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Renal care 

Renal care
Renal care

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

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date: 09 May 2021

Acute kidney injury (AKI)

Acute kidney injury (AKI) can be defined as a rapid reduction in renal function (within 48 h) resulting in a failure to maintain fluid, electrolyte, and acid–base balance. The clinical outcomes of AKI include increased length of stay, critical care admission, higher mortality, and long-term dialysis. A worse outcome is linked to post-admission AKI.

AKI is usually associated with oliguria, which is due to a sudden and sustained drop in renal perfusion causing the glomerular filtration rate (GFR) to fall, resulting in a decrease in urine output. The kidneys are highly susceptible to ischaemia and/or toxins. The resultant vasoconstriction, endothelial injury, and inflammatory changes contribute to loss of glomerular or tubular function, interstitial oedema, and reabsorption of toxins.

Causes of acute kidney injury

Pre-renal conditions

These are conditions that decrease blood flow to the renal artery.

  • Hypovolaemia—for example, haemorrhage, burns, gastrointestinal losses, excessive diuresis, and third spacing (ascites, pancreatitis).

  • Hypotension—low cardiac output states, such as myocardial dysfunction, arrhythmias, valvular dysfunction, and obstructive states (pulmonary embolus, pericardial tamponade).

  • Sepsis—septic changes to renal vasculature lead to reduced GFR despite increased cardiac output. Septic AKI has a greater likelihood of recovery compared with non-septic causes of AKI.

Intra-renal conditions

These are conditions that produce a direct ischaemic or toxic effect.

  • Hepatorenal syndrome—seen in advanced cirrhosis without significant glomerular or tubular abnormalities.

  • Cortical necrosis—nephrotic syndrome, renal artery occlusion or thrombosis, glomerulonephritis, vasculitis (see Renal care p. [link]).

  • Acute tubular necrosis—nephrotoxins (e.g. radiographic contrast, aminoglycosides, rhabdomyolysis).

  • Acute interstitial nephritis—drugs including penicillins and NSAIDs.

  • Vascular—emboli.

Post-renal conditions

These are conditions that hinder urine flow to the remainder of the urinary tract.

  • Raised intra-abdominal pressure—impedes renal venous drainage.

  • Intra-ureteral conditions—calculi, tumour, blood clot.

  • Extra-ureteral conditions—retroperitoneal fibrosis, tumour, aneurysm.

  • Bladder obstruction—prostatic hypertrophy, bladder tumour, blood clot, calculi, functional neuropathy.

  • Urethral obstruction—stricture, phimosis, blocked urinary catheter.

Specific disorders associated with AKI

Acute glomerulonephritis

This refers to a specific set of renal diseases in which an immunological mechanism triggers inflammation and proliferation of glomerular tissue. This can result in damage to the basement membrane or capillary endothelium. Sudden-onset haematuria, oliguria, and proteinuria accompany renal dysfunction. Granular red cell casts are present in the urine. Clinically it is associated with hypertension and peripheral oedema.

Causes of acute glomerulonephritis

Systemic causes

  • Wegener’s granulomatosis—necrotizing vasculitis affecting small and medium-sized vessels in the kidneys, lungs, and nasal cartilage.

  • Collagen vascular diseases (e.g. systemic lupus erythematosus)—causes renal deposition of immune complexes.

  • Hypersensitivity vasculitis—often associated with eosinophilia.

  • Polyarteritis nodosa—causes vasculitis of the renal arteries.

  • Henoch–Schönlein purpura—causes generalized vasculitis.

  • Goodpasture’s syndrome—antibodies to type IV collagen may rapidly result in oliguric renal failure and haemoptysis.

  • Drug-induced (e.g. gold, penicillamine).

  • Cryoglobulinaemia—abnormally high plasma levels of cryoglobulin.

Post-infectious causes

  • Group A streptococcal infection (e.g. sore throat, upper respiratory tract infection)—usually occurs 1 week or more after the acute infection.

  • Other specific agents—other bacteria, fungi, viruses, and parasites (e.g. malaria, filariasis), and atypicals (e.g. Legionnaire’s disease).

Renal diseases

  • Berger’s disease—immunoglobulin-related nephropathy due to deposition of IgA and IgG.

  • Membranoproliferative glomerulonephritis—deposition of complement causes expansion and proliferation of mesangial cells.

  • Idiopathic rapidly progressive glomerulonephritis.

Hepatorenal syndrome

This is the development of AKI in patients with chronic liver disease presenting with ascites and portal hypertension. It may be caused by alterations in splanchnic circulatory tone and renal blood supply. The renin–angiotensin–aldosterone and sympathetic nervous systems are activated with profound renal vasoconstriction. It is associated with a high mortality. Liver transplantation is the definitive treatment, with normalization of renal function occurring soon after the transplant. Risk factors include:

  • infection (e.g. bacterial peritonitis)

  • acute alcoholic hepatitis

  • large-volume paracentesis without albumin replacement

  • gastrointestinal and variceal bleeding.


This is the breakdown of striated muscle, resulting in release of myoglobin, which causes a combination of pre-renal, nephrotoxic, and obstructive renal failure.


  • Direct trauma, crush injury, or burns.

  • Muscle compression from prolonged immobility (e.g. surgery, coma).

  • Metabolic illness (e.g. diabetic metabolic decompensation).

  • Myositis or excessive muscle activity.

  • Temperature extremes.

  • Toxins—alcohol, solvents, drug abuse.

  • Muscular dystrophies.

Substances released by damaged muscle

  • Potassium, leading to hyperkalaemia, which may be resistant to glucose and insulin therapy and require urgent haemodialysis or haemodiafiltration (dialysis is more effect than filtration alone).

  • Hydrogen ions, leading to metabolic acidosis (see Renal care p. [link]).

  • Phosphate, leading to hyperphosphataemia.

  • Creatine, leading to elevated creatinine kinase activity (usually > 5000 IU/L).

  • Myoglobin, leading to myoglobinuria; myoglobin is oxidized by hydroperoxides in the kidney, generating potent oxidizing ferryl-myoglobin. This is nephrotoxic, especially with coexisting acidosis and volume depletion, as it can obstruct renal tubules.


  • Maintain an effective circulating volume to meet perfusion needs (e.g. to ensure high urine output).

  • Forced alkaline diuresis, with 6–10 L fluid/day to maintain urine pH > 6 using 1.24% sodium bicarbonate. Alkalinization stabilizes the oxidized form of myoglobin.

  • Treat hyperkalaemia.

  • Renal replacement therapy may be needed if AKI is established.

  • Compartment syndrome may require treatment (referral to surgeons is needed) with decompression fasciotomy.

  • Avoid NSAIDs and use opiate analgesia.

  • Treat the underlying cause.

Further reading

Bagshaw S et al. Acute kidney injury in critical illness. Canadian Journal of Anaesthesia 2010; 57: 985–98.Find this resource:

Clec’h C et al. Multiple-center evaluation of mortality associated with acute kidney injury in critically ill patients: a competing risks analysis. Critical Care 2011; 15: R128.Find this resource:

National Confidential Enquiry into Patient Outcome and Death (NCEPOD). Acute Kidney Injury: adding insult to injury NCEPOD: London, 2009. Renal

Identification and detection of AKI

Investigate by measuring serum creatinine concentration and comparing it with baseline values in any adult with acute illness if any of the following are likely or present:

  • chronic kidney disease (adults with an estimated GFR of < 60 mL/min/1.73 m2 are at particular risk)

  • heart failure

  • liver disease

  • diabetes

  • history of AKI

  • oliguria (urine output < 0.5 mL/kg/h)

  • neurological or cognitive impairment, which may mean limited access to fluids due to reliance on a carer

  • hypovolaemia

  • use of drugs with nephrotoxic potential (NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists, and diuretics) within the past week, especially if hypovolaemic

  • use of iodinated contrast agents within the past week

  • symptoms or history of urological obstruction, or conditions that may lead to obstruction

  • sepsis

  • deteriorating NEWS score

  • age 65 years or over.


Perform urine dipstick testing for blood, protein, leucocytes, nitrites, and glucose in all patients as soon as AKI is suspected or detected.

Assess the risk of AKI in adults before surgery. Be aware that increased risk is associated with emergency surgery, especially when the patient has sepsis or hypovolaemia, intraperitoneal dialysis, or chronic kidney injury. When adults are at risk of AKI, ensure that systems are in place to recognize and respond to oliguria.


  • Maintain effective blood pressure—MAP > 65 mmHg or patient specific, give inotropes as required.

  • Maintain effective circulating volume—monitor fluid status, give IV fluids as required; avoid hydroxyethyl starches.

  • Maintain effective cardiac output—monitor cardiac output and end-organ perfusion, give inotropes as required.

  • Caution is needed with nephrotoxic medications—withhold or adjust the dose.

Detection of AKI

Detection of AKI is based on serum creatinine levels and urine output. The latest 2012 classification is from Kidney Disease Improving Global Outcomes (KDIGO),1 which builds on the RIFLE and the AKIN criteria (see Table 9.1).

Table 9.1 AKI classification


Serum creatinine (within 48 h)

Urine output

1 Risk

Increase by ≥ 26 μ‎mol/L or 1.5–1.9 times baseline

< 0.5 mL/kg/h for 6 h

2 Injury

2–2.9 times baseline

< 0.5 mL/kg/h for 12 h

3 Failure

Increase by ≥ 44 μ‎mol/L or 3 times baseline

< 0.3 mL/kg/h for 24 h or anuria for 12 h


1 KDIGO. KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements 2012; 2 (Suppl.): 1–138.Find this resource:

Further reading

National Institute for Health and Care Excellence (NICE). Acute Kidney Injury: prevention, detection and management of acute kidney injury up to the point of renal replacement therapy. CG169. NICE: London, 2013. Renal this resource:

Management of AKI

Airway and breathing

  • Monitor respiratory rate and pattern (Kussmaul breathing is a pattern of rapid deep respirations that may develop secondary to acidosis).

  • Monitor arterial blood gases.

  • Respiratory failure, necessitating endotracheal intubation and ventilation, may develop secondary to:

    • deterioration in conscious level (secondary to uraemia)

    • pulmonary oedema (secondary to fluid overload).


  • Continuous monitoring, including ECG, CVP, and also cardiac output if necessary.

  • Maintain adequate circulating volume, blood pressure, and cardiac output.

  • Treat arrhythmias (secondary to hyperkalaemia).

  • Monitor K+ levels—treat hyperkalaemia promptly with 10 mL of 10% calcium gluconate to stabilize the myocardium, followed by 50 mL of 50% glucose containing 10 units of soluble insulin infused over 30 min and if necessary oral calcium resonium.

Fluid balance

  • Monitor fluid input and output hourly. Avoid fluid overload.

  • Suspect catheter blockage if sudden oligoanuria develops, and exclude by bladder irrigation and/or replacement of catheter. In patients with nephrostomies, stents, or urostomies, rule out the possibility of obstruction. In patients post-surgery or trauma, consider the possibility of blood clots causing obstruction, an anastomotic leak, or ureteric rupture.

  • If obstruction has been excluded and the patient remains oliguric, optimize the circulating volume by giving a fluid challenge.

  • Consider loop diuretics (e.g. furosemide) only to manage fluid overload or oedema, not just diuresis.

  • If the circulating fluid volume has been optimized and the patient remains oliguric, fluid intake should be restricted to replace urine output and insensible losses only, and renal replacement therapy should be considered.


The patient with AKI is often catabolic, and nutrition should be commenced as soon as possible. Enteral nutrition is preferable to parenteral, as it has fewer complications (e.g. line-related sepsis) and maintains gut integrity. Special consideration should be given to the following:

  • use of higher-concentration feeds if fluid restriction is required

  • amino acid losses occur with haemofiltration

  • B-group vitamins are water soluble and can be removed during renal replacement therapy

  • electrolytes and trace elements should be administered either routinely or according to blood levels.

Other considerations

  • Drug dosages or timings may need to be adjusted if they are renally excreted (e.g. penicillins, aminoglycosides, digoxin). A pharmacist should be consulted and blood levels measured.

  • If the patient is anuric, remove the urethral catheter to reduce the risk of infection.

Renal replacement therapy: basic principles

Indications for renal replacement therapy

  • Metabolic acidosis: pH < 7.3.

  • Hyperkalaemia: > 6 mmol/L.

  • Fluid overload.

  • Pulmonary oedema.

  • Severe uraemic symptoms: encephalopathy, pericarditis.

  • Elevated urea (> 30 mmol/L) and creatinine (> 300 µmol/L).

  • Clearance of nephrotoxins or other toxins.

Aims of renal replacement therapy

Discuss any potential indications for renal replacement therapy with the nephrologist and/or critical care specialist and the patient or carer. Include discussion and agreement on the escalation and ceiling of treatment, and the benefits and risks of commencing treatment.

The filter pore sizes are around 30 000 daltons. Molecules of low molecular weight (> 500 daltons) will pass freely through the filter, intermediate- molecular-weight molecules will move by diffusion or convection, and high-molecular-weight molecules will be retained. This will determine which if any molecules will require replacement or addition to the replacement fluid or dialysate (see Table 9.2).

Table 9.2 Molecular weight and solute removal guide


Molecular weight in daltons









Uric acid




Vitamin B12



17 000


68 000


150 000

Medications removed by renal replacement therapy

Drugs that are removed are those unbound to protein and those with a low molecular weight. They include:

  • lithium

  • methanol

  • ethylene glycol

  • salicylates

  • barbiturates

  • metformin

  • aminoglycosides, metronidazole, carbapenems, cephalosporins, and most penicillins.

Medications not removed by renal replacement therapy

These include:

  • digoxin

  • tricyclics

  • phenytoin

  • gliclazide

  • beta blockers (except atenolol)

  • benzodiazepines

  • macrolide and quinilone antibiotics

  • warfarin.

Types of renal replacement therapy

  • Continuous venovenous haemofiltration (CVVH).

  • Continuous venovenous haemodialysis (CVVHD).

  • Continuous venovenous haemodiafiltration (CVVHDF).

  • Intermittent haemodialysis (IHD).

  • Slow continuous ultrafiltration (SCUF).

A double-lumen cannula is inserted into a large vein (e.g. internal jugular, femoral, or subclavian vein). Blood is drawn from the patient through one lumen, while blood is simultaneously returned through the other lumen. This lumen enters the vein more proximally to prevent recirculation (see Figure 9.1). The therapy is continuous over a 24-h period to allow for gentle removal of fluid and solutes without causing dramatic fluid shifts or cardiovascular instability.

Figure 9.1 Vascular catheter for renal replacement therapy.

Figure 9.1 Vascular catheter for renal replacement therapy.

(Reproduced from Adam SK and Osborne S, Critical Care Nursing: science and practice, Second Edition, 2005, with permission from Oxford University Press.)

Physiological principles


  • This is movement of solutes across a semi-permeable membrane from a high solute concentration to a low solute concentration (i.e. movement down a concentration gradient).

  • Diffusion occurs when blood flows on one side of the filter membrane, and there is counter-current flow of dialysate solution on the other side.

  • It is a passive transport mechanism, so is less predictable than convection in terms of solute clearance.

  • Diffusion is affected by the resistance of the membrane, which is related to its thickness and the size and shape of the pores.

  • Diffusion is utilized in haemodialysis and haemodiafiltration.


  • This is the movement of fluid across a semi-permeable membrane under hydrostatic pressure.

  • The hydrostatic pressure is generated to push water and small molecules across the semi-permeable membrane.

  • Fluid removal occurs mainly by ultrafiltration, and minimal solute clearance occurs by convection during ultrafiltration.

  • Ultrafiltration is utilized in haemofiltration and slow continuous ultrafiltration.


  • This is the movement of fluid across a semi-permeable membrane by creating a solute drag.

  • The pressure difference between the blood and the ultrafiltrate filters water, causing solvent drag as molecules move across the membrane with the water.

  • It is an active transport mechanism, so solute clearance is predictable for a given amount of therapy and dependent on the substitution fluid flow rate.

  • Solute clearance is affected by the amount of ultrafiltration, the solute concentration of plasma, and the size and shape of pores in the membrane.

  • Convection is utilized in haemofiltration and haemodiafiltration.

Buffers (replacement fluid)

  • To treat metabolic acidosis a buffer must be provided in either the dialysate fluid or the replacement fluid for haemofiltration.

  • Lactate is commonly used as the buffer for haemofiltration, and is metabolized to bicarbonate in the liver. Excess lactate can cause a metabolic alkalosis, so a replacement fluid with a lower lactate content should be used. Conversely, in liver failure the lactate will not be metabolized, so serum lactate levels will increase.

  • Bicarbonate itself can be used as a buffer for renal replacement therapy, but cannot be given with calcium because of the risk of chalk formation.


Replacement fluid is added to blood before passing through the filter.


  • It dilutes the blood, preventing an increase in haematocrit.

  • It reduces the clotting risk.

  • It increases filter-membrane efficiency.


  • It decreases the concentration of solutes removed.

  • It decreases the clearance rate.


Replacement fluid is added to blood after passing through the filter.


  • It increases the concentration of solutes removed.

  • It increases the clearance rate.


  • It increases the haematocrit.

  • It increases the clotting risk.

  • It decreases filter-membrane efficiency.

Mixed dilution (i.e. pre- and post-dilution) may also be an option to consider. A one-third pre-dilution and two-thirds post-dilution split may be used both to achieve effective clearance and to extend the filter life.

Types of renal replacement therapy

Continuous venovenous haemofiltration (CVVH)

Filtrate is removed from the blood by convection using a replacement fluid, which is replaced either pre-dilution or post-dilution (i.e. before or after the blood passes through the filter). The blood on one side of the membrane exerts a hydrostatic pressure, causing solute molecules small enough to pass through the membrane to be dragged across with the water by the process of convection. The filtered fluid (ultrafiltrate) is discarded and the replacement fluid is added.

  • Goal: solute removal and fluid management.

  • Indications: uraemia, electrolyte imbalance, acid–base disturbance, removal of small and medium-sized molecules, low-molecular-weight proteins, and water.

  • Physiological principles: ultrafiltration and convection.

Continuous venovenous haemodiafiltration (CVVHDF)

Filtrate is removed from the blood by diffusion using a dialysate solution running through the filter in a counter-current direction to the blood on the opposite side of the membrane, in order to maintain concentration gradients. Filtration still occurs because a pressure gradient exists, but diffusion can be utilized to facilitate the removal of solutes without the need to remove such large volumes of fluid. Therefore some fluid and solutes are removed by convection and then replaced post dilution. Fluid is also passed through the filter to create a concentration gradient for diffusion of solutes. When removal of water is required, the pressure on the blood side of the membrane has to be increased, forcing water molecules to pass into the dialysate.

  • Goal: solute removal and fluid management.

  • Indications: uraemia, electrolyte imbalance, acid–base disturbance, and removal of small molecules.

  • Physiological principles: diffusion, ultrafiltration, and convection.

CVVHDF has the benefits of both techniques, but to a lesser extent than when either technique is used on its own.

General principles for renal replacement therapy

  • Fluid balance recordings must be documented carefully to avoid confusion and prevent accidental hypo- or hypervolaemia.

  • Blood flow through the circuit should be in the range 100–200 mL/min in order to reduce the clotting risk without damaging the filter with extreme pressures.

  • Continuous anticoagulation of the circuit is usually necessary unless the patient is significantly auto-anticoagulated.

  • Filters are usually hollow-fibre membranes made from biocompatible products (e.g. polyacrylonitrile).

  • Vascular access should be in view or inspected regularly (particularly after a position change or patient movement).

  • Adherence to infection prevention and control is essential, and aseptic non-touch technique must be used when accessing the vascular access device.

  • Circuit tubing should be supported or clamped in position and checked for kinking, undue tension, or inadvertent disconnection.

Example of a prescription for renal replacement therapy

A typical prescription for a 75 kg patient requiring renal replacement therapy for AKI would be as follows:


  • Unfractionated heparin—5000 IU bolus followed by a pre-filter infusion at 500 IU/h.

  • Aim to anticoagulate the filter, but ensure that the activated partial thromboplastin time ratio (APTTR) is < 2.

Fluid balance over 24 h

  • Aim for an even balance if the patient is euvolaemic.

  • Aim for the appropriate negative balance if the patient is fluid overloaded (e.g. < 1500 mL/24 h).

Type of replacement fluid/dialysate

  • Use solutions without potassium if serum potassium levels are high, but switch to potassium-containing solutions as serum potassium concentration normalizes.

  • Use a bicarbonate-based buffer rather than a lactate-based buffer if there are concerns about lactate metabolism, or if serum lactate concentration is > 8 mmol/L.

  • Note: An intravenous bicarbonate infusion may be required if a lactate-based buffer is used.

Exchange rate/treatment dose

  • This should be 1500 mL/h (75 kg × 20 mL/kg/h). The treatment dose is usually prescribed as an hourly exchange rate, which is the desired hourly flow rate adjusted for the patient’s weight. In CVVH, the exchange rate represents the ultrafiltration rate, whereas in CVVHDF it represents a combination of the ultrafiltration rate and the dialysate flow rate. In CVVHDF, the ratio of ultrafiltration to dialysate flow is often set at 1:1, but it can be altered to favour either the dialysis component or the filtration component.

Nursing interventions


  • Haemodynamic monitoring should be continuous in order to detect hypovolaemia, hypotension, and arrhythmias.

  • Monitor plasma potassium levels at least 4-hourly.

  • Monitor core temperature and maintain at > 36°C. Heat loss from blood in the extracorporeal circuit and infusion of large volumes of room-temperature replacement fluid can reduce body temperature.

  • Monitor circuit pressures and blood coagulation laboratory profiles.

Rest and sleep

Ensure that the patient is allowed adequate rest and sleep. Position the circuit tubing so as to prevent kinking and obstruction of blood flow, and thus avoid setting off machine alarms and increasing the risk of filter or circuit clotting.

Psychological care

The sight of large volumes of blood in the extracorporeal circuit can be frightening for the patient and their relatives. To reduce anxiety, discussion about renal replacement therapy as a treatment should be introduced before its commencement. A constant and reassuring nursing presence will also support the patient and their family.


  • The aim is to prevent platelet and coagulation activation in response to contact of blood with a foreign surface (i.e. the filter or circuit).

  • Too little anticoagulation can cause clotting in the filter. This is time-consuming to replace, expensive, and decreases efficiency as well as risking blood loss (a circuit contains 150–200 mL of blood).

  • Too much anticoagulation can cause bleeding from cannula sites or spontaneous bleeds in the brain, bowel, or lung.

  • Heparin is the most commonly used anticoagulant.

  • Usually 5–20 IU/kg/h heparin is infused proximal to the filter.

  • A pre-filtration heparin bolus of 2000–5000 IU may also be given if there are problems with filter clotting.

  • If the patient has an adverse reaction to heparin (e.g. heparin-induced thrombocytopenia) or is at risk of bleeding (e.g. post-surgery), prostacyclin/epoprostenol (PG12) or alprostadil (PGE1) can be given at 2.5–10 ng/kg/min. Observe the patient for hypotension.

  • Alternatively, citrate can be given in order to anticoagulate the circuit and filter without anticoagulating the patient. Citrate is both an anticoagulant and a buffer. It chelates ionized calcium, and the associated regional hypocalcaemia in the filter inhibits the generation of thrombin. The citrate is partially removed by filtration, and the remaining citrate is rapidly metabolized to bicarbonate in the liver, muscle, and renal cortex. Calcium infusion is required.

Anticoagulation tests required during heparin infusion

Activated clotting time (ACT)

ACT is normally maintained at 200–250 s for haemodialysis and 150–220 s for haemofiltration.

Whole blood partial thromboplastin time (WBPTT)

During haemodialysis the WBPTT must be maintained at the baseline value plus 40–80% (approximately 120–140 s), and during haemofiltration at the baseline value plus 50%.

Activated partial thromboplastin time (APTT)

  • APTT should be checked 4–6 h after starting a heparin infusion.

  • Aim for 1.5–2.5 times the control value.

Troubleshooting frequent filter clotting

  • Ensure that the filter has been adequately primed prior to use.

  • Check for kinking or obstruction of the double-lumen cannula.

  • If arterial (outflow) circuit pressures are high, check the vascular access for signs of obstruction.

  • If filter pressures are high, check the filter for signs of clotting, and if necessary reduce the blood flow rate if above 150 mL/min.

  • Consider swapping access on the double-lumen cannula (this will result in recirculation of the blood between 20–40%).

  • Consider changing the cannula if pressures remain high and filter clotting is likely.

  • If repeated filter clotting occurs with full anticoagulation, consider pre-dilution using replacement fluid added prior to the filter to reduce viscosity (this will reduce filter efficiency).

Filtration fraction

This is the measure of filtrate removed as a percentage of blood flow. It indicates the haemoconcentration of the filter (i.e. how long the filter circuit will last). The lower the filtration fraction (FF), the longer the filter will last. To decrease the filtration fraction, increase the blood flow rate (BFR) or decrease the ultrafiltration rate (UFR). The ideal range for the filtration fraction is 20–30%. If the filtration fraction is higher than 30% there is an increased risk of clotting.

Filtration fraction formula:

FF(%)=(UFR × 100)/QPQP=BFR × ( Hct)

For example:

UFR = 1500 mL/h = 25 mL/min.

QP (filter plasma flow rate) = blood flow rate 150 mL/min × 0.6 (1 – 0.40 Hct) = 90 mL/min.

Therefore FF = (25 mL/min × 100)/90 mL/min = 27%.