Recommendations

Urgent

Immediate management is supportive and guided by the cause.

  • In most patients with AKI, the priority is to treat hypovolaemia and correct electrolyte imbalances.[13]

Use a simple care bundle - STOP AKI is a good option although others are available:[62][64]

  • Sepsis - perform an urgent septic screen and implement your local care bundle (e.g., Sepsis Six) within 1 hour if infection is suspected. See our Sepsis in adults topic for more information. 

  • Toxins - identify and stop (or avoid exposure to):[1][13]

    • Nephrotoxic drugs (e.g., non-steroidal anti-inflammatory drugs [NSAIDs], aminoglycoside antibiotics, iodinated contrast agents)[1]

    • Nephrotoxins (a contributor in 20%-30% of cases of AKI).[1]

  • Optimise volume status and blood pressure (BP).

    • If hypovolaemic, give an immediate intravenous bolus of crystalloid (choose a balanced crystalloid unless hyperkalaemia is confirmed or suspected, in which case use normal saline).[62][65]

    • Withhold drugs that may exacerbate AKI, particularly ACE inhibitors or angiotensin-II receptor antagonists.

    • Consider withholding diuretics and other antihypertensive medications.

    • Escalate to critical care for consideration of vasopressors if the patient remains severely hypotensive despite adequate volume resuscitation.

  • Prevent harm

    • Identify and treat reversible causes (e.g., relief of any urinary tract obstruction).

    • Treat life-threatening complications (e.g., hyperkalaemia and acidosis).

    • Review and modify doses of all medications in line with the degree of kidney injury.[13][64]

Refer the following life-threatening complications for emergency renal replacement therapy (RRT):[13][64]

  • Refractory hyperkalaemia (potassium >6.5 mmol/L)

  • Refractory metabolic acidosis (pH <7.15)

  • Refractory volume overload with or without pulmonary oedema

  • End-organ complications of uraemia (e.g., pericarditis, encephalopathy, uraemic bleeding) or other end-organ involvement (e.g., neuropathy, myopathy)

  • Severe AKI and poisoning/drug overdose (e.g., ethylene glycol, lithium).

Key Recommendations

It is crucial to identify the cause and severity of the AKI when formulating your management plan for the patient.[1][62]

In most patients, successful management consists of:[1][62][13][64][65]

  • Supportive therapy with close ongoing monitoring of volume status and electrolytes

  • Prompt identification and management of the underlying cause (e.g., sepsis, nephrotoxic medication, urinary tract obstruction)

  • Early recognition and correction of life-threatening complications (e.g., hyperkalaemia, acidosis, volume overload).

Most patients with AKI do not need referral to nephrology.[62]Do refer if there is:[3][64]

  • Uncertainty about the cause or a poor response to treatment or complications that fail to respond to medical management

  • A specific diagnosis that might need specialist treatment (e.g., vasculitis, glomerulonephritis, myeloma)

  • Stage 3 AKI or AKI in a patient with pre-existing CKD stage 4 or 5

  • A history of kidney transplant.

Management of volume status

Prompt correction of volume depletion or volume overload can often reverse or improve AKI.

Hypovolaemia is common at presentation.

  • Start immediate intravenous fluid resuscitation to improve kidney perfusion but take care to use close monitoring to avoid volume overload.[1][62][13][64]

  • Give a 500 mL intravenous bolus of crystalloid over 15 minutes and then continue with goal-directed fluid therapy.

  • Escalate for senior review if no improvement after two boluses.[62][96]

If the patient is volume overloaded, consider the need for a loop diuretic or RRT - consult the nephrology team.[1][13]

  • Never use loop diuretics in AKI without specialist supervision.

Specific treatment of the underlying cause

No specific treatment has been shown to be effective in pre-kidney AKI that is secondary to hypovolaemia and/or sepsis.[13]

  • A key principle is to correct the haemodynamic status of the patient to improve kidney perfusion.[62][64]

Specific management of intrinsic AKI depends on the aetiology and is led by the nephrology team so early referral is important.[62] For example:

  • Interstitial nephritis - stop causative drugs and manage with a corticosteroid.

  • Acute glomerulonephritis/vasculitis - managed with a cytotoxic or immunomodulating agent.

In obstructive AKI, relief of the obstruction is key.[9][64]

  • Insert a bladder catheter if obstruction is suspected clinically and cannot be quickly ruled out by ultrasound. Input from the urology and/or radiology team will be needed.

  • Refer immediately to urology and/or radiology if the patient has pyonephrosis (ensure an ultrasound within 6 hours), an obstructed single kidney, bilateral upper urinary tract obstruction, or complications secondary to obstruction.[3]

Management of complications

Hyperkalaemia - management depends on the severity but may include:

  • Immediate cardiac protection with intravenous calcium chloride or calcium gluconate - ensure ongoing ECG monitoring

  • Adjunctive therapy to drive potassium intracellularly with intravenous insulin/glucose (beware the risk of hypoglycaemia) and nebulised salbutamol

  • Treatment to remove potassium from the body with a cation-exchange resin (e.g., calcium polystyrene sulfonate)

  • Withholding culprit medications (e.g., ACE inhibitor, angiotensin-II receptor antagonist, potassium-sparing diuretics)

  • RRT is indicated for severe refractory hyperkalaemia.

Acidosis - severe metabolic acidosis may need treatment with intravenous sodium bicarbonate (only under expert supervision due to the risk of volume overload and/or hypernatraemia).

  • RRT is indicated for refractory acidosis.

Pulmonary oedema - often results from overzealous fluid resuscitation in a patient who presented with hypovolaemic AKI. For immediate management:[62][64]

  • Sit the patient upright

  • Give high-flow oxygen and intravenous glyceryl trinitrate

  • Seek senior support

  • A loop diuretic may be used to manage associated volume overload but only with specialist supervision

  • Never allow these holding measures to delay initiation of RRT if indicated.[13]

Full recommendations

Determine the cause and severity of AKI when formulating your management plan for the patient.[1][62]

  • Monitor electrolytes and acid-base balance and correct any abnormalities. Tailor the frequency of monitoring to individual patient risk factors and the severity (stage) of AKI.

In most patients, successful management of AKI consists of:[1][62][13][64][65]

  • Supportive therapy and close ongoing monitoring of volume status and electrolytes.

    • Focus in particular on giving adequate intravenous fluids to ensure rapid correction of hypovolaemia if present (e.g., from haemorrhage, gastrointestinal losses, inadequate fluid intake) - but take care to avoid volume overload.

  • Prompt identification and treatment of any reversible underlying cause, for example:

    • Sepsis - perform an urgent septic screen and implement your local care bundle (e.g., Sepsis Six) within one hour if infection is suspected. See our Sepsis in adults topic for more information. 

    • Discontinuation/avoidance of nephrotoxic medications or any other drugs that might cause indirect harm to kidney function.

    • Relief of any urinary tract obstruction - refer urgently to urology and/or radiology as appropriate.[3]

  • Recognition and management of life-threatening complications (e.g., hyperkalaemia, acidosis, pulmonary oedema, uraemia).

RRT is indicated in patients who have refractory volume overload or other complications that fail to improve with medical management.[1][3][13][64]

In rarer forms of intrinsic AKI, more specific management interventions will be needed.[13]

Practical tip

The UK Royal College of Physicians suggests the use of the STOP AKI acronym as an aide-memoire to recall the immediate steps needed for management of AKI:[62]

  • Sepsis - implement the your local care bundle (e.g., Sepsis Six) within 1 hour if sepsis is suspected or confirmed. Identify and treat the source of infection. 

  • Toxins - stop/avoid nephrotoxins (e.g., NSAIDs, aminoglycoside antibiotics, iodinated contrast agents).[1]

  • Optimise volume status/BP - assess volume status and give intravenous fluids as needed; hold antihypertensive medication and diuretics; consider vasopressors if patient does not respond.[3] 

  • Prevent harm - treat complications; identify and treat the cause of AKI; review all medications and adjust doses appropriately; closely monitor intravenous fluid therapy.

Specialist referral

Most patients with AKI do not need referral to nephrology.[62]

  • Do not refer if there is a clear cause and the AKI is responding to medical management.[3][97][98]

Refer immediately to critical care and/or nephrology if:

  • The patient meets (or is anticipated to meet) the criteria for RRT[3][64]

  • There are severe complications that cannot be managed medically (such as hyperkalaemia, pulmonary oedema, acidosis, or uraemia)[64]

  • The patient remains haemodynamically unstable after appropriate supportive care and/or there are signs of multi-organ failure.[64]

    Check local protocols for referral criteria and pathways. 

Refer for urgent discussion with nephrology (as soon as possible and within 24 hours at the latest) if any one or more of the following is present:[3][64]

  • Uncertainty about the cause of AKI or a poor response to treatment

  • A possible diagnosis that may need specialist treatment (e.g., vasculitis, glomerulonephritis, tubulointerstitial nephritis, myeloma)

  • Complications associated with AKI that are not responding to medical treatment

  • Stage 3 AKI

  • AKI in a patient with pre-existing chronic kidney disease (CKD) stage 4 or 5

  • The patient has a kidney transplant.

Refer to urology and/or radiology if the patient has an upper urological tract obstruction.[3]

  • Refer immediately in any case of pyonephrosis, an obstructed solitary kidney, bilateral upper urinary tract obstruction, or complications of AKI associated with obstruction.

After recovery from an episode of AKI, consider referral to nephrology if:[3]

  • Estimated glomerular filtration rate (eGFR) is ≤30 mL/min/1.73 m2  

  • There is hypertension or proteinuria (1+) on an early morning urine dipstick (particularly in a child or young person). 

There is little evidence available to support routine referral to the nephrology team for every patient with stage 2 AKI.

Evidence is lacking on whether outcomes are improved by routine rapid referral to nephrology (within 12 hours) for all patients with stage 2 or 3 AKI that does not need critical care input.[3]

  • The large number of AKI cases among patients admitted acutely to hospital makes it impractical to refer every patient with suspected or confirmed AKI to nephrology.

  • Initial management for most patients encompasses identification and treatment of sepsis, avoidance of nephrotoxins, fluid replacement, and correction of hypotension. These steps can be commenced by any medical or surgical team.

  • Potential benefits of routine nephrology referral include a faster diagnosis in patients with primary kidney disease, prevention of progressive AKI and the potential need for RRT, avoidance of a delayed transfer to critical care, improved chances of kidney recovery, and a shorter hospital stay.

  • However, there is very little evidence to support routine nephrology referral for all patients with stage 2 or 3 AKI.[3]

    • Very low quality evidence from one large retrospective study suggested that for non-critically ill patients with AKI, early compared with delayed referral to nephrology may reduce in-hospital mortality, the number of patients needing RRT, and length of hospital stay.[99]

An assessment of the patient’s volume status is a crucial part of your initial examination.[1][62][13][64]

  • Prompt correction of volume depletion or volume overload (especially if associated with worsening cardiac output) can reverse or improve AKI.

  • Both hypovolaemia and volume overload are associated with worse outcomes, so careful management of fluid balance is vital.[1]

Pre-kidney AKI (80% of all cases) is most often caused by hypovolaemia and/or hypotension

  • A key principle is to improve the haemodynamic status of the patient and restore kidney perfusion.[62][64]

Look for signs of hypovolaemia. Your assessment should cover:[62][13]

  • Peripheral perfusion (capillary refill time)

  • Pulse rate

  • BP (including a check for postural hypotension) - taking into account the patient’s baseline BP

  • Jugular venous pressure

  • Dry axillae/mucous membranes

  • Skin turgor.

Practical tip

An early fluid challenge can be both diagnostic and therapeutic for pre-kidney AKI.

  • In AKI that is secondary to hypovolaemia, kidney function may improve rapidly in response to administration of intravenous fluids.

Signs of volume overload are less common at presentation; for example:[64]

  • Respiratory rate - tachypnoea suggests fluid overload and/or acidosis

  • Crackles on auscultation of lungs may suggest pulmonary oedema

  • Peripheral oedema.

Ensure at least daily ongoing monitoring of volume status for any patient with established AKI or at risk of AKI, via:[13][64]

  • Review of haemodynamic status, including postural BP

  • Weight monitoring 

  • Fluid input/output chart

    • Routine urinary catheterisation is not appropriate, so weigh up the benefits and risks (in particular, infection and trauma) for the individual patient.[64] Catheterisation is indicated if fluid balance management is crucial in an acutely unwell patient (e.g., hourly monitoring of fluid balance is needed) or if the patient is too ill or frail to use a bottle or commode 

  • Urea and electrolytes.

Management of hypovolaemia

Fluid resuscitation

If the patient is hypovolaemic, start immediate intravenous fluid resuscitation to improve kidney perfusion - but take care to avoid volume overload.[1][62][13][64]

  • Give a 500 mL intravenous bolus of fluid over 15 minutes.

  • Use a wide bore cannula to allow adequate fluid resuscitation.

  • A crystalloid fluid is preferred.[1][62][13][64]

  • A smaller bolus (e.g., 250 mL) may be more appropriate if the patient has a history of cardiac failure.[65]

Use a balanced crystalloid unless hyperkalaemia is suspected or confirmed.[62][65]

  • Balanced crystalloid options include Hartmann’s solution, Ringer’s acetate, or Plasma-Lyte 148® (a solution of sodium chloride, sodium gluconate, sodium acetate trihydrate, potassium chloride, and magnesium chloride hexahydrate).

  • Use normal saline (0.9% sodium chloride) instead if hyperkalaemia is present (potassium >5.5 mmol/L) or suspected (e.g., rhabdomyolysis). This is because balanced crystalloids all contain potassium.

    • Once hyperkalaemia has been treated and resolved, switch to a balanced crystalloid due to the risk of hyperchloraemic metabolic acidosis associated with excessive use of normal saline.[62]

Reassess haemodynamic status after the initial fluid bolus and consider whether further 250 to 500 mL boluses are required.

  • Goal-directed fluid therapy is recommended.[13]

  • Reassess the patient’s response to each fluid challenge through careful clinical examination (ABCDE approach) and monitoring of:[96]

    • BP

    • Pulse rate

    • Jugular venous pressure

    • Capillary refill time

    • Signs of pulmonary oedema

    • Urine output.

  • If no improvement is seen after two fluid challenges, escalate the patient for senior review.[62][96]

    • If the patient has already had ≥2 L of fluid, or is in shock, seek immediate senior help so that critical care involvement for vasopressor support can be considered.[62]

    • In a patient with profound sepsis it can take >24 hours for antibiotics to act and the vascular permeability to reverse and BP to respond to intravenous fluids.

As soon as haemodynamic stability is restored and the patient is euvolaemic, review and adjust the intravenous fluid prescription to match the patient’s ongoing fluid requirements.[62][96]

  • It is vital to recognise when to de-escalate intravenous fluid therapy. Failure to do so can result in volume overload and precipitate pulmonary oedema.

    • There is a particular risk from over-aggressive fluid resuscitation if the patient is oliguric/anuric or has a history of heart failure.[13][96]

Practical tip

Passive leg raising can help predict fluid responsiveness in critically ill patients.[62][13]

  • In the context of acute hypovolaemia, passive leg raising can improve the venous return and the response in BP can be recorded.

  • A rise in BP confirms hypovolaemia and the need for further fluid resuscitation.[62]

  • Passive leg raising is most commonly practised on critical care units.

Practical tip

Always be clear about the purpose of the intravenous fluid therapy you are prescribing.

  • The UK National Institute for Health and Care Excellence (NICE) has categorised these as Resuscitation, Replacement, or Routine maintenance:[100] 

    • Resuscitation fluid therapy is aimed at re-establishing haemodynamic stability by restoring intravascular volume.

    • Replacement fluid therapy provides daily maintenance water and electrolyte requirements and replaces any ongoing abnormal fluid losses.

    • Maintenance fluid therapy must provide daily ongoing water and electrolyte requirements (i.e., sodium 1 mmol/kg, potassium 1 mmol/kg, and water 25-35 mL/kg)

      • Never give maintenance fluids at a rate of >100 mL/hour.

Never prescribe intravenous fluid therapy for more than 24 hours at once due to the risk of causing volume overload.

Blood transfusion will be indicated if hypovolaemia is secondary to significant blood loss.

  • This is generally not given unless more than one unit is anticipated, based on local guidelines and the clinical assessment of the patient.[5]

  • Note that this may worsen hyperkalaemia.

Vasoactive drugs

Vasopressor support is recommended if the patient remains severely hypotensive despite adequate volume resuscitation (e.g., in septic/hypovolaemic shock).[1][62][13][96]

  • Escalate to critical care. Vasopressors should only be used with continuous haemodynamic monitoring in place.

  • A reasonable goal is to maintain mean arterial pressure (MAP) ≥65 mmHg, but this target may need adjusting according to the patient’s baseline BP.[1][13][64]

  • In the setting of vasomotor shock where the patient has persistent hypotension despite optimisation of intravascular volume through aggressive fluid resuscitation, preservation and improvement of kidney perfusion can only be achieved by the use of systemic vasopressors.[1]

Noradrenaline (norepinephrine) is the usual vasopressor of choice, with the addition of vasopressin if needed.

  • There is little good evidence available to guide the choice of vasopressor in patients with AKI and septic shock.[1][13]

  • Do not use low-dose dopamine to treat AKI.[1][3][13]

    • There is no evidence to support its use and it can worsen kidney perfusion in patients with AKI.

Consider the potential need for an inotrope (e.g., dobutamine) to optimise cardiac output if kidney hypoperfusion is caused by impaired cardiac function due to poor left ventricular systolic function.[13]

It is not known which vasopressor agent is most effective for prevention or treatment of AKI and septic shock.

There is insufficient evidence to say that one vasoactive agent is better than another in preventing or treating AKI.[1]

  • Small open-label studies have shown improvement in creatinine clearance after a 6- to 8-hour infusion of noradrenaline.[101]

  • Vasopressin, when compared with noradrenaline in one RCT, was found to increase BP and enhance diuresis, but has not yet been proven to enhance survival or reduce the need for RRT.[102]

    • A post-hoc analysis of the same RCT used the RIFLE criteria for AKI to compare the effects of vasopressin versus noradrenaline.[103] Vasopressin was associated with a trend to a lower rate of progression of the AKI, and a lower rate of use of RRT. 

    • According to the Kidney Disease: Improving Global Outcomes (KDIGO) guideline group, this study suggests that vasopressin may reduce progression to kidney failure and mortality in patients with septic shock who have or are at risk of AKI.[1]

  • Dopamine has no significant clinical benefits in patients with AKI.[13]

    • A large randomised controlled trial (RCT) comparing dopamine with noradrenaline as the initial vasopressor in patients with shock showed no significant differences between groups with regard to kidney function or mortality.[104]

      • However, there were more arrhythmic events among the patients treated with dopamine than among those treated with noradrenaline, and dopamine was associated with an increased rate of death at 28 days among the patients with cardiogenic shock.

    • Both the NICE and KDIGO guidelines include a recommendation not to offer low-dose dopamine to treat AKI.[1][3]

Management of volume overload

Volume overload in a patient with AKI can occur as a result of:

  • Overaggressive fluid resuscitation in a patient who initially presented with hypovolaemic pre-kidney AKI. This is most commonly seen in patients with sepsis.

  • Oliguria in intrinsic or post-kidney AKI.

If the patient is volume overloaded, consider the potential need for a diuretic or RRT. Discuss with the nephrology team.

  • Patients with volume overload need careful monitoring and management to reduce the risk of a poor outcome.

  • Failure to manage volume overload can lead to complications including pulmonary oedema.[62] In critically ill patients, a positive fluid balance (>5% body weight) has been found to be associated with an increase in mortality at up to 1 year follow-up when compared to neutral or negative (<5%) fluid balance.[13]

  • Management of volume overload may include:

    • Sodium restriction

    • Cautious use of a loop diuretic under specialist supervision[1][13]

    • RRT - immediate RRT is indicated for refractory volume overload or volume overload associated with severe complications of AKI.[62][13][64] For more details, see the section further down on Indications for RRT.

Consider a loop diuretic (under specialist supervision) to treat volume overload.[1][13]

  • A loop diuretic such as furosemide may be useful in achieving euvolaemia in a patient with fluid overload (with or without pulmonary oedema).[1] This must be done with caution and under the supervision of the nephrology team.

    • Note that there is no evidence to support the routine use of loop diuretics for management of AKI in the absence of volume overload.[1][3][13]

    • Never use a loop diuretic if the patient is hypovolaemic or hypotensive. The diuretic will exacerbate the haemodynamic instability.

  • Do not allow the use of loop diuretics to delay more definitive management of volume overload.

    • Careful monitoring of response is important (e.g., urine output). Stop the diuretic if there is no response.

    • Proceed without delay to more definitive management with RRT if the response to diuretics is unsuccessful.[64]

Loop diuretics have no routine role in the management of AKI. They should be reserved for specific indications (such as volume overload) and only used under specialist supervision.

There is no evidence for any benefits from the routine use of loop diuretics in patients with AKI - but there is some evidence to suggest harm.

  • The theoretical rationale for the use of loop diuretics to treat AKI is based on their potential to reduce oxygen consumption in the ascending loop of Henle, thereby reducing any ischaemic damage to the kidneys. They may also be used to convert oliguric AKI to non-oliguric AKI.[1][13]

    • However, diuretics can also excessively reduce circulating volume and so cause a pre-kidney insult that could worsen established AKI. Hence an evaluation of the available evidence is vital to determine their appropriate role. 

  • There is no evidence to support the use of loop diuretics in routine treatment of AKI.

    • One RCT found furosemide to be ineffective in treating AKI and epidemiological data suggest the use of loop diuretics may increase mortality in patients with critical illness and AKI.[105][106]

    • Two systematic reviews on the use of furosemide to prevent or treat AKI found no significant effect on in-hospital mortality, risk for requiring RRT, the number of dialysis sessions needed, or even the proportion of patients with persistent oliguria.[107][108]

    • Prophylactic furosemide has been shown to increase the risk of AKI when given to prevent AKI in patients having cardiac surgery.[109] 

  • There is no evidence to support the use of loop diuretics for managing AKI-associated hyperkalaemia.[110]

    • However, in practice their use may be considered (with specialist supervision) as an adjunct to other therapies provided the patient is fluid replete.

Whenever AKI is suspected or confirmed, review all medications and stop/avoid any nephrotoxic drugs and other drugs that may affect kidney function.[13][64][65]

  • Common nephrotoxic drugs include aminoglycoside antibiotics, NSAIDs, and iodinated contrast agents.[1] Consult a pharmacist for a full list of nephrotoxic drugs.

  • ACE inhibitors, angiotensin-II receptor antagonists, and other renin-angiotensin modifying agents can exacerbate AKI by reducing the kidney’s ability to adapt to changes in perfusion pressure.[9]

  • Diuretics or other antihypertensives increase the risk of hypovolaemia/hypotension.

  • If there are overriding reasons why a potentially harmful drug must be continued, seek specialist pharmacist advice to minimise negative effects (e.g., dose adjustment, keep the treatment course as short as possible, monitor blood levels of the drug if feasible).

Review and adjust doses of all other medications in line with the patient’s degree of kidney injury.[13][64]

  • Any medication that is cleared via the kidneys has the potential to accumulate during an episode of AKI. Dose adjustment is therefore important to prevent toxicity and patient harm.

  • Inappropriate drug dosing in patients with AKI is an important cause of adverse drug events.[13]

When restarting drugs after an episode of AKI, ensure:

  • Any medications that were used for the treatment of pre-existing heart failure are re-started as soon as clinically reasonable and re-titrated to achieve the best control of fluid balance and blood pressure[13]

  • All medications are reviewed before discharge and a plan is put in place to reintroduce any medications that have been withheld, at an appropriate time, with re-titration to the optimum dose continued in primary care as appropriate[96]

    • Ensure a process is in place for measurement of serum creatinine and potassium 1 to 2 weeks later. This may need to be part of discharge planning.[13]

Alongside supportive therapy and management of any complications, it is important to identify and treat the specific underlying cause of AKI.

Pre-kidney AKI

No specific pharmacological treatment has been proven to treat AKI that is secondary to hypovolaemia and/or sepsis.[13]

  • Pre-kidney AKI is most often caused by hypovolaemia and/or hypotension.

  • A key principle is to improve the haemodynamic status of the patient and restore kidney perfusion through careful administration of intravenous fluid resuscitation (plus vasopressor therapy if needed).[62][64]

Intrinsic AKI

Specific management of intrinsic AKI depends on the aetiology and is led by the nephrology team.[62]

  • Immunological tests and kidney biopsy are needed to confirm acute glomerulonephritis, ANCA-associated vasculitis, anti–glomerular basement membrane (anti-GBM) antibody disease (Goodpasture syndrome if associated with pulmonary hypertension), and lupus nephritis.

    • Treatment will require corticosteroids, cytotoxic agents, immunomodulating drugs, and/or plasma exchange.

  • Atypical haemolytic uraemic syndrome (HUS) is treated with the monoclonal antibody eculizumab or plasma exchange.[111]

  • Thrombotic thrombocytopenic purpura (TTP) is treated with plasma exchange.[112]

  • Acute allergic interstitial nephritis is treated with a corticosteroid (after excluding infection) and stopping potential causative medications (e.g., proton-pump inhibitors, NSAIDs, antibiotics).[113]

Obstructive AKI

Relief of the obstruction is key in the management of obstructive AKI.[9][64]

  • Insert a bladder catheter in any case of AKI when bladder outlet obstruction is suspected clinically and cannot be quickly ruled out by ultrasound.

    • Refer to urology within 24 hours if obstruction is confirmed on ultrasound.[3][64]

Refer immediately to urology and/or radiology if one of more of the following is present:[3]

  • Pyonephrosis - if pyonephrosis is suspected, ensure the patient has an ultrasound within 6 hours (because of the risk of septic shock)[3]

  • Obstructed single kidney

  • Bilateral upper urinary tract obstruction

  • Complications of AKI secondary to urological obstruction.

Refer to urology and/or radiology for ureteral stenting, urinary diversion, debulking procedures, or other case-specific requirements.[64]

  • Nephrostomy or ureteral stenting must be undertaken as quickly as possible and at the latest within 12 hours of diagnosis.[3]

  • Ureteral stenting may be indicated if there is a ureteral stricture, stone, or extrinsically obstructing mass. 

  • Lithotripsy or surgical removal may be needed if obstruction is caused by stones at the ureteropelvic junction.

  • Exploratory laparotomy may be indicated if a compressing tumour is suspected that may require surgical removal; this may be done following ureteral stenting.

  • Percutaneous nephrostomy (placement of a catheter into the renal pelvis percutaneously for drainage of urine from a distal obstruction) may be undertaken by a urologist, surgeon, or interventional radiologist.

RRT may be needed while the underlying obstruction is being addressed if there is severe acidosis, volume overload, or electrolyte or uraemic complications.

Hyperkalaemia[62]

Hyperkalaemia is a common complication of AKI. It can lead to:

  • Muscle weakness

  • Cardiac arrhythmias (e.g., bradycardia, bundle branch block, ventricular tachycardia, ventricular fibrillation, asystole).

Treatment depends on the severity and presence of muscular and/or cardiac complications. The principles of treatment are:[110]

  • Immediate cardiac protection with intravenous calcium chloride or calcium gluconate

  • Adjunctive therapy to drive potassium intracellularly

    • Intravenous insulin/glucose

    • Nebulised salbutamol

  • Removal of potassium from the body

    • Cation-exchange resin (e.g., calcium polystyrene sulfonate)

  • Correction of exacerbating factors:

    • Manage the AKI

    • Withhold culprit medications (e.g., ACE inhibitor, angiotensin-II receptor antagonist, potassium-sparing diuretics)

    • Restrict dietary intake - avoid potassium-rich foods and fluids[80]

  • Close ongoing monitoring of potassium and glucose.

Refer for RRT if the patient has moderate or severe hyperkalaemia that fails to respond to medical management.[13][64]

Check your local protocols - many hospitals have institutional guidelines for managing hyperkalaemia.

Management of mild hyperkalaemia (potassium 5.5 to 5.9 mmol/L)[62][80]

In mild hyperkalaemia, always look for and treat the underlying cause.

  • Review medications that might be responsible (e.g., ACE inhibitor, angiotensin-II receptor antagonist, potassium-sparing diuretics).

    • Treatment of hyperkalaemia only results in a temporary intracellular shift of potassium so the cause of hyperkalaemia must be identified and corrected.[62]

    • Consult a pharmacist for a full list of medications that can cause hyperkalaemia.

A cation-exchange resin can be considered.[110]

  • This will help remove potassium from the body.[80]

  • Do not use if the patient has obstructive bowel disease.

Management of moderate hyperkalaemia (potassium 6.0 to 6.4 mmol/L)[62][80]

Check for any acute ECG changes:

  • Features of hyperkalaemia include peaked t waves, flattened p waves, broad QRS complexes.

If there are ECG changes consistent with hyperkalaemia, treat in the same way as severe hyperkalaemia (see below).

If there are no acute ECG changes consistent with hyperkalaemia:

  • Give an infusion of insulin/glucose to push potassium intracellularly[62][80]

    • Give over 15 minutes

    • Acts within 10 to 20 minutes

    • Lasts 4 to 6 hours

    • Monitor hourly for hypoglycaemia

  • Consider further adjunctive treatment with nebulised salbutamol if necessary

    • Decide whether this is needed based on the ECG and the rate of rise of serum potassium[80]

    • Use caution if there is a history of ischaemic heart disease and avoid if there is a history of tachyarrhythmias.[62][80]

Always look for and treat the underlying cause.

Management of severe hyperkalaemia (potassium ≥6.5 mmol/L)[62][80]

Check for any acute ECG changes.

If the patient has severe hyperkalaemia or moderate hyperkalaemia with associated ECG changes: [80]

  • Seek expert advice from the nephrology or ICU team to consider whether immediate RRT may be needed

    • RRT is indicated if severe hyperkalaemia (potassium ≥6.5 mmol/L) fails to respond quickly to medical management[13]

  • Monitor the patient in a high-dependency area.[62]

Give immediate intravenous calcium for cardiac protection.[62][80]

  • Give over 5 to 10 minutes, then repeat the ECG and consider a further dose if ECG changes persist.[80]

    • Use a wide bore cannula and avoid extravasation.

    • Ensure cardiac monitoring.

  • Intravenous calcium antagonises the cardiac membrane excitability and so protects the heart against arrhythmias.[110]

    • Effective within 3 minutes and lasts 30 to 60 minutes.

  • Seek senior advice if the ECG fails to normalise after one dose.[62]

Give an immediate infusion of insulin/glucose to push potassium intracellularly:[62][80]

  • Give over 15 minutes

  • Acts within 10 to 20 minutes

  • Lasts 4 to 6 hours

  • Monitor hourly for hypoglycaemia.

Give further adjunctive treatment with nebulised salbutamol.[80]

  • Use caution if there is a history of ischaemic heart disease and avoid if there is a history of tachyarrhythmias.[62]

Always look for and treat the underlying cause.

Routine use of sodium bicarbonate is not recommended.

  • Sodium bicarbonate is often used to treat acute hyperkalaemia in clinical practice although there is little evidence to support its use.[110]

  • It can be considered in the setting of hyperkalaemia with hypovolaemia and acidosis.

    • Use only with expert supervision due to the risk of causing volume overload and/or hypernatraemia.

There is no evidence to support the use of loop diuretics for managing AKI-associated hyperkalaemia.[110]

  • However, in practice their use may sometimes be considered as an adjunct to other therapies, provided the patient is fluid replete (but only with supervision from the nephrology team).

The role of loop diuretics in the management of AKI-associated hyperkalaemia remains controversial.

  • Loop diuretics may be used under specialist supervision for volume management in patients with AKI and there is a theoretical rationale to suggest they could be beneficial in managing hyperkalaemia.[1]

    • Loop diuretics promote potassium excretion in the urine through their action in inhibiting the Na+-K+-2Cl co-transporter on the ascending limb of Henle, thereby reducing uptake of potassium (as well as sodium and chloride).

  • However, the 2014 UK Renal Association guideline on acute hyperkalaemia concluded that there is no evidence to support the use of diuretics in the management of AKI-associated hyperkalaemia.[110]

  • Both the NICE and KDIGO guidelines are clear that loop diuretics should not be used routinely to manage AKI.[1][3] The use of loop diuretics is indicated (under specialist supervision) only if a patient with AKI-associated hyperkalaemia also has volume overload (which is a clear indication for their use).[3]

Acidosis (pH <7.25) [62][64]

Metabolic acidosis is a common metabolic disturbance in AKI.

  • It occurs primarily due to impaired excretion of the normal load of metabolic acid in the setting of a low glomerular filtration rate (GFR).

  • Other factors may also contribute (e.g., increased production of lactic acid in patients with sepsis).

  • Note that there will be relative resistance to vasopressors in the presence of severe metabolic acidosis.

If the patient has severe acidosis, seek expert supervision as intravenous sodium bicarbonate may be needed.[64]

  • Severe metabolic acidosis (pH <7.2) is an indication for intravenous sodium bicarbonate.

  • This should only be given under expert supervision due to the risk of causing volume overload and/or hypernatraemia.

    • Consider referring to ICU.

  • Sodium bicarbonate should only be used if venous bicarbonate is <16 mmol/L with no signs of volume overload.[64]

    • Ionised Ca2+ falls with rapid correction and this can trigger tetany, seizures and cardiac instability. Prior to administration of sodium bicarbonate, correct low ionised Ca2+ via a different intravenous route due to the incompatibility of bicarbonate and calcium solutions.[64]

Refer for RRT if the patient has:[13][64]

  • Refractory acidosis (pH <7.15) that is not responding to initial management

  • Severe acidosis in the setting of volume overload (hence sodium bicarbonate must not be given).

Pulmonary oedema[62][64]

Pulmonary oedema may occur:

  • As a result of overzealous intravenous fluid resuscitation in a patient who presented with hypovolaemic pre-kidney AKI[96]

  • At presentation in some types of AKI, for example:

    • Renal artery stenosis - flash pulmonary oedema

    • Renal tract obstruction - salt and water retention

    • Cardiac failure with AKI.

Mortality is high in acute pulmonary oedema so emergency management is vital.

For immediate management of pulmonary oedema:[62][64]

  • Sit the patient upright

  • Give high-flow oxygen (15 L/minute via a reservoir mask) and, if available, consider continuous positive airway pressure ventilation

  • Give intravenous glyceryl trinitrate - titrate the dose upwards, aiming to maintain systolic BP (SBP) >95mmHg

  • Consider a loop diuretic (under specialist supervision) provided the patient is haemodynamically stable and well filled intravascularly[1][62][13]

    • For more details, see the section on Management of volume overload above

  • Seek senior support.

Refractory pulmonary oedema is an indication for emergency RRT.[13][64]

  • The use of an intravenous nitrate and a loop diuretic such as furosemide can be a useful holding measure but do not delay proceeding to definitive management with kidney support if needed.

Indications for RRT

Renal replacement therapy (RRT) is the cornerstone for treatment of severe AKI with complications that are not responding to medical management.

  • It can be used to manage refractory hyperkalaemia, restore metabolic homeostasis, and correct volume overload.[3]

Refer immediately to the nephrology team for consideration of RRT if a patient with AKI has any one or more of the following indications for emergency kidney support:[13][64]

  • Refractory hyperkalaemia (potassium >6.5 mmol/L)

  • Refractory metabolic acidosis (pH <7.15)

  • Refractory volume overload with or without pulmonary oedema

  • End-organ complications of uraemia (e.g., pericarditis, encephalopathy, uraemic bleeding) or other end-organ involvement (e.g., neuropathy, myopathy)

  • Severe AKI and poisoning/drug overdose (e.g., ethylene glycol, lithium).

The decision to start RRT must be based on the patient’s overall condition and not on any isolated urea, creatinine, or potassium value.[1][3]

  • The potential metabolic and fluid benefits of earlier initiation of RRT must be balanced with the potential harm for the individual patient (e.g., complications related to line insertion, anticoagulation).[13]

  • In the absence of any of the emergency indications for RRT listed above, there is little clear evidence available to guide decisions on whether and when to start RRT, with individual studies reaching conflicting findings and meta-analyses hampered by varied definitions of ‘early’ and ‘late’ initiation.[13]

  • In practice, the decision to start RRT is based on a combination of clinical, physiological, and laboratory parameters used to assess the patient’s fluid, electrolyte, and metabolic status.[1][13]

  • Factors to consider include:[13]

    • The trend as well as the absolute values of biochemical parameters (e.g., potassium, pH, urea)

    • The uraemic solute burden (which is increased in tumour lysis syndrome, rhabdomyolysis, and hypercatabolic states)

    • The need for intravascular space to allow administration of therapeutic interventions such as blood products or nutrition

    • The degree and duration of oliguria

    • Whether or not the underlying kidney insult has resolved

    • Any signs of organ dysfunction (which will affect the patient’s ability to tolerate uraemic complications)

    • The presence of any other electrolyte disturbances that may be corrected by RRT (e.g., hypercalcaemia).

There may be some patients with pre-existing comorbidities for whom RRT will not offer any realistic benefits.[114][13]

  • This needs to be a shared decision between the patient and their family members/carers after discussion with the multidisciplinary team.

Pre-assessment for RRT requires careful consideration and must include:[114]

  • Clinical preparation

  • Discussion with the patient around the types of RRT that are available and the acute process (it must be made clear that RRT is supportive treatment that is doing the work of the kidneys)

  • If it is unclear whether the patient has a reversible form of AKI, discussion about the longer term options and the impact they may have on the patient’s life

  • Psychological assessment and support.

Choice of RRT modality

The nephrology team will select the best modality of RRT after assessment of the patient's overall medical condition and comorbidities.[63]

  • Various options exist for supporting kidney function.

  • There is no evidence that one modality is better than another in terms of outcomes among patients with AKI.[115]

  • If your patient is in a non-renal centre and is too unwell to transfer, the critical care team will lead the decision-making.

The choice of RRT modality depends on several factors, including:[63]

  • Individual patient factors:

    • Haemodynamic stability (and hence the patient’s physiologic reserve to tolerate metabolic shifts and fluctuations in fluid status) is a key determinant of the most appropriate RRT modality[13]

    • Severity of electrolyte and acid base balance disorders

    • Risk of ongoing catabolism with cellular breakdown and acidosis.

    • Any need for rapid poison removal (e.g., lithium or ethylene glycol)

  • Availability of modality and staff skill mix.

The options for RRT include:[115][13]

  • Intermittent haemodialysis (IHD) - usually the preferred option in haemodynamically stable AKI patients, but generally avoided in haemodynamically unstable patients, as it often precipitates hypotensive events.[1]

    • Duration up to 4 hours so the patient can participate in active rehabilitation.

    • Fast removal of toxins (e.g., urea, ethylene glycol). In the case of lithium, rebound can occur after IHD as the drug redistributes from the intracellular to extracellular compartment. 

    • May risk dialysis disequilibrium syndrome through over-rapid solute removal and attendant osmolar shifts.

    • Fast correction of acidosis/hyperkalaemia with risk of rebound following the treatment.

    • Hybrid versions of IHD include:

      • Sustained low-efficiency dialysis (SLED)

      • Extended daily dialysis (EDD)[116]

      • Prolonged intermittent renal replacement therapy (PIRRT).

  • Continuous renal replacement therapy (CRRT) - preferred in haemodynamically unstable patients.[117][118][119]

    • Duration 24 to 72 hours, depending on blood circuit clotting.

    • Slower blood flow.

    • Slower but continual removal of toxins allowing more gradual restoration of metabolic homeostasis and avoidance of rebound (e.g., lithium toxicity). 

    • Slows patient rehabilitation when recovering.

    • There are several different types of CRRT but no evidence to support one form over another in terms of better outcomes:

      • Continuous venovenous haemofiltration (CVVH)[120][121][122]

      • Continuous venovenous haemodialysis (CVVHD)

      • Continuous venovenous haemodiafiltration (CVVHDF).[116][117][118][119]

  • Peritoneal dialysis - rarely used in the developed world except in paediatric patients.

RRT (whether IHD or CRRT) is performed through a large double lumen catheter placed into the central venous system, such as the internal jugular or femoral vein.

CRRT and IHD have similar outcomes in AKI.

Mortality outcomes are similar in critically ill AKI patients treated with CRRT and IHD.

  • Several RCTs have compared CRRT to IHD in AKI patients, including the Hemodiafe study, the SHARF study, the CONVINT study and the OUTCOMEREA study. None has found any survival advantage from one modality over the other.[13]

  • A Cochrane systematic review that analysed 15 RCTs in 1550 AKI patients concluded that outcomes were similar in the CRRT and IHD groups in terms of hospital mortality, ICU mortality, length of hospitalisation, and kidney recovery.[123]

Peritoneal dialysis has generally been thought ineffective in adults with AKI and hypercatabolic states, although some studies now suggest equal effectiveness in appropriate subjects.[124][125]

  • However, one study was stopped early because there was a significant benefit to patients being on CRRT rather than PD.[126]

  • In practice, PD is rarely used in adult patients in high-income countries although it is an option for children with AKI.[13]


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