The first dialysis session

Planned initiation of haemodialysis in end-stage kidney disease (ESKD) differs greatly from dialysis started for acute uraemia.

In chronic kidney disease, preparation often proceeds gradually for months before dialysis becomes necessary, reflecting the slow development of the uraemic state. Acute kidney injury is different: it is commonly caused by a serious disorder that may require dialysis urgently, so treatment is almost always started through a temporary dialysis catheter.

Factors that need to be considered include:

• Session duration.

• Blood-flow rate.

• Choice of dialyser.

• Anticoagulation.

• Dialysate composition.

• Fluid removal by ultrafiltration.

• The experience of the nursing team and availability of medical staff.

1. Session duration

Together with blood flow, treatment time is a major determinant of the dialysis dose delivered.

The main concern during initial treatment is dialysis disequilibrium syndrome, which can occur when severe uraemia is corrected too rapidly. It may develop in either acute or chronic kidney disease when blood urea falls very quickly or the starting urea concentration is extremely high. The source therefore recommends limiting the fall in urea during the first treatment to no more than about 30%.

For many patients, the source describes an initial session of approximately two hours. Some people require daily dialysis for several days—often three consecutive treatments—before moving to a conventional chronic schedule of three sessions per week.

The dialysis dose is also commonly increased stepwise before the full standard prescription is reached: for example, the second session may last three hours and the third 3.5–4 hours. Urea values must be interpreted carefully. Persistently high urea on the second or third day does not by itself justify a rapid increase in treatment intensity, particularly when substantial post-dialysis urea rebound is expected.

2. Blood flow

The source describes a blood-flow rate of 150–200 mL/min for the first session. A larger patient may require a slightly longer treatment, such as 2.5 hours, or a modestly higher blood flow, such as 250 mL/min.

3. Dialyser

A standard dialyser is generally sufficient. A high-efficiency dialyser with KoA above 400 is not usually required for the first session. If one is used, treatment time or blood flow should be reduced to lower the risk of disequilibrium syndrome.

Evidence is conflicting as to whether more biocompatible membranes improve morbidity or recovery of kidney function after acute kidney injury.

Atopic patients may be more susceptible to a reaction to ethylene-oxide sterilisation. In rare cases, a patient receiving an angiotensin-converting-enzyme inhibitor (ACE inhibitor) can develop a hypersensitivity reaction during dialysis with an AN69® membrane.

4. Anticoagulation

The source favours avoiding heparin or other anticoagulants during the first dialysis session when feasible, in order to reduce the risk of pericardial bleeding, bleeding from a newly placed vascular access, or intracranial bleeding in severe hypertension. The actual choice must be individualised according to the competing risks of bleeding and circuit clotting.

5. Dialysate settings for the first session

Bicarbonate

Bicarbonate is preferred to acetate because it is less likely to contribute to hypotension. Patients at risk of severe alkalaemia may need a lower bicarbonate concentration, cited here as below 35 mmol/L.

In metabolic alkalosis, hyperventilation can raise systemic pH further. In severe metabolic acidosis, serum bicarbonate should not be corrected too abruptly; the source describes an initial serum target of 15–20 mmol/L and possible reduction of dialysate bicarbonate to avoid overcorrection.

Sodium

Dialysate sodium is generally set between 135 and 145 mmol/L. In a patient with serum sodium below 130 mmol/L, the source recommends limiting the dialysate-to-plasma gradient to about 5–10 mmol/L and avoiding overly rapid correction of hyponatraemia through the dialysate prescription.

For hypernatraemia, the source states that dialysate sodium should be equal to or only slightly higher—by 1–3 mmol/L—than plasma sodium.

If dialysate sodium is substantially lower than blood sodium, the venous blood returning to the patient can become relatively hyponatraemic. Water then moves out of the vascular compartment, which may contribute to an acute fall in blood pressure.

Potassium

Blood potassium will often fall as acidosis is corrected.

The source describes dialysate potassium of 4–4.5 mmol/L when serum potassium is at least 4.5 mmol/L, a concentration of 2–3 mmol/L when serum potassium is above 5.5 mmol/L, and 4 mmol/L when serum potassium is 4–5 mmol/L. The expected fall in potassium as metabolic acidosis is corrected must be considered. These examples require individual prescription and continuous clinical review.

Calcium

Avoid an excessive fall in calcium, because it may contribute to hypotension.

6. Ultrafiltration

Substantial fluid removal during the first session is reserved in the source for severe oedema with marked hypertension, such as acute pulmonary oedema or decompensated heart failure. Otherwise it is discouraged during the first treatment. The source recommends removing no more than two litres during the first haemodialysis session.

Conversely, some patients need additional fluid rather than fluid removal.

7. Medical and nursing team

The first haemodialysis session requires skilled staff who can monitor the patient and the equipment while also providing reassurance.

Complications can be severe or unexpected.

Complications during haemodialysis

Common complications during dialysis

The frequency estimates below are those quoted in the source and vary widely between patient populations, definitions, and dialysis practices:

• Hypotension: reported in 25%–60% of treatments.

• Cardiac arrhythmia: reported in 5%–60% of patients.

• Muscle cramps: 5%–25%, often associated with excessive fluid removal.

• Nausea and vomiting: 5%–15%.

• Headache: 5%–10%, particularly during early sessions.

• Back pain: 2%–5%.

• Chest pain: 2%–5%; a cardiovascular emergency must always be excluded.

• Pruritus: 1%–5%.

• Fever: approximately 1%; vascular-access infection must always be considered.

Other, less common complications

• Air embolism.

• Seizures.

• Haemolysis.

• Dialysis disequilibrium.

• First-use syndromes.

• Acute urticaria.

• Cardiac tamponade.

Dialysis disequilibrium syndrome

This syndrome can occur in acute or chronic kidney disease when blood urea falls too rapidly, especially in severe uraemia or when the patient already has an altered mental state.

It presents with a spectrum of acute neurological symptoms during or after dialysis, including headache, nausea, confusion, restlessness, and blurred vision. Severe manifestations include seizures, coma, and death.

The proposed mechanism is cerebral oedema after a rapid fall in plasma osmolality as osmotically active retained solutes are removed from blood. Water moves from the intravascular compartment into the brain before solutes have equilibrated across cell membranes. Intracerebral acidosis may also contribute.

The syndrome is uncommon when the initial prescription for severe uraemia is deliberately gentle—for example, a short session of about two hours with low blood flow and a first-session urea reduction below approximately 30%.

The source reports historical use of phenytoin, with a 1,000 mg loading dose followed by 300 mg/day. Symptoms are usually self-limiting over several hours, but any neurological deterioration during dialysis is an emergency and requires immediate clinical assessment rather than routine self-treatment.

For severe cases, the source describes intravenous mannitol 10–15 g or 5 mL of 23% hypertonic saline. Such hyperosmolar treatment requires specialist emergency management and monitoring.

Intradialytic hypotension (IDH)

IDH is reported in approximately 6%–30% of haemodialysis sessions and is particularly common in people with heart disease. It may be episodic or, less commonly, persistent. Mechanistically, it can be classified as hypovolaemic, distributive, or cardiogenic.

IDH can create a vicious cycle that perpetuates fluid overload and hypertension. The immediate response is often normal or hypertonic saline, which can leave the patient above target weight after the session. This may then worsen interdialytic hypertension and lead to further antihypertensive treatment.

Groups at greater risk include older adults, women, and people with diabetes, high serum phosphate, coronary artery disease, or autonomic neuropathy.

Correct and repeated assessment of dry or target weight is central to preventing IDH.

Common causes can be divided into patient-related and treatment-related factors.

1. Patient-related causes

• Diabetes and autonomic polyneuropathy.

• Heart failure.

• Cardiac arrhythmia.

• Poor nutritional status.

• Large interdialytic weight gain.

• Eating during dialysis, which diverts blood to the splanchnic circulation.

• Sepsis.

• Adenosine release during organ ischaemia, including ischaemia caused by hypotension. Adenosine is a vasodilator and inhibits release of norepinephrine.

• Subclinical myocardial ischaemia.

2. Treatment-related causes

• Rapid fluid removal and a high ultrafiltration rate.

• Antihypertensive medicines that blunt cardiac compensation or vascular reflexes.

• A rapid fall in plasma osmolality, causing water to move from the vascular to the interstitial compartment.

• High dialysate temperature.

• Low dialysate sodium.

• Low dialysate osmolality.

• Use of acetate rather than bicarbonate; acetate can promote vasodilatation.

• Bioincompatibility.

Less common important causes include:

• Pericardial effusion or tamponade.

• Hypersensitivity to a dialyser membrane.

• A high dialysate magnesium concentration.

• Gastrointestinal bleeding.

• Myocardial infarction.

• Haemolysis.

• Air embolism.

The source additionally reports chronic, persistent hypotension in up to 75% of long-term dialysis patients, particularly after more than five years of treatment, with pre-dialysis systolic blood pressure often below 90 mmHg. The exact frequency depends heavily on definition and population.

Reduced left-ventricular function or valvular disease may explain chronic hypotension, but often no single cause is identified. Accumulation of poorly dialysed vasodilators such as nitric oxide and adrenomedullin, together with diminished adrenergic responsiveness, may contribute.

Hypotension caused by excessive ultrafiltration

As ultrafiltration removes water from the intravascular space, circulating volume is maintained by movement of fluid from tissues back into the vessels—vascular refilling. Because this movement is relatively slow, rapid ultrafiltration commonly leads to hypotension.

The source gives a general vascular-refilling rate of 15–25 mL/kg/hour and therefore advises keeping ultrafiltration below 20 mL/kg/hour, particularly in patients with cardiac disease. Modern practice generally uses substantially lower individualised ultrafiltration rates; no single threshold is safe for every patient.

Two broad groups of forces affect refilling: Starling forces and osmotic forces. They act continuously, often in opposing directions.

Starling forces, together with capillary permeability, govern fluid movement between the vascular and interstitial spaces. Refilling may be impaired by hypoalbuminaemia, right-sided heart failure, increased capillary permeability or capillary-leak syndrome, and increased capillary hydrostatic pressure.

Dihydropyridine calcium-channel blockers dilate the precapillary sphincter, which can increase capillary hydrostatic pressure and reduce vascular refilling.

Osmotic forces arise from dissolved substances in plasma and help draw fluid from the interstitium into blood vessels. These solutes fall rapidly after dialysis starts as they cross into the dialysate, allowing Starling forces that favour movement toward the interstitium to predominate until a new equilibrium develops. This effect is especially relevant when dialysate sodium is more than about 4 mEq/L below plasma sodium.

Heart failure and the diastolic dysfunction common in dialysis patients are also important. Dialysis-induced cardiac stunning—a transient form of treatment-related myocardial ischaemia—may occur.

Factors that make uncontrolled ultrafiltration more likely

• Haemodialysis or ultrafiltration without volumetric control.

• An excessively high blood-flow rate may also contribute.

• Large interdialytic fluid intake that makes target weight difficult to reach. High salt intake, often hidden in processed food, is commonly the main driver. The source states that 0.5 g/day of additional salt can produce a mean 1.5 kg weight gain in an anuric 70 kg patient; this estimate should be interpreted cautiously and not as a universal quantitative rule.

• An incorrectly low target weight causes hypotension. This is especially relevant during recovery from acute illness, when lost muscle mass is regained.

Management of hypotension

Hypotensive episodes are extremely uncomfortable for patients, markedly reduce quality of life, increase morbidity, and may contribute to cardiovascular mortality.

Frequent, careful reassessment of dry or target weight is essential.

Immediate management centres on restoring effective circulating volume and identifying the cause. The source describes:

• Lowering the patient’s head.

• Administering 100–250 mL of normal saline. It also lists historical alternatives used by some units: 10 mL of 23% saline, 30 mL of 7.5% saline, 50 mL of 20% mannitol, or albumin solution.

• Reducing the ultrafiltration rate to zero.

• Giving further saline if blood pressure does not recover promptly.

Hypertonic saline can increase thirst, prevent achievement of target weight, and worsen fluid overload. If blood pressure does not improve after adequate fluid treatment, other causes must be sought urgently, particularly cardiac disease, gastrointestinal bleeding, and sepsis.

In many episodes, excessive ultrafiltration is the cause and blood pressure improves rapidly when fluid removal is stopped and volume is restored.

If hypotension recurs, review:

• Whether target weight is too low.

• Use of short-acting antihypertensive medicines before dialysis; selected medicines may be moved until after treatment, although this does not apply automatically to modern long-acting agents.

• The ultrafiltration rate.

• Interdialytic weight gain, with particular attention to salt and hidden fluids such as soups. The source suggests limiting weight gain to about 1 kg/day, but the appropriate limit is individual.

• Dialysate sodium; a concentration above plasma sodium can temporarily support blood pressure but may increase sodium loading and thirst.

• Use of bicarbonate rather than acetate.

• Lowering dialysate temperature to approximately 34–36°C, while recognising that some patients find this uncomfortable.

• Correction of clinically important anaemia.

• Avoiding food during dialysis when eating reliably precipitates hypotension, while recognising that dialysis may be the only practical opportunity for nutritional support in some patients.

If non-pharmacological measures fail, the source describes medicines that have sometimes been used:

• Levocarnitine 20 mg/kg at the end of dialysis; good evidence for improvement of IDH is lacking.

• Midodrine, an oral alpha-1 agonist, 2.5–10 mg approximately 30 minutes before dialysis. It increases peripheral vascular resistance, venous return, and cardiac output. A second dose has sometimes been used during the session.

• Sertraline 50–100 mg/day.

Preventing hypotension

Hypotension is distressing for both patient and clinical team. It makes euvolaemia difficult to achieve and can perpetuate fluid overload followed by interdialytic hypertension.

Because cardiovascular disease is the leading cause of death in ESKD, volume and blood-pressure control are important.

Dialysis duration

Extending the session often helps control recurrent hypotension by permitting slower fluid removal, although patients may find longer treatments burdensome.

Sodium ramping or profiling

Sodium profiling has been used to reduce hypotension and cramping by supporting vascular refilling. Dialysate sodium is set high—for example, 144–155 mmol/L—during the first one or two hours and then lowered in steps or gradually over the following three hours.

It may help selected patients, but the prescription requires great care. Trials have reported fewer hypotensive episodes but also greater thirst and subsequent fluid intake because of sodium loading, which can negate the benefit.

The time-averaged dialysate sodium concentration, not merely the end-of-session value, should generally avoid a positive sodium balance relative to plasma.

Sequential ultrafiltration and isovolaemic dialysis

This strategy can help some patients reach target weight without hypotension, although the source considers it less effective than sodium profiling. Isolated ultrafiltration is performed during the first one or two hours, removing fluid while maintaining or increasing plasma urea and sodium concentrations and thereby supporting faster vascular refilling. Dialysis then follows with minimal ultrafiltration.

The method tends to lengthen the total treatment time.

Temperature

The patient’s temperature can be kept approximately 0.5°C below baseline by cooling dialysate to about 35–36.5°C. This promotes cutaneous vasoconstriction and can be very effective in preserving blood pressure during haemodialysis.

Carnitine

Some evidence has suggested that carnitine deficiency may contribute to intradialytic hypotension, muscle fatigue, cardiomyopathy, and anaemia. The source describes regular intravenous levocarnitine or oral levocarnitine 500 mg/day, alone or with oral vitamin E 200 IU/day, although benefit is not established for every patient.

Calcium

Low dialysate calcium can impair myocardial contractility. Prospective studies cited in the source reported less IDH with dialysate calcium of 1.5 or 1.75 mmol/L than with 1.25 mmol/L. A higher calcium concentration can, however, produce a positive calcium balance.

Haemofiltration and haemodiafiltration

Convective treatments may provide greater cardiovascular stability than routine haemodialysis. The source also cites the 2023 CONVINCE trial by Blankestijn and colleagues, which found a lower risk of death with high-dose haemodiafiltration than with high-flux haemodialysis in the studied population.

Several possible mechanisms have been proposed:

• A slower fall in serum osmolality during convective transport, because water and solutes are removed together.

• Better removal of larger molecules. Some retained larger molecules have been proposed as contributors to vasodilatation; improved removal might therefore reduce hypotension.

• Lower temperature. Replacement fluid is often not warmed during haemofiltration, so blood temperature may be lower and vasodilatation reduced.

• Use of a biocompatible membrane. Convective therapies generally use more permeable synthetic membranes associated with less complement activation and cytokine production.

Peritoneal dialysis

Some patients with persistent, uncontrollable IDH may need to consider a switch to peritoneal dialysis.

Blood-volume monitoring: Crit-Line

Continuous optical measurement of haematocrit or plasma-protein concentration can estimate changes in blood volume through changes in haemoglobin or plasma-protein concentration. Specialist software can identify blood-volume patterns that precede symptomatic hypotension and intervene, for example by slowing ultrafiltration.

As a general rule quoted in the source, a fall in relative blood volume exceeding 8%–10% per hour suggests that hypovolaemia is approaching. Individual thresholds differ, however, and some patients become hypotensive without crossing a conventional relative-volume threshold.

Other complications during haemodialysis

Hypertension during or at the end of dialysis

Some patients paradoxically develop a rise in blood pressure during dialysis, usually in the final hour. Studies have associated intradialytic hypertension with adverse outcomes. Proposed mechanisms include volume excess from an inaccurate target weight, an altered nitric-oxide/endothelin-1 balance, and endothelial dysfunction.

Other possible contributors include:

• A fall in potassium, which may stimulate renin or act directly on the circulation.

• Use and dialytic removal of beta blockers such as atenolol and metoprolol.

• Changes in calcium; higher calcium may also raise blood pressure.

• Sympathetic activation.

• Continued presence of the native kidneys.

• Erythropoiesis-stimulating therapy.

• Removal during dialysis of dialysable antihypertensive drugs, including metoprolol, atenolol, and some ACE inhibitors.

Management begins by reviewing these causes and reassessing target weight. If appropriate, a highly dialysable antihypertensive may be replaced with a less dialysable, more protein-bound agent, such as an angiotensin-receptor blocker or carvedilol. A lower dialysate sodium concentration may also be considered within an individualised prescription.

Muscle cramps

Muscle cramps are common, especially near the end of dialysis. The source states that up to 90% of patients have experienced them at some point. They are an important cause of early termination and therefore of a lower delivered dialysis dose. The cause is not always clear, but cramps are closely associated with low sodium, hypotension, and hypovolaemia; hypoxia and carnitine deficiency have also been proposed.

Treatment of muscle cramps

Patient education about fluid limits and reduction of interdialytic weight gain is central to preventing both cramps and intradialytic hypotension.

For an acute episode, the source describes normal or hypertonic saline and hypertonic glucose, including 50% glucose, as rapidly effective options. Saline can raise blood pressure and add to extracellular volume.

Massage can provide relief. The source also describes vitamin E 200–400 IU/day, carnitine, and quinine sulphate as treatments that may help selected patients.

It states that quinine is best given two hours before dialysis and describes intravenous carnitine 20 mg/kg after each session or oral levocarnitine 500 mg/day. Quinine can cause serious adverse effects and is not a routine self-treatment; any use requires a current, individual medical decision.

Nausea, vomiting, and headache

These symptoms are common and usually accompany hypotension. They may indicate mild dialysis disequilibrium after a large fall in urea or occur in severe, longstanding uraemia. Less commonly, withdrawal from caffeine or alcohol during dialysis contributes.

Treatment

Treat and prevent hypotension. An antiemetic and paracetamol may help after the cause has been assessed.

Reducing blood flow by 25%–30% during the first hour sometimes helps, but the total session must then be extended to preserve the prescribed dialysis dose. Bicarbonate is preferable to acetate.

Chest pain

Chest pain is commonly related to myocardial ischaemia or hypotension, but it may also occur with disequilibrium syndrome, haemolysis, or air embolism. A comprehensive and urgent cardiovascular assessment is required.

Air embolism

Possible manifestations include acute breathlessness and neurological symptoms such as loss of consciousness or a seizure.

Air embolism is rare because air detectors clamp the venous blood line when air is detected in the return circuit.

The patient’s position influences where air travels and therefore the clinical presentation.

If air enters through a peripheral vascular access such as a fistula or graft while the patient is sitting upright, it may travel toward the cerebral circulation and cause acute neurological injury, seizures, altered consciousness, or coma.

Air entering through a central venous catheter may reach the right ventricle and cause severe hypoxaemia through pulmonary arterial air embolism. It may obstruct right-ventricular outflow, leading to low cardiac output, acute right-sided heart failure, or profound hypoxia.

In a head-down Trendelenburg position, air may move toward lower-limb veins and compromise limb perfusion.

Foam may be visible in the venous blood line, and abnormal “mill-wheel” cardiac sounds may sometimes be heard.

Emergency management

Clamp the venous line and stop the blood pump immediately. The source describes placing the patient in the left lateral position with the head and chest down, administering 100% oxygen, and providing cardiopulmonary support as required.

Percutaneous aspiration of air from the right ventricle may occasionally be necessary in specialist care.

Haemolysis

Possible symptoms include generalised pain, breathlessness, headache, and nausea.

Severe haemolysis is rare but may cause chest, abdominal, or back pain, chest tightness, headache, nausea, and malaise. It can produce life-threatening hyperkalaemia if not recognised promptly. Suspicion should be especially high when several patients develop similar symptoms at the same time.

Causes include:

• Excessive dialysate temperature, above 45°C, because of a technical machine fault.

• Chemical contamination with substances such as bleach, formaldehyde, or peroxide during water treatment or reprocessing.

• Chloramine, nitrate, or copper contamination of the water supply. Chloramine is normally removed by activated-carbon beds; if more than one patient is affected, this treatment stage and the carbon beds require immediate investigation.

• Hypotonic dialysate.

• Kinks in the blood tubing.

• Malfunction of the blood pump.

Management: stop the blood pump immediately and clamp the lines. Do not return potentially haemolysed circuit blood because of the risk of severe hyperkalaemia. Check potassium and haemoglobin and begin emergency treatment as indicated.

Haemolysis can continue for several hours after the precipitating exposure has ended. Identify the cause urgently, because a problem with water or a central dialysis system may affect several patients.

Dialyser hypersensitivity reactions

These reactions are also called first-use syndromes because they have often occurred with new dialysers, although they can also occur with reprocessed dialysers.

They are traditionally divided into severe anaphylactic or anaphylactoid type A reactions, usually beginning within the first few minutes but occasionally up to 30 minutes after dialysis starts, and milder type B reactions, commonly presenting with back or chest pain from minutes to hours after initiation.

Type A reaction

Symptoms begin within minutes and range from breathlessness, wheeze, warmth, urticaria, and cough to hypotension, shock, or cardiac arrest.

Many historical cases were related to an immune reaction to ethylene oxide (EtO). Increased IgE antibodies against EtO-modified proteins were demonstrated, and reactions became uncommon when residual EtO was removed by thorough rinsing, supporting a causal role.

Reactions can also occur in patients taking an ACE inhibitor who are dialysed with an AN69® membrane, and rarely with other polyacrylonitrile membranes.

AN69® can increase or activate bradykinin even in a patient not taking an ACE inhibitor; ACE inhibition then prevents normal bradykinin degradation.

Type A-like reactions have also been reported with endotoxin-contaminated water or dialysate and, occasionally, with heparin.

Whether other sterilant impurities or dialysate constituents cause similar reactions is less certain. The association with ACE inhibitors is well documented. Reports exist with other membranes, including polyacrylonitrile and polysulfone, but the evidence is strongest for AN69®.

Anaphylactoid reactions have also been reported with high-flux dialysers and bicarbonate dialysate; bicarbonate concentrate can support microbial contamination if handling and disinfection are inadequate.

Type B reaction

Type B reactions are more common but much milder. They often begin 20–40 minutes after dialysis starts and usually cause back or chest pain. The cause is uncertain and incidence has declined.

The historical literature also describes a syndrome of acute deafness and blindness in the 1990s among patients treated with very old cellulose-acetate dialysers, more than 11 years old. None of the reported patients recovered, and all died within one year. Degradation products from the membrane were suspected.

In 2002, several patients died after use of Baxter Althane cellulose-diacetate dialysers. Residual perfluorocarbon within the dialysers was identified as the cause. This volatile, hydrophobic liquid was insoluble in water and produced extensive gas formation in the right side of the heart with obstruction of pulmonary capillaries. Perfluorocarbon had been used during manufacture to repair leakage from hollow fibres.

Management

Type A: avoid dialysers sterilised with ethylene oxide and rinse the dialyser thoroughly. Stop the ACE inhibitor when an AN69® or related polyacrylonitrile membrane is implicated. If reactions recur with different dialysers, change membrane type and consider whether heparin is the trigger.

Type B: first change the membrane type—for example, from cellulose to modified cellulose or a synthetic membrane.