Acute kidney injury: quick reference for management

Acute management on call

Acute kidney injury, AKI, is a syndrome of rapidly deteriorating renal function. Management is governed not by the creatinine value alone but by the course, urine output, volume status, electrolytes, acid-base status and the underlying cause. KDIGO recommends prompt investigation of reversible causes, continuing staging, and treatment directed at both the cause and the severity [1].

Three questions must be answered immediately:

1. Is there obstruction to urine flow?
2. Is the patient hypovolaemic, adequately filled or fluid overloaded?
3. Is there, or is there approaching, an indication for dialysis?

AKI occurs in about one fifth of adults during a hospital episode in international studies and is linked to substantial mortality, even though incidence and prognosis vary widely between patient groups and care settings [2].

Practical first actions

Do the following in parallel, not sequentially:

1. Check previous creatinine values and establish the time course.
2. Measure the urine output. Perform a bladder scan in oliguria, anuria or unexplained AKI.
3. Assess the circulation and volume status, including signs of both hypovolaemia and venous congestion.
4. Take an urgent panel: creatinine, urea, sodium, potassium, bicarbonate or blood gas, calcium, phosphate, glucose and a full blood count.
5. Take a urine dipstick and, where the cause is unclear or a renal cause is suspected, urine microscopy and urinary albumin or protein.
6. Perform an ECG in hyperkalaemia or where a rapid rise in potassium is suspected.
7. Review all medication, including over-the-counter preparations, herbal remedies, contrast media and recently stopped drugs.
8. Treat sepsis, bleeding, shock, hypoxia and any other underlying cause immediately.
9. Request ultrasound of the kidneys and urinary tract when a postrenal cause cannot confidently be excluded.
10. Contact nephrology early in severe, progressive or diagnostically unclear AKI.

Definition and staging according to KDIGO

Acute kidney injury is present when at least one of the following criteria is met [1]:

• A rise in creatinine of at least 26.5 µmol/L within 48 hours.
• A rise in creatinine to at least 1.5 times baseline, known or presumed to have occurred within 7 days.
• Urine output below 0.5 mL/kg/h for at least 6 hours.

Use whichever criterion gives the higher stage. A patient can thus be stage 3 by urine output despite a less marked rise in creatinine.

Limitations of creatinine and urine output

Creatinine is a late marker of function and may rise only after a substantial fall in glomerular filtration. The value is affected by muscle mass, nutrition, drugs and fluid balance. Fluid administration can dilute the creatinine and mask the deterioration, while dehydration can concentrate it. In older, malnourished, amputee or muscle-wasted patients, an apparently normal creatinine may therefore correspond to markedly impaired renal function [3].

Urine output can change before creatinine but is not a pure marker of filtration. Oliguria may be due to hypovolaemia, shock, obstruction or advanced renal injury. Conversely, significant AKI may be non-oliguric, particularly after nephrotoxins, sepsis or diuretic treatment [4].

An automatically reported eGFR is less reliable when creatinine is changing rapidly, since the calculation assumes a steady state. Dosing and clinical decisions should therefore be based on the whole course, not on a single eGFR.

Step 1: confirm the course and assess severity

Establish the baseline

Look for previous creatinine values in the record, preferably from before the current illness. A creatinine taken after several days of vomiting, sepsis or hypotension is not a reliable baseline.

Ask specifically about:

• Previous chronic kidney disease, albuminuria or haematuria.
• Diabetes, hypertension, heart failure, cirrhosis or vascular disease.
• Recent surgery, hypotension, bleeding, diarrhoea or vomiting.
• Fever, infection, rash, arthralgia, muscle pain or dark urine.
• Urinary symptoms, flank pain, a poor stream or inability to empty the bladder.
• Cancer, monoclonal gammopathy or immunotherapy.
• New drugs started over the past few weeks.

Assess immediately life-threatening complications

Check in particular:

• Potassium and the ECG.
• pH, bicarbonate and lactate.
• Work of breathing, oxygenation and signs of pulmonary oedema.
• Level of consciousness and other possible uraemic symptoms.
• Pericardial pain, a friction rub or a new pericardial effusion.
• Bleeding tendency.
• Suspected dialysable poisoning.

A high creatinine is not in itself an urgent indication for dialysis. A patient with rapidly rising potassium, severe acidosis or pulmonary oedema may by contrast need dialysis before the creatinine has had time to become very high.

Step 2: exclude a postrenal cause

Bladder scan and catheter

Perform a bladder scan early in:

• Oliguria or anuria.
• Suprapubic pain or a palpable bladder.
• Prostate-related symptoms.
• Neurogenic bladder dysfunction.
• Treatment with drugs that can cause retention.
• Unexplained AKI where urinary retention cannot confidently be excluded.

Insert a urinary catheter in retention, when accurate hourly urine measurement is needed, or when a blocked catheter is suspected. Check that an existing catheter is not kinked, blocked or misplaced. A catheter should not be inserted as a matter of routine simply because the patient has mild AKI, since the risk of infection must be weighed against the benefit.

Ultrasound of the kidneys and urinary tract

Request ultrasound when obstruction is possible or the cause is unclear. The examination can show hydronephrosis, bladder distension, kidney size and certain structural abnormalities. Point-of-care ultrasound can in addition help assess cardiac function, pulmonary congestion and venous congestion, but the result is operator dependent and must be integrated with the rest of the clinical picture [5].

Ultrasound does not have to be done immediately in every patient with entirely obvious and rapidly reversible prerenal AKI. The threshold should, however, be low in anuria, pelvic tumour, previous urinary tract surgery, suspected stones, prostatic enlargement, a single kidney or failure to improve.

The absence of hydronephrosis does not always exclude obstruction. Early obstruction, marked dehydration, retroperitoneal fibrosis and certain infiltrative tumours can cause obstruction without clear dilatation. Where clinical suspicion is strong, further radiological and urological investigation is required.

Relieve the obstruction promptly

Distal retention is usually treated with a urinary catheter. Higher obstruction may require a ureteric stent or nephrostomy. Contact a urologist urgently in an infected obstructed kidney, obstruction of a single functioning kidney, bilateral obstruction, anuria or rapidly progressive renal failure.

Post-obstructive polyuria may follow relief of the obstruction. Follow hourly urine output, blood pressure, weight and electrolytes. Do not automatically replace the entire urine volume millilitre for millilitre; individualise fluid administration according to the circulation, thirst, sodium and ongoing losses.

Step 3: prerenal, renal or mixed cause

The classification is useful but simplified. The same patient may simultaneously have hypovolaemia, sepsis-related tubular injury, a drug effect and renal venous congestion.

Volume status is more than hypovolaemia versus fluid overload

Assess:

• Blood pressure, pulse and the postural response.
• Peripheral temperature and capillary refill.
• Raised JVP, oedema, ascites and crackles.
• Daily weight and cumulative fluid balance.
• Ongoing gastrointestinal, renal or other losses.
• Cardiac function and signs of right ventricular failure.
• Lung ultrasound or echocardiography when the clinical assessment is uncertain.

Venous congestion can impair renal function even though the patient has a low or normal blood pressure. An oedematous patient with heart failure or cirrhosis should therefore not automatically be given more fluid for a rising creatinine.

A fluid challenge only where fluid responsiveness is plausible

If the history and examination suggest hypovolaemia, a limited volume of isotonic crystalloid can be given with immediate reassessment of blood pressure, peripheral perfusion, breathing and urine output. Repeated fluid boluses without demonstrated benefit can cause pulmonary oedema, tissue oedema and renal venous congestion.

The fact that creatinine does not fall immediately after fluid does not prove acute tubular injury. Creatinine responds slowly, and the result is influenced by both continuing illness and dilution.

Urine sodium and fractional excretion

Urine sodium, the fractional excretion of sodium and the fractional excretion of urea can lend support but must not by themselves determine the diagnosis or fluid treatment. A low urine sodium can occur in heart failure, cirrhosis, glomerulonephritis, early obstruction and sepsis. A higher value may be caused by diuretics, chronic kidney disease or tubular injury.

A fractional excretion of sodium below 1 percent classically indicates sodium retention, whereas higher values may indicate tubular dysfunction. The diagnostic performance is degraded by diuretics and sepsis among other things. A fractional excretion of urea below about 35 percent has been proposed as indicating prerenal physiology, but this measure too has limited accuracy in the critically ill [6].

Urine dipstick, albuminuria and sediment

The urine dipstick should be part of the early work-up

Assess:

• Blood.
• Protein.
• Leucocytes and nitrite.
• Glucose and ketones.
• Specific gravity where it is clinically relevant.

Quantify significant proteinuria with a urinary albumin to creatinine ratio or protein to creatinine ratio. A large amount of albumin argues more for glomerular injury, whereas certain tubular and monoclonal proteins can produce substantial total proteinuria with relatively little albumin.

The urinary sediment gives aetiological information

The urinary sediment is often more informative than an isolated urinary electrolyte, particularly in sepsis and suspected renal disease [6].

Common causes

Sepsis-related AKI

Sepsis-related AKI is not always a simple consequence of low renal blood flow. Microcirculatory dysfunction, inflammation, endothelial involvement, altered tubular metabolism and venous congestion all contribute. Sepsis accounts for a large proportion of AKI in the critically ill [7].

Treat the infection and the circulatory failure. Take cultures without delaying antibiotics in sepsis. Dose the initial antibiotic treatment so that adequate exposure is achieved, and then adjust according to renal function, the pharmacokinetics of the drug, any concentration measurement and the clinical response.

Acute tubular injury

Acute tubular injury often follows prolonged hypoperfusion, sepsis, major surgery or nephrotoxic exposure. The diagnosis is supported by a typical sediment and by failure to improve despite a corrected circulation and treatment of the underlying cause. The condition is often multifactorial.

There is no specific drug treatment to promote regeneration. Management consists of treating the underlying cause, careful fluid balance, electrolyte monitoring, adjustment of medication and dialysis for complications.

Acute interstitial nephritis

Common triggers are beta-lactam antibiotics, proton pump inhibitors, NSAIDs, sulfonamides, quinolones, allopurinol and certain antiepileptic drugs. The classic triad of fever, rash and eosinophilia occurs in only a minority. The absence of eosinophilia or leucocyturia therefore does not exclude the diagnosis. Urinary eosinophils have insufficient diagnostic accuracy [8].

Stop the suspected drug and contact nephrology. A renal biopsy is often needed when the diagnosis is uncertain or when steroid treatment is being considered.

Immune checkpoint inhibitors can cause tubulointerstitial nephritis and, less often, glomerular disease. AKI has been reported in about 2 to 5 percent of treated patients. Concomitant use of proton pump inhibitors, NSAIDs and certain antibiotics may increase the risk. Contact both the oncologist and nephrology before deciding on continued immunotherapy or immunosuppression [9].

Glomerulonephritis and vasculitis

Suspect glomerulonephritis in:

• AKI with haematuria and albuminuria.
• Red cell casts or dysmorphic red cells.
• A rapid rise in creatinine without another explanation.
• Purpura, arthralgia, haemoptysis, sinusitis, neuropathy or systemic symptoms.
• Severe hypertension and oedema.

According to local practice, take a full blood count, albumin, complement, ANA, ANCA, anti-GBM antibodies, hepatitis serology and relevant infection tests among others. Always discuss the tests with nephrology. Suspected pulmonary haemorrhage together with AKI is an emergency.

Proteinuria and haematuria on the dipstick should not reflexly be equated with glomerulonephritis, since catheter trauma, urinary tract infection and other renal injury can produce the same findings. The combination with albuminuria, the sediment and the clinical picture determines how urgent the situation is.

Thrombotic microangiopathy

Think of thrombotic microangiopathy in AKI together with thrombocytopenia and microangiopathic haemolysis. Take a blood film, LDH, haptoglobin, bilirubin, reticulocytes and coagulation tests. Severe hypertension, neurological symptoms, diarrhoea, pregnancy, transplantation, malignancy and certain drugs provide important clues [10].

Thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome overlap clinically. Suspected TTP requires immediate haematological management and a sample for ADAMTS13 without delaying life-saving treatment. Complement-mediated haemolytic uraemic syndrome requires prompt specialist assessment [11].

Rhabdomyolysis

Suspect rhabdomyolysis with muscle pain, weakness, immobilisation, seizures, heat injury, trauma, poisoning or dark urine. The dipstick reacts to blood, while the sediment contains few or no red cells. Check CK, potassium, phosphate, calcium and acid-base status. A CK above five times the upper reference limit is a common diagnostic criterion, but the risk of AKI is not determined by the CK alone [12].

Treat the underlying cause and give isotonic crystalloid early when the patient is not fluid overloaded. Fluid administration must be guided by the circulation and urine output, particularly in heart failure or established oliguria. The evidence for routine bicarbonate treatment or mannitol in addition to fluid is insufficient [12].

Myeloma and monoclonal light chains

Consider myeloma in unexplained AKI with anaemia, hypercalcaemia, bone pain, a high total protein level or a discrepancy between total proteinuria and albuminuria. Take serum free light chains and serum and urine electrophoresis according to local practice.

Light chain cast nephropathy can cause rapidly progressive AKI requiring dialysis. Prompt rehydration where appropriate, correction of precipitating factors and urgent haematological treatment to reduce light chain production are decisive [13].

Cirrhosis and hepatorenal syndrome

AKI in cirrhosis may be due to hypovolaemia, infection, acute tubular injury, drugs or hepatorenal syndrome. Look actively for infection, including spontaneous bacterial peritonitis. Withhold diuretics and other drugs that worsen the circulatory failure where clinically justified.

Hepatorenal syndrome is a diagnosis of exclusion after treatment of precipitating factors and adequate assessment of volume. Albumin and vasoconstrictor treatment, usually terlipressin or noradrenaline (norepinephrine) depending on the care setting and availability, should be managed together with a gastroenterologist, hepatologist or intensive care. Albumin can cause pulmonary oedema and requires careful monitoring of volume [14].

Medication review

Basic principle

Go through the whole medication list. For every drug, four questions must be answered:

1. Could the drug have contributed to the AKI?
2. Does the drug or its active metabolites accumulate?
3. Is the drug still necessary during the acute illness?
4. When and how should it be restarted?

Write a documented plan. Otherwise a drug stopped during AKI is often permanently forgotten despite a continuing cardiac, vascular or renal indication.

Drugs usually to be withheld or reconsidered

ACE inhibitors and ARBs are not generally nephrotoxic. They can reduce the filtration pressure during hypovolaemia or hypotension but are often prognostically important in heart failure, albuminuric kidney disease and hypertension. Observational data do not show an increased risk of a further AKI in previous users who continued treatment after an episode of AKI compared with those who stopped [15]. Restart once the circulation, potassium and renal function allow.

Drugs requiring dose adjustment or a switch

An eGFR based on a rapidly changing creatinine must not be used uncritically. In severe infection an adequate loading dose may still be needed despite AKI, followed by an individualised dosing interval and concentration measurement.

Contrast media

Necessary contrast-enhanced imaging must not be delayed if it is expected to change acute treatment, for example in suspected aortic catastrophe, pulmonary embolism, severe bleeding or another life-threatening illness.

The term contrast-associated AKI describes AKI that arises after contrast, whether or not the contrast was the cause. The true risk of contrast-induced AKI has historically been overestimated. The risk is greatest in ongoing AKI and severely impaired renal function. International consensus recommends intravenous saline prophylaxis in AKI or an eGFR below 30 mL/min/1.73 m² when the patient is not on maintenance dialysis, provided fluid can be given safely [16]. Swedish radiological practice and local thresholds may differ and should be followed.

Supportive treatment

Fluids and circulation

Use isotonic crystalloids in genuine intravascular volume depletion. Balanced crystalloids reduce hyperchloraemic acidosis and may give a small reduction in AKI compared with sodium chloride in some critically ill patients, but the differences in mortality and need for dialysis are uncertain [17,18]. The choice must be adapted in, for example, traumatic brain injury and marked electrolyte disturbances.

Avoid hydroxyethyl starch where AKI is a risk or is established. Albumin is not routinely the first choice for general volume expansion, but has specific indications in certain cirrhosis-related conditions among others.

In vasodilatory shock, a vasopressor must not be withheld for fear of renal injury once an adequate initial assessment of volume has been made. The aim is a sufficient perfusion pressure without unnecessary fluid overload.

Diuretics

Loop diuretics treat fluid overload but do not repair the kidney. In established AKI, diuretics do not clearly reduce mortality or the need for dialysis and can increase hypotension and arrhythmias [19].

Use diuretics when the aim is to treat pulmonary congestion, oedema or other clinically relevant fluid overload. Absent diuresis despite an adequate dose may be a sign of severe tubular dysfunction, but must not by itself be used as an indication for dialysis.

A standardised furosemide stress test has been studied for risk assessment and can predict progression and the need for dialysis, but it should be performed according to a local protocol and under specialist supervision. It is not a treatment for the renal injury itself [20].

Electrolytes and acid-base status

Follow at least:

• Potassium.
• Sodium.
• Calcium.
• Phosphate.
• Magnesium.
• Bicarbonate or a blood gas.
• Glucose.

The sampling interval is governed by the rate of change and the clinical state. In severe hyperkalaemia the ECG must be monitored and acute treatment started without waiting for a nephrology opinion.

Bicarbonate may be appropriate in selected severe metabolic acidosis, but the sodium and volume load must be taken into account. Dialysis should be considered in refractory acidosis or when medical treatment cannot be given safely.

Nutrition

Avoid starving the patient or restricting protein merely to postpone dialysis. Enteral nutrition is preferred where possible. Protein requirements are affected by catabolism and by whether the patient is receiving renal replacement therapy. A dietitian should be involved in prolonged or severe AKI [1].

Monitoring

• Hourly urine output where it affects management.
• Daily weight.
• Fluid intake and losses.
• Creatinine and electrolytes at least daily in unstable AKI, more often with rapid changes.
• Regular assessment of the lungs and circulation.
• Daily medication review.
• A documented plan for sampling, escalation and specialist contact.

When should nephrology be contacted?

Contact them early in:

• KDIGO stage 3.
• Rapid progression or a rising creatinine despite initial measures.
• Oliguria or anuria.
• Refractory hyperkalaemia, acidosis or fluid overload.
• Suspected glomerulonephritis, vasculitis, interstitial nephritis or thrombotic microangiopathy.
• Suspected myeloma kidney.
• Unexplained AKI where the diagnosis affects specific treatment.
• AKI in a renal transplant.
• Suspected poisoning requiring dialysis.
• A need for renal biopsy.
• Uncertainty about the timing or modality of dialysis.

A renal biopsy can change treatment in unexplained renal AKI once prerenal and postrenal causes have been excluded, particularly with an active urinary sediment, systemic disease, significant proteinuria or suspected interstitial nephritis [21].

Indications for urgent dialysis

The decision is based on the overall clinical picture. There is no single creatinine or urea value that automatically triggers dialysis.

Dialysable poisonings include lithium, methanol and ethylene glycol among others. Salicylate and metformin-associated lactic acidosis may also require dialysis depending on the clinical severity, acid-base status, concentrations and treatment response. Metformin can accumulate in AKI and cause severe high anion gap acidosis with a high mortality [22]. Contact your national or regional poison control centre and nephrology immediately.

Do not start dialysis early simply as a matter of routine

In critically ill patients with severe AKI but without an urgent indication for dialysis, a strategy of earlier initiation has not been shown to give lower mortality than a standard or watchful approach. Early treatment does by contrast increase the risk of hypotension, arrhythmia, hypophosphataemia and catheter-related infection [23].

Do not wait when there is a clear indication or when the patient's physiological reserve is insufficient for continued conservative treatment. Contact nephrology before the complication has become immediately life-threatening.

Red flags and common pitfalls

Red flags

• Anuria or a rapidly falling urine output.
• Hyperkalaemia with ECG changes.
• Pulmonary oedema and a rising oxygen requirement.
• Severe acidosis.
• Haemoptysis together with haematuria and AKI.
• AKI, thrombocytopenia and haemolysis.
• Severe hypertension with neurological symptoms or haemolysis.
• Dark urine and a markedly raised CK.
• AKI with hypercalcaemia, anaemia or suspected monoclonal light chains.
• Fever or sepsis combined with an obstructed urinary tract.
• AKI in a patient with a renal transplant.
• Suspected dialysable poisoning.

Pitfalls

• Waiting for the creatinine to rise. The urine output and the clinical situation can show the deterioration earlier.
• Regarding a normal creatinine as normal renal function. Low muscle mass can conceal markedly impaired filtration.
• Not performing a bladder scan. Retention is easy to treat but easy to miss.
• Excluding obstruction on the basis of a single early normal ultrasound.
• Giving repeated fluid boluses to a patient who is not fluid responsive.
• Interpreting a low urine sodium as proof of hypovolaemia.
• Stopping diuretics in a clearly fluid overloaded patient merely because the creatinine is rising.
• Using diuretics to treat the renal injury itself.
• Forgetting the urine dipstick and sediment.
• Missing interstitial nephritis because there is no rash or eosinophilia.
• Delaying a life-saving contrast study out of exaggerated fear of renal injury.
• Using eGFR uncritically when the creatinine is changing rapidly.
• Reducing the first antibiotic dose so much that sepsis is undertreated.
• Forgetting accumulating sedatives, anticoagulants and diabetes drugs.
• Delaying contact with nephrology until the indication for dialysis is already fulminant.
• Failing to document when withheld drugs should be restarted.

Recovery and follow-up

AKI does not always end when the creatinine starts to fall. Persisting impairment of renal function between 7 and 90 days is termed acute kidney disease and may represent a transition to chronic kidney disease [24,25].

The following should be documented before discharge:

• The probable cause and the highest KDIGO stage.
• Previous and current creatinine.
• Whether dialysis has been needed.
• Current urine output and volume status.
• Which drugs have been withheld.
• A clear plan for restarting them and for checking doses.
• The date for checking creatinine, potassium, blood pressure and a urine sample.
• The need for nephrological follow-up.

KDIGO recommends assessment after three months to establish whether renal function has recovered or whether new or worsened chronic kidney disease is present [1]. Earlier review is needed after severe AKI, incomplete recovery, persisting albuminuria or haematuria, heart failure, cirrhosis, a transplanted kidney or drugs that need to be restarted.

Survivors of AKI are at increased risk of chronic kidney disease, cardiovascular events, further AKI and death. Follow-up should therefore cover renal function, albuminuria, blood pressure, volume status, medication reconciliation and information on what the patient should do in the event of future dehydration or acute illness [26].

References

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