating agents or hypoxia-inducible factor prolyl hydroxylase inhibitors are typically needed to prevent dependence on red blood cell transfusions. The doses of these agents should be minimized as much as possible to reduce the risk of adverse effects. (See 'Therapy for anemia' above.)

•Heart failure with preserved ejection fraction (HFpEF) – Patients with HFpEF on dialysis should receive monitoring and optimization of volume status and should receive treatment for conditions commonly associated with HFpEF (eg, hypertension, obesity) as described elsewhere.

There is no specific pharmacologic regimen to treat HFpEF in patients on dialysis. In patients with HFpEF who receive dialysis, we suggest not treating with an MRA or an SGLT2 inhibitor (Grade 2C).

●Other types of heart failure – In patients on dialysis who have HF with mid-range ejection fraction (HFmrEF; left ventricular ejection fraction [LVEF] 41 to 49 percent) or asymptomatic LV systolic dysfunction, the management is the same as that for patients on dialysis with HFrEF. (See 'Heart failure with reduced ejection fraction (HFrEF)' above.)

●Refractory heart failure – In patients with refractory HF, we avoid use of digoxin, and options for therapy include kidney transplantation, heart-kidney transplantation, and palliative care. (See 'Refractory heart failure' above.)

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