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Kidney failure, defined by an estimated glomerular filtration rate below 15 mL/min/1.73 m², represents the terminal stage of chronic kidney disease and requires renal replacement therapy or supportive care. Dialysis is a cornerstone treatment that removes metabolic waste products and excess fluid while maintaining electrolyte and acid–base balance. Over 3.5 million individuals worldwide receive dialysis, most commonly hemodialysis, with diabetes mellitus and hypertension accounting for the majority of cases of end-stage renal disease. This course outlines the 2 primary dialysis modalities: intermittent and continuous hemodialysis and peritoneal dialysis, and their indications, which should be guided primarily by clinical symptoms rather than eGFR alone, emphasizing individualized decision-making. This activity reviews hemodialysis principles, indications, timing, and complications. Additionally, the value of coordinated interprofessional management to optimize outcomes and quality of life for patients with kidney failure is discussed, as cardiovascular disease remains the leading cause of mortality among dialysis patients, underscoring the importance of cardioprotective strategies and interprofessional care. Participants will also gain an understanding of modality selection, dialysis adequacy, cardiovascular risk reduction, and patient-centered decision-making. This activity for healthcare professionals is designed to enhance the learner's competence in identifying candidates for hemodialysis, preventing complications, and implementing an appropriate interprofessional approach when managing kidney failure with this procedure. Objectives: Identify the various forms of hemodialysis. Assess the recommended techniques of dialysis hemodialysis modalities. Screen for the associated complications of hemodialysis. Collaborate with interprofessional teams to improve care collaboration and outcomes for renal failure patients. Access free multiple choice questions on this topic.

Kidney failure is defined by an estimated glomerular filtration rate (eGFR) of less than 15 mL/min/1.73 m² and can be managed through kidney transplantation, hemodialysis, peritoneal dialysis, or supportive care. The term "dialysis" is derived from the Greek words dia, meaning "through," and lysis, meaning "loosening or splitting." Dialysis is a treatment for kidney failure that helps remove waste products and excess fluid from the blood while maintaining the proper balance of essential minerals for normal body function.[1] Over 3.5 million people worldwide, including about 540,000 in the United States, receive dialysis for chronic kidney failure, with nearly 90% undergoing hemodialysis.[2][3] The end-stage renal disease (ESRD) burden is attributed mainly to diabetes mellitus and hypertension, besides rarer causes like polycystic kidney disease, obstructive nephropathy, and glomerulonephritis. Dialysis for kidney failure can be classified into 2 broad types: hemodialysis and peritoneal dialysis. Hemodialysis includes several modalities, eg, intermittent hemodialysis (IHD) and continuous renal replacement therapy (CRRT), while peritoneal dialysis relies on the patient’s peritoneum as a natural filter for waste removal. Determining the optimal timing for initiating long-term dialysis in patients with kidney disease remains uncertain, with considerable variation across health systems.[4] According to the United States Renal Data System, the proportion of patients starting dialysis at an eGFR 10 mL/min/1.73 m² or greater rose from 13% in the mid-1990s to 43% in 2010, then declined slightly to 39% in 2015.[5] The IDEAL study in 2010 found that planned early initiation of dialysis at eGFR 10 to 14 mL/min/1.73 m² in stage V chronic kidney disease patients did not improve survival or clinical outcomes compared with late initiation at eGFR 5 to 7 mL/min/1.73 m².[6] In practice, most late-start patients (76%) began dialysis at a mean eGFR of 9.8 mL/min/1.73 m² due to symptoms, eg, uremia or fluid overload, indicating that clinical presentation often guides timing more than eGFR alone.[7] Guidelines differ internationally: the United Kingdom recommends dialysis initiation at eGFR 5 to 7 mL/min/1.73 m² or with symptom onset, whereas Japanese guidelines suggest continuing conservative treatment until eGFR falls below 8 mL/min/1.73 m², even if symptoms occur.[8][9]

According to the United States Renal Data System, the proportion of patients starting dialysis at an eGFR 10 mL/min/1.73 m² or greater rose from 13% in the mid-1990s to 43% in 2010, then declined slightly to 39% in 2015.[5] The IDEAL study in 2010 found that planned early initiation of dialysis at eGFR 10 to 14 mL/min/1.73 m² in stage V chronic kidney disease patients did not improve survival or clinical outcomes compared with late initiation at eGFR 5 to 7 mL/min/1.73 m².[6] In practice, most late-start patients (76%) began dialysis at a mean eGFR of 9.8 mL/min/1.73 m² due to symptoms, eg, uremia or fluid overload, indicating that clinical presentation often guides timing more than eGFR alone.[7] Guidelines differ internationally: the United Kingdom recommends dialysis initiation at eGFR 5 to 7 mL/min/1.73 m² or with symptom onset, whereas Japanese guidelines suggest continuing conservative treatment until eGFR falls below 8 mL/min/1.73 m², even if symptoms occur.[8][9] The Renal Physicians Association identifies patients with 2 or more of the following characteristics—age 75 years or older, high comorbidity burden (modified Charlson Comorbidity Index ≥8), significant functional impairment (Karnofsky Performance Status <40), or severe chronic malnutrition (serum albumin <2.5 g/dL)—as having a poor prognosis. Patients in this population should understand that dialysis may not improve survival or functional status and carries burdens that can reduce quality of life. Mortality among dialysis patients predominantly results from cardiovascular causes, followed by sepsis.[NIH. End Stage Renal Disease: Chapter 5. End Stage Renal Disease: Chapter 5. 2020]

The Renal Physicians Association identifies patients with 2 or more of the following characteristics—age 75 years or older, high comorbidity burden (modified Charlson Comorbidity Index ≥8), significant functional impairment (Karnofsky Performance Status <40), or severe chronic malnutrition (serum albumin <2.5 g/dL)—as having a poor prognosis. Patients in this population should understand that dialysis may not improve survival or functional status and carries burdens that can reduce quality of life. Mortality among dialysis patients predominantly results from cardiovascular causes, followed by sepsis.[NIH. End Stage Renal Disease: Chapter 5. End Stage Renal Disease: Chapter 5. 2020] High cardiovascular mortality may relate to chronic inflammation, extracellular volume shifts, dystrophic vascular calcification, and altered cardiovascular dynamics during dialysis. The SHARP study demonstrated a 17% reduction in major atherosclerotic events among patients with chronic kidney disease (CKD) receiving simvastatin–ezetimibe therapy.[10] Hypertension contributes to ESRD risk both as a cause and consequence of CKD. Cardioprotective strategies, including beta-blockers, aspirin, and renin-angiotensin-aldosterone system inhibitors, are recommended based on individual cardiovascular risk. Effective interprofessional collaboration among physicians, nurses, pharmacists, and other healthcare professionals is critical to optimizing outcomes for patients with ESRD who require dialysis.

Several complications are commonly associated with hemodialysis. Intradialytic Hypotension Intradialytic hypotension is defined as a decrease in systolic blood pressure of 20 mm Hg or greater, or a decrease in mean arterial blood pressure of 10 mm Hg, accompanied by associated clinical events.[44] This causes poor long-term outcomes due to increased mortality and increased rate of regional wall motion abnormalities during dialysis, known as myocardial stunning. A nadir systolic blood pressure lower than 90 mm Hg is associated with higher mortality.[45] Intradialytic hypotension may reflect severe underlying conditions, eg, infection, arrhythmias, myocardial ischemia, tamponade, hemorrhage, air embolism, or dialyzer reactions that require urgent recognition. This complication can result from rapid or excessive ultrafiltration, reduced plasma osmolality, autonomic dysfunction, diminished cardiac reserve, intake of antihypertensive medications, or dialysate-related factors, eg, temperature and electrolyte composition.[46][47][48] Intradialytic hypotension usually presents as dizziness, light-headedness, nausea, dyspnea, or subtle symptoms. Management includes reducing the ultrafiltration rate, maintaining the patient in the Trendelenburg position, and administering oxygen and a normal saline fluid bolus. Intradialytic Hypertension Volume overload, sympathetic overactivity, activation of the renin-angiotensin system, medications, and arteriosclerosis can contribute to intradialytic hypertension.[49][50][51] Intradialytic hypertension can be treated by using antihypertensive medications and achieving euvolemia. Muscle Cramps The pathogenesis of muscle cramps in patients on dialysis is unknown. The origin of the cramps is considered neural and typically involves the lower extremity muscles; however, upper extremity muscles can also be involved. Electrolyte shifts (eg, hypokalemia and hypomagnesemia), changes in plasma osmolality, and plasma volume contraction can predispose individuals to cramps. Tissue hypoxia and other factors that trigger vasoconstriction and muscle hypoperfusion impair muscle relaxation. Treatment includes slowing the rate of ultrafiltration, increasing plasma osmolality with hypertonic saline, mannitol, or dextrose, using medications (eg, gabapentin or amitriptyline), massaging the affected extremity, and using warm compresses.[52][53]

The pathogenesis of muscle cramps in patients on dialysis is unknown. The origin of the cramps is considered neural and typically involves the lower extremity muscles; however, upper extremity muscles can also be involved. Electrolyte shifts (eg, hypokalemia and hypomagnesemia), changes in plasma osmolality, and plasma volume contraction can predispose individuals to cramps. Tissue hypoxia and other factors that trigger vasoconstriction and muscle hypoperfusion impair muscle relaxation. Treatment includes slowing the rate of ultrafiltration, increasing plasma osmolality with hypertonic saline, mannitol, or dextrose, using medications (eg, gabapentin or amitriptyline), massaging the affected extremity, and using warm compresses.[52][53] Dialysis Disequilibrium Syndrome Dialysis disequilibrium syndrome is more common in patients during or soon after their first treatment. This complication is a clinical syndrome characterized by neurologic deterioration, restlessness, mental confusion, headache, occasional muscle twitching, and coma. It occurs due to a substantial gradient in urea concentration between CSF and blood, which causes water to move into the central nervous system, thereby raising intracranial pressure. Patients undergoing fast dialysis develop seizures and cerebral edema more often. A reasonable goal for urea concentration reduction is 40% over 2 hours, with a urea reduction ratio of 0.4. Adding an osmotic agent to the blood could prevent the gradient from forming. Sodium, mannitol, high-glucose dialysate, and glycerol are usually added. Increasing the dialysate’s sodium concentration throughout treatment may be beneficial.[54][55] Dialyzer Reactions

Dialysis disequilibrium syndrome is more common in patients during or soon after their first treatment. This complication is a clinical syndrome characterized by neurologic deterioration, restlessness, mental confusion, headache, occasional muscle twitching, and coma. It occurs due to a substantial gradient in urea concentration between CSF and blood, which causes water to move into the central nervous system, thereby raising intracranial pressure. Patients undergoing fast dialysis develop seizures and cerebral edema more often. A reasonable goal for urea concentration reduction is 40% over 2 hours, with a urea reduction ratio of 0.4. Adding an osmotic agent to the blood could prevent the gradient from forming. Sodium, mannitol, high-glucose dialysate, and glycerol are usually added. Increasing the dialysate’s sodium concentration throughout treatment may be beneficial.[54][55] Dialyzer Reactions Anaphylactic type A reactions can present from mild-to-moderate symptoms, eg, itching, urticaria, coryza, watery eyes, abdominal cramping, fever, nausea, vomiting, and diarrhea to severe symptoms, eg, dyspnea, a feeling of impending doom, and hemodynamic instability. Symptoms may begin at any time during the first 30 minutes following dialysis.[56] The reaction can be due to hypersensitivity to ethylene oxide, used to sterilize dialyzers, or to bacterial peptide contamination. Anaphylactoid reactions are common in patients taking ACE inhibitors who undergo hemodialysis with AN-69 membranes, likely due to the enhanced generation of bradykinin from the membrane’s negatively charged surface, combined with ACE inhibition.[57][58][59] Surface-modified AN-69 membranes (AN-69 ST) or adjusting priming conditions can reduce bradykinin release and prevent these reactions, even in patients who continue to take ACE inhibitors.[60] Management includes termination of dialysis treatment, treatment with intravenous antihistamines, steroids, and epinephrine. Proper rinsing of dialyzers before use eliminates residual allergens and helps prevent them.

Anaphylactic type A reactions can present from mild-to-moderate symptoms, eg, itching, urticaria, coryza, watery eyes, abdominal cramping, fever, nausea, vomiting, and diarrhea to severe symptoms, eg, dyspnea, a feeling of impending doom, and hemodynamic instability. Symptoms may begin at any time during the first 30 minutes following dialysis.[56] The reaction can be due to hypersensitivity to ethylene oxide, used to sterilize dialyzers, or to bacterial peptide contamination. Anaphylactoid reactions are common in patients taking ACE inhibitors who undergo hemodialysis with AN-69 membranes, likely due to the enhanced generation of bradykinin from the membrane’s negatively charged surface, combined with ACE inhibition.[57][58][59] Surface-modified AN-69 membranes (AN-69 ST) or adjusting priming conditions can reduce bradykinin release and prevent these reactions, even in patients who continue to take ACE inhibitors.[60] Management includes termination of dialysis treatment, treatment with intravenous antihistamines, steroids, and epinephrine. Proper rinsing of dialyzers before use eliminates residual allergens and helps prevent them. Type B reactions, which occur in patients dialyzed with new cellulosic membranes, are generally less severe than type A reactions and present with chest or back pain, dyspnea, nausea, vomiting, and hypotension. Symptoms usually appear within 15 to 30 minutes of starting dialysis and often improve as treatment continues. These reactions are mediated by complement activation and can be minimized by dialyzer reuse or by using more biocompatible membranes.[61][62] Chest Pain and Dyspnea Chest pain and dyspnea most often result from myocardial ischemia, volume shifts with rapid ultrafiltration, hypotension, or hypervolemia, but may also reflect severe conditions, eg, arrhythmias, hemolysis, air embolism, infection, or dialyzer reactions. Immediate management includes stopping ultrafiltration, reducing blood flow, positioning the patient in a supine position, administering oxygen, assessing vital signs, and evaluating for cardiac, hemolytic, or air embolic causes. Persistent symptoms, hypotension, hypoxemia, or suspected life-threatening etiologies require discontinuation of dialysis and urgent transfer to a hospital setting. Hemolysis

Chest pain and dyspnea most often result from myocardial ischemia, volume shifts with rapid ultrafiltration, hypotension, or hypervolemia, but may also reflect severe conditions, eg, arrhythmias, hemolysis, air embolism, infection, or dialyzer reactions. Immediate management includes stopping ultrafiltration, reducing blood flow, positioning the patient in a supine position, administering oxygen, assessing vital signs, and evaluating for cardiac, hemolytic, or air embolic causes. Persistent symptoms, hypotension, hypoxemia, or suspected life-threatening etiologies require discontinuation of dialysis and urgent transfer to a hospital setting. Hemolysis Acute hemolysis during dialysis is a medical emergency characterized by port-wine appearance in the venous blood line, a marked fall in hematocrit, and a pink-colored plasma centrifuged blood sample. The patient should undergo hematologic investigations and be monitored for potential delayed hemolysis. A dialysate sample must be investigated to find the cause. Air Embolism Air embolism is a rare complication but can lead to hemodynamic collapse, cardiac arrest, and fatal consequences. Venous air embolism is often challenging to diagnose, and visualization of intracardiac air on transesophageal echocardiography is considered the most definitive diagnostic test.[63][64] Management includes placing the patient in the left lateral decubitus position with the head down or in the Trendelenburg position, administering 100% and hyperbaric oxygen, and withdrawing air from the cardiac chambers using a percutaneously inserted needle or a cardiac catheter.[65] Fever Patients undergoing hemodialysis are at increased risk for infection, and the development of fever during a hemodialysis session should prompt concern for a vascular access–related infection. Other Complications Other complications of hemodialysis include nausea and vomiting, headache, chest and back pain, and pruritus.[54][66][67][68] These symptoms may be related to an underlying disorder, hypotension, an early manifestation of disequilibrium syndrome, dyselectrolytemia, hypoglycemia, or psychological factors.[69][70] Acetaminophen and antiemetics administered during dialysis can help alleviate the symptoms.

Other complications of hemodialysis include nausea and vomiting, headache, chest and back pain, and pruritus.[54][66][67][68] These symptoms may be related to an underlying disorder, hypotension, an early manifestation of disequilibrium syndrome, dyselectrolytemia, hypoglycemia, or psychological factors.[69][70] Acetaminophen and antiemetics administered during dialysis can help alleviate the symptoms. In patients with recurrent and severe dialysis-associated headaches, reducing the duration of individual hemodialysis sessions to mitigate symptoms while increasing treatment frequency to preserve dialysis adequacy may be beneficial.[71] Switching to a different type of dialyzer membrane could reduce itching caused by low-grade hypersensitivity to blood circuit components. Vascular Access Dysfunction Vascular access dysfunction most commonly manifests as stenosis of arteriovenous access, which is the strongest determinant of the quality of life of a patient undergoing dialysis. This leads to reduced blood flow and an increased risk of thrombosis.[72] The formation of a catheter-related fibro-epithelial sheath also hampers blood flow. Urokinase instillation, endovascular catheter stripping, or replacement of the indwelling dialysis catheter in a subcutaneous tunnel reestablishes access.[73][74] Electrolyte Imbalances Electrolyte imbalances should be remediated by dialysis; however, they can also be precipitated by dialysis. Hyperkalemia is the most common and clinically significant complication in noncompliant patients, besides hypermagnesemia, hyponatremia, and hypocalcemia.[75] A cardiac arrest is twice as likely in patients undergoing hemodialysis as in those on peritoneal dialysis 3 months after dialysis initiation. Sudden cardiac deaths are most likely during the first 2 months after the initiation of hemodialysis. The predominant arrhythmias identified are ventricular fibrillation, pulseless electrical activity, and asystole. In the vascular access process, death may occur from cardiac arrhythmias, pulmonary edema, or contrast medium reaction.[72]

Electrolyte imbalances should be remediated by dialysis; however, they can also be precipitated by dialysis. Hyperkalemia is the most common and clinically significant complication in noncompliant patients, besides hypermagnesemia, hyponatremia, and hypocalcemia.[75] A cardiac arrest is twice as likely in patients undergoing hemodialysis as in those on peritoneal dialysis 3 months after dialysis initiation. Sudden cardiac deaths are most likely during the first 2 months after the initiation of hemodialysis. The predominant arrhythmias identified are ventricular fibrillation, pulseless electrical activity, and asystole. In the vascular access process, death may occur from cardiac arrhythmias, pulmonary edema, or contrast medium reaction.[72] Vascular access precautions include avoiding additional trauma to the access arm, eg, wearing tight clothing or jewelry, carrying heavy objects, or sleeping on the affected limb. Blood draws and blood pressure measurements should not be performed on this arm. Needle insertion sites should be rotated to preserve access integrity, and gentle pressure should be applied after needle removal to achieve hemostasis. Patients should be instructed to contact a health care practitioner if bleeding persists or becomes profuse (>30 minutes). Bleeding, often related to heparin use during dialysis, can be effectively treated with protamine sulfate. Continuous monitoring of venous and arterial pressures is essential for detecting line disconnections. Needles should be securely taped, and safety measures such as wetness detectors and closed connector devices should be employed. Regular inspection of the access site for signs of infection (eg, redness, warmth, pain) is necessary. Loss of the normal bruit should prompt evaluation for access thrombosis to prevent limb ischemia.

Dialysis serves as a life-sustaining therapy for patients with advanced kidney disease or end-stage renal disease, offering two primary modalities: hemodialysis and peritoneal dialysis. Hemodialysis can be delivered intermittently (IHD) or continuously (CRRT), with IHD providing rapid ultrafiltration for acute volume overload and CRRT offering continuous fluid and solute removal to maintain hemodynamic and metabolic stability in critically ill patients. Appropriate timing for initiating dialysis depends on clinical symptoms, volume status, and functional decline rather than kidney function alone. Early counseling regarding treatment options, including home or in-center hemodialysis, peritoneal dialysis, kidney transplantation, or conservative management, supports informed decision-making for patients and their caregivers. Mortality among dialysis patients is predominantly cardiovascular, highlighting the need for risk mitigation through pharmacologic strategies and careful monitoring. Effective management of dialysis requires coordinated interprofessional collaboration. Physicians, general practitioners, and advanced practitioners assess disease progression, determine timing and modality selection, and monitor clinical and laboratory parameters. Nurses provide patient education, monitor hemodynamic stability, and facilitate adherence to treatment plans. Pharmacists optimize medication management, ensure safe dosing, and support cardiovascular protection. Dietitians guide nutritional interventions, and social workers support patients and assist with resource access. Consistent communication across the care team ensures timely recognition of complications, individualized therapy adjustments, and comprehensive patient-centered care, ultimately improving clinical outcomes, safety, and quality of life for patients requiring dialysis.

Home hemodialysis causes an additional burden for both caregivers and patients. However, imparting adequate pre-dialysis education, motivation, and training of patients and caregivers, assisted cannulation, home visits by nurses, and an organized framework for providing nursing, technical support, and respite care for patients have been shown to improve the adoption of home hemodialysis. Sticking to a healthy diet has been shown to improve outcomes in patients undergoing hemodialysis.[77] A study has shown that periodic text messaging to advise dialysis patients on healthy eating habits has improved adherence to dietary recommendations and reduced the need for phosphate binder therapy. The reminders focus on guidance related to potassium, phosphorus, sodium, and fluid intake, as well as broader nutrition and lifestyle advice. These include encouraging the consumption of fresh, unprocessed foods to limit phosphate intake commonly found in packaged products; advising patients to read food labels carefully and select items containing less than 400 mg of sodium per 100 g; and recommending alternatives, eg, pasta, rice, and sweet potato, consumed 3 to 4 times per week, in place of regular potatoes to better control potassium intake.

Commencing home hemodialysis creates unique psychosocial issues affecting the patient and care partner. The home hemodialysis health care team must provide proactive interprofessional support, respite care, travel support, peer support, and financial support. Improper redressal of these aspects could cause patients to return to in-center hemodialysis. Some centers provide real-time monitoring of home hemodialysis treatments, and a panic button/alarm may be present to contact the local paramedic unit.[78]