AKI is easily missed; most patients present asymptomatically, with non-specific symptoms or with symptoms solely related to the precipitating illness (e.g., sepsis).
Perform a septic screen and implement your local care bundle (e.g., Sepsis Six) if infection is suspected.
Stop/avoid exposure to any nephrotoxins (e.g., non-steroidal anti-inflammatory drugs [NSAIDs], aminoglycoside antibiotics) and to any other agents that may reduce kidney function (e.g., ACE inhibitors, angiotensin-II receptor antagonists).
Review and adjust dosing of all other medications in line with the degree of kidney injury.
Definition and staging of AKI
AKI can often be non-oliguric.
A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours
A rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the past 7 days (in practice you can use the lowest value from the past 3 months as the baseline for the patient)
Urine volume <0.5 ml/kg/hour for at least 6 hours.
Stage the AKI according to the KDIGO staging criteria.
A higher stage of AKI is associated with a greater risk of death as well as increased likelihood of needing renal replacement therapy (RRT).
AKI is often asymptomatic so a high index of suspicion is vital for prompt recognition and treatment.
A relevant history is a key part of the assessment. Check for:
Your examination should prioritise volume status and a sepsis screen.
Causes of AKI
Sepsis (e.g., pneumonia, cellulitis)
Fluid loss (e.g., vomiting and diarrhoea, or blood loss)
Reduced fluid intake - a particular problem in frail, elderly patients.
Prolonged pre-kidney AKI that progresses to overt cellular damage is the most common cause.
Nephrotoxins (e.g., iodinated contrast agents, NSAIDs, aminoglycoside antibiotics). See our Primary prevention section for information about preventing AKI.
Rare causes (e.g., vasculitis, glomerulonephritis).
Most common in older men with prostatic hyperplasia
Other causes include kidney stones and tumours.
If positive for both protein and blood (in the absence of a urinary tract infection or catheterisation), consider the possibility of an intrinsic cause (e.g., glomerulonephritis).
Nitrites and leukocytes may indicate infection - send urine culture.
There is no clear cause of AKI
Pyelonephritis or pyonephrosis is suspected (if pyonephrosis is suspected, ensure the patient has an ultrasound within 6 hours because of the risk of septic shock)
Urinary tract obstruction is suspected (the ultrasound should be performed within 24 hours at the latest).
AKI is a medical emergency. Prompt recognition and treatment are vital to improve patient outcomes and preserve long-term kidney function.
Kidney function often does not return to the baseline level after recovery from AKI, especially if the patient has pre-existing CKD.
Age ≥ 65 years
History of any one or more of CKD, heart failure, liver disease, diabetes, dementia
Previous AKI episode
Exposure within the previous week to:
Iodinated contrast agent
Any other nephrotoxin (e.g., NSAID, aminoglycoside antibiotic)
Renin-angiotensin-system modifying agent (e.g., ACE inhibitor/angiotensin-II receptor antagonist)
Symptoms or history of urological obstruction
Suspected or confirmed sepsis
Hypovolaemia (with or without hypotension) - may be related to dehydration or over-diuresis
Hypotension (SBP <90 mmHg or a fall of >40mmHg from baseline BP)
Oliguria (urine output <0.5ml/kg/hour).
Because AKI is so common in acutely ill patients, the UK Royal College of Physicians recommends that a NEWS2 score of 5 or above should prompt a check for AKI (kidney function, fluid balance, and urine output).
But be aware that some patients with AKI may not have an elevated early warning score. This is because urine output is not included in commonly used scores such as NEWS2 - so oliguria (an indicator of possible AKI) will not trigger any increase in the patient’s score.
AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly in acutely ill patients.
Most patients with AKI present asymptomatically, with non-specific symptoms or with symptoms solely related to the precipitating illness (e.g., sepsis).
A 2009 report from the UK’s National Confidential Enquiry into Patient Outcome and Death (NCEPOD) identified an unacceptable delay in post-admission diagnosis of AKI in 43% of patients who died in hospital from the condition.
AKI is diagnosed based on an acute rise in serum creatinine and/or a sustained reduction in urine output.
Acute kidney injury has replaced the term ‘acute renal failure’.
AKI is a sudden reduction in kidney function that makes it difficult to maintain fluid, electrolyte, and acid-base balance.
The condition covers the full spectrum of kidney damage ranging from less severe kidney injury through to kidney failure requiring RRT.
A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours
A rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the past 7 days
Urine volume <0.5 ml/kg/hour for at least 6 hours (at least 8 hours in children/young people).
These criteria were defined in the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) guideline.
One additional criterion for diagnosing AKI applies only to children/young people: a fall in estimated glomerular filtration rate (eGFR) of ≥25% over the past 7 days.
Baseline serum creatinine is best considered clinically as the lowest value over the previous 3 months.
If no recent creatinine value is available, provided the patient does not have progressive CKD, it is reasonable to assume that creatinine levels will have been stable for some time, so that a measurement from 6 months or even 1 year ago can be used as the baseline.
If there is no previous serum creatinine within the previous year, and AKI is suspected, consider repeating the creatinine within 12 hours - and certainly within 24 hours.
You may work in an institution with an automatic alert system for AKI that is based on serum creatinine results.
The algorithm used in the UK NHS alert system for AKI determines baseline serum creatinine as the lowest value in the past 7 days. If there is no creatinine value available from that period, it uses a median value over the previous 12 months.
In England and Wales a system is mandated across both primary and secondary care, whereby an AKI alert is triggered by rises in serum creatinine, based on the KDIGO definition and staging system.
In practice, both the serum creatinine and urine output criteria present diagnostic challenges.
Rises in creatinine are delayed for approximately 24 hours following kidney injury.
A reduction in urine output is an earlier indicator of AKI in some patients but AKI can also present without oliguria.
It is important to differentiate AKI from a progression of CKD at initial presentation.
This can be difficult if there are no recent comparison creatinine values. The clinical context will be important in helping you assess whether a rise in serum creatinine has been acute or occurred over a longer period.
Small kidneys on ultrasound (sometimes scarred) - suggestive of advanced CKD.
If the patient is acutely unwell or hypovolaemic, this points towards AKI.
Remember that pre-existing CKD is a risk factor for AKI.
Repeat blood testing along with reference to historical creatinine values is the key to confirming or ruling out AKI.
Recent use of trimethoprim can lead to a rise in serum creatinine that does not reflect any change in glomerular filtration rate
Serum creatinine falls during pregnancy so a rise in creatinine after recent delivery may be a false positive.
Staging the AKI
The stage of AKI is determined by the extent to which serum creatinine rises or urine output falls.
The 2012 KDIGO AKI definition and staging criteria are internationally recognised. They harmonised the earlier RIFLE (Risk, Injury, Failure, Loss of kidney function, and End stage kidney disease) and AKIN (Acute Kidney Injury Network) definitions.
A higher stage of AKI is associated with a greater risk of death as well as increased likelihood of needing RRT.
Serum creatinine (SCr) criteria*
Urine output criteria
*Baseline SCr is the lowest level in the last 7 days or, if not available, the lowest within the previous 3 months.
Even relatively minor changes in serum creatinine levels are associated with a significant increase in mortality.
In a person with normal kidney function, a rise of creatinine above the normal range reflects a loss of more than 50% of function and a significant loss in kidney reserve.
Mortality rises sharply with increasing stage of AKI.
A comparison of the RIFLE, AKIN, and KDIGO staging systems found they were all good predictors of mortality. Whichever system was used, the key message was that mortality increases with severity as determined by rising serum creatinine.
One study of more than 20,000 patients showed a nearly linear increase in in-hospital mortality with increasing RIFLE stage.
Patients at Risk (R) had triple the mortality rate of patients without AKI.
Patients with Injury (I) had close to twice the mortality of R.
Patients with Failure (F) had 10 times the mortality rate of inpatients without AKI.
The RIFLE and KDIGO criteria map to each other approximately as:
R = KDIGO stage 1
I = KDIGO stage 2
F = KDIGO stage 3
KDIGO diagnostic and staging criteria
The international KDIGO guideline group harmonised the previous definitions and staging criteria for AKI to produce a widely accepted consensus.
Prior to the 2012 KDIGO definitions, there were a large number of different definitions of AKI.
In one study of 50,000 patients that compared the incidence of AKI using the RIFLE, AKIN, and KDIGO criteria, 11.6% of hospitalised patients were diagnosed as having AKI with the KDIGO criteria and 11.0% with the RIFLE criteria, whereas only 4.8% were classified as having AKI under the AKIN criteria.
A comparison of the RIFLE definition with the modified AKIN definition demonstrated that there were subsets of patients defined as having AKI by each definition that were not detected by the other.
The RIFLE criteria failed to detect 9% of cases that were detected by AKIN criteria.
The AKIN criteria missed 26.9% of cases detected by RIFLE.
The advent of agreed AKI definitions has allowed a better understanding of the incidence and outcomes of patients with AKI. This has in turn stimulated the development of new potential therapeutic interventions for AKI.
In practice, AKI is sometimes multi-factorial.
Sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI)
Often due to acute illness in a patient with background risk factors
In such patients, AKI is a strong indicator of a very sick patient who needs urgent recognition and management
Exposure to nephrotoxins (intrinsic AKI).
If AKI is not secondary to either of these, then consider the possibility of obstruction or a less common intrinsic cause.
The most appropriate management plan will depend on both the severity of AKI and the underlying cause.
1. Pre-kidney AKI (80%)
Pre-kidney AKI is caused by reduced kidney perfusion often resulting from sepsis, excessive fluid loss, and/or hypotension associated with acute illness.
By definition this is a functional process whereby there is no cellular damage.
Hypovolaemia/dehydration. For example, due to:
Vomiting and diarrhoea
Insufficient maintenance or replacement fluids to cover losses
Hypotension (SBP <90 mmHg or a drop of >40 mmHg from baseline BP)
May be related to antihypertensive medications.
After major surgery
Ileus (sequestration of fluid)
High output ileostomy.
2. Intrinsic AKI (10%-20%)
Intrinsic AKI occurs when there is cellular damage within the kidneys.
If you suspect an intrinsic cause (e.g., vasculitis), seek early specialist input.
Prolonged pre-kidney AKI leading to acute tubular injury (the most common cause)
Nephrotoxins (e.g., iodinated contrast agents, aminoglycoside antibiotics, NSAIDs) - see our Primary prevention section for information on preventing AKI
Tubulointerstitial nephritis (e.g., triggered by infection or nephrotoxic drugs)
Acute glomerulonephritis (e.g., post-streptococcal glomerulonephritis)
Vasculitis (e.g., anti-neutrophil cytoplasmic antibodies [ANCA]-associated vasculitis)
Microangiopathy (e.g., accelerated hypertension, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura)
3. Post-kidney AKI (5%-10%)
Age ≥65 years (frail older people are at particular increased risk).
History of any one or more of CKD, heart failure, liver disease, diabetes, dementia (or any other neurological/cognitive impairment that may result in limited access to oral fluids).
Suspected or confirmed sepsis.
Hypovolaemia (with or without hypotension).
May be related to haemorrhage or dehydration due to poor fluid intake, over-diuresis, illness (e.g., diarrhoea and vomiting) or insufficient replacement fluids in a hospital inpatient.
Hypotension (SBP <90 mmHg or a fall of >40mmHg from baseline BP).
Exposure within the previous week to iodinated contrast.
Recent surgery (especially cardiac).
History of urinary tract symptoms that might suggest an obstructive cause.
Recent vascular intervention - raises the possibility of cholesterol embolisation (livedo reticularis), contrast-induced AKI. See our Primary prevention section for information about preventing AKI.
NSAID or aminoglycoside antibiotic use (nephrotoxic potential - can cause drug-induced interstitial nephritis).
ACE inhibitor/angiotensin-II receptor antagonist.
Renin-angiotensin system modifying agents reduce the kidney’s ability to adapt to changes in perfusion pressure by lowering efferent glomerular arteriolar tone, making it more difficult for the kidney to maintain glomerular filtration pressure in the event of hypovolaemia/hypotension.
Diuretic or any other antihypertensive - particularly if started (or dose changed) in the last 7 days.
These medications increase the risk of hypovolaemia and/or hypotension.
Aciclovir, methotrexate, triamterene, indinavir, or sulfonamides (can cause tubular obstruction by forming crystals).
Recreational drug use.
Over-the-counter drugs and herbal remedies.
If symptoms do occur they may include:
Postural hypotension secondary to hypovolaemia suggests pre-kidney AKI.
Thirst is another common symptom of hypovolaemia.
Decreased urine output
Oliguria is one of the diagnostic criteria for AKI and is an earlier indicator of impaired kidney function than rising creatinine.
Urine output <0.5 ml/kg/hour for at least 6 consecutive hours (at least 8 hours in children/young people) is diagnostic of AKI.
But be aware that patients with AKI are often not oliguric.
Anuria suggests either an obstructive cause or severe AKI from a pre-kidney or intrinsic cause.
Vomiting may cause pre-kidney AKI or can be a later manifestation of AKI-related uraemia.
Lower urinary tract symptoms (urgency, frequency, nocturia, or hesitancy)
Suggestive of an obstructive cause.
Altered mental status
Usually secondary to a primary kidney insult (e.g., sepsis) but may also result from AKI-related uraemia.
Suspect intrinsic AKI secondary to rhabdomyolysis and tubular toxicity from myoglobin in the setting of acidosis.
Haematuria (visible or non-visible)
May be related to pyelonephritis, kidney stones, papillary necrosis, tumour, or acute glomerulonephritis.
Less commonly, symptoms of volume overload can be seen at presentation:
From pulmonary oedema or AKI-related acidaemia.
Suggests salt/water overload - from an obstructive cause or in patients with nephrotic syndrome secondary to glomerulonephritis.
Fever, rash, and/or joint pain
Suspect small-vessel vasculitis (e.g., granulomatosis with polyangiitis, microscopic polyangiitis), or interstitial nephritis.
Suspect small vessel vasculitis or anti-glomerular basement membrane antibody disease.
Hypercalcaemia, hyperuricaemia, bone pain, and lytic lesions
Suspect multiple myeloma.
Volume status - signs of hypovolaemia are often present (less commonly, signs of volume overload are seen at presentation). Check:
Peripheral perfusion (capillary refill)
Blood pressure (BP) - including a check for postural hypotension
Jugular venous pressure
Dry axillae/mucous membranes
Auscultation of lungs (crackles may suggest pulmonary oedema)
Respiratory rate (tachypnoea suggests fluid overload and/or acidosis).
May be affected by precipitating illness (e.g., sepsis).
Confusion can result from encephalopathy in a patient with AKI-related uraemia.
Asterixis is another possible symptom of uraemia.
Perform a septic screen and implement your local care bundle (e.g., Sepsis Six) if infection is suspected. See our Sepsis topic for more information.
Clinical findings that may support a specific underlying diagnosis include:
Rash - for example, petechiae or purpura (intrinsic AKI, e.g., interstitial nephritis, vasculitis, glomerulonephritis)
Jaundice (hepatorenal syndrome)
Joint swelling/pain (vasculitis)
Hypotension (pre-kidney or intrinsic AKI)
Note that hypotension might be absolute (SBP <90 mmHg) or relative (BP fall of >40 mmHg from the patient’s baseline).
May be secondary to sepsis and vasodilation and/or hypovolaemia, resulting in reduced kidney perfusion and pre-kidney AKI.
Prolonged hypotension can then cause cell damage and acute tubular injury, resulting in intrinsic AKI.
Abdominal bruit (renovascular disease)
Abdominal distension and/or palpable bladder and/or enlarged prostate (obstruction).
Baseline bloods and urine analysis
The key investigations in suspected or confirmed AKI are baseline bloods and urine analysis.
Urea and electrolytes (including creatinine) are essential.
The initial serum creatinine level, followed by ongoing serum creatinine monitoring, forms the basis of diagnosing, staging, and monitoring the progress of any patient with AKI.
An acutely elevated serum creatinine may be the only sign of AKI.
Hyperkalaemia is a common complication of AKI.
Urgent treatment is required if potassium >6.0 mmol/L and/or ECG changes are seen.
For any hospital inpatient with AKI, ensure daily monitoring of urea and electrolytes until the AKI has resolved (i.e., a return to actual or presumed baseline kidney function or the establishment of steady state kidney function).
Request bicarbonate if it is not part of the standard panel.
Alternatively, if previously taken bloods indicate AKI and bicarbonate was not included, request a venous blood gas.
Low bicarbonate suggests acidosis.
Venous blood gases can help with further evaluation of acidosis.
Liver function tests (will aid diagnosis of hepatorenal syndrome)
CRP (a marker of inflammation; will be elevated in vasculitis)
Leukocytosis may suggest infection.
High or low WBC can occur with sepsis.
If platelets are low, request a blood film and lactate dehydrogenase to check for rare disorders such as haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, cryoglobulinaemia.
Blood cultures - if infection is suspected
Serum creatine kinase - if rhabdomyolysis is suspected.
Do not use the urea:creatinine ratio as an indicator of the cause of AKI.
An elevated urea: creatinine ratio can occur in AKI. This is because urea and creatinine are both freely filtered at the glomerulus, but urea is reabsorbed by the tubules whereas creatinine is not.
The urea:creatinine ratio is sometimes suggested as a useful indicator to distinguish pre-kidney AKI from intrinsic or post-kidney causes, with a higher ratio considered to be suggestive of a pre-kidney cause.
However, there is no reliable evidence to support this and there are multiple confounders that affect the ratio, including gastrointestinal bleeding, drug-induced increases (e.g., corticosteroids) and a high-protein diet.
Perform urine dipstick testing for specific gravity, blood, protein, leucocytes, nitrites, and glucose as soon as AKI is suspected or diagnosed.
Use a clean-catch specimen.
Consider the possibility of intrinsic AKI if urinalysis is positive for both blood and protein in the absence of an obvious alternative cause (e.g., urinary tract infection or trauma from urinary catheterisation).
Proteinuria together with haematuria may indicate an active urinary sediment due to glomerular disease.
Patients with glomerular disease typically present with proteinuria and haematuria with hypertension and oedema. An early referral to nephrology is indicated.
However, there remains a wide differential diagnosis for blood and protein on dipstick (e.g., infection, trauma, papillary necrosis).
Careful microscopy of freshly collected, freshly spun urine for the presence of red cell casts can confirm glomerular origin haematuria. But if this is not available, the absence of catheter trauma or urinary tract infection should raise concerns about glomerular disease.
Other causes of an active urinary sediment (dysmorphic red cells and red cell casts) include infection, tumours, calculi, venous thrombosis, and myoglobinuria (rhabdomyolysis).
Send urine culture if clinical features of urinary tract infection are present and/or urinalysis is positive for blood, protein, leukocytes, or nitrites.
Start urine output monitoring (hourly if catheterised, 4-hourly if not).
Routine urinary catheterisation is not appropriate in patients with AKI. Carefully weigh up the benefits against the risks for the individual patient.
Oliguria is one of the diagnostic criteria for confirming AKI, but urine output is difficult to measure accurately without catheterisation
Urinalysis can be performed on a sample obtained following catheterisation (but be aware that any proteinuria/haematuria might have resulted from catheter-related trauma)
Hourly urinary output monitoring aids assessment of the patient’s response to treatment
Catheterisation can be both diagnostic and therapeutic for bladder neck obstruction.
Catheterisation is indicated:
In any case where fluid balance management is crucial
If the patient is too ill to use a bottle or commode
If bladder neck obstruction is suspected and cannot be quickly ruled out by ultrasound.
Consider requesting urine electrolytes to measure fractional excretion of sodium or urea - but beware the potential pitfalls.
In principle, calculation of fractional excretion of sodium (FENa) may be helpful in distinguishing pre-kidney from intrinsic AKI. In practice it is rarely performed and results are often difficult to interpret, particularly if loop diuretics have been used within the last 24 hours.
Fractional excretion of sodium (FENa) of <1% suggests pre-kidney AKI but may also be seen in glomerulonephritis, hepatorenal syndrome, some cases of obstruction, and even acute tubular necrosis (if tubular function remains intact).[ Fractional Excretion of Sodium (SI units) ]
Fractional excretion of urea (FEUr) is more useful if the patient has received loop diuretics - although results are also difficult to interpret so the test is rarely performed in clinical practice.
Urea excretion is not significantly affected by diuretics.
A fractional excretion of urea <35% supports a diagnosis of pre-kidney AKI.
The fractional excretion of urea is calculated as: 100% X (urine urea x plasma creatinine)/(plasma urea x urine creatinine).
Urine sodium concentration
<20 mmol/L (20 mEq/L) suggests pre-kidney AKI with preserved tubule function/sodium retention.
Raised levels are seen in intrinsic AKI where there is tubule damage or in response to diuretics.
Urine osmolality is rarely requested.
Urine osmolality is the number of moles of solute per kg of solvent and it depends on tubule response to anti-diuretic hormone (ADH).
However this should not be interpreted as confirming pre-kidney AKI because intact tubule function (particularly in the early stages) may be seen in various forms of kidney disease (e.g., glomerulonephritis).
Urine osmolality <300 mOsm/kg suggests tubule damage (intrinsic AKI) as urinary concentration is impaired.
Urine microscopy can be useful if there is a finding of blood and protein on urinalysis.
It is not widely used in the UK but is more commonly performed in other countries (e.g., USA, China).
It may reveal:
Granular casts in acute tubular injury
Red cell casts in glomerulonephritis/vasculitis
Oxalate crystals - suggestive of ethylene glycol poisoning.
Urinary eosinophil counts may be of some use in patients with pyuria.
A result above 5% to 7% supports a diagnosis of acute allergic interstitial nephritis but is not diagnostic because of low sensitivity and specificity. The test is dependent on the expertise of the microscopist.
It has a negative predictive value of >90% for patients with AKI and may be useful in excluding the disease process.
Eosinophiluria may be seen with atheroembolic disease as well.
Other initial tests
Request a chest x-ray. It may demonstrate signs of:
Haemorrhage (e.g., ANCA-associated vasculitis, Goodpasture syndrome [pulmonary haemorrhage, rapidly progressive glomerulonephritis, and anti-glomerular basement membrane antibodies])
Request an ECG.
It may demonstrate features consistent with severe hyperkalaemia (peaked T waves, increased PR interval, widened QRS, atrial arrest, deterioration to a sine wave pattern).
Investigations to consider
The presence of dilated renal calyces suggests obstruction and hydronephrosis.
Ultrasound has high sensitivity (90%-98%) but lower specificity (65%-84%) for diagnosing upper tract obstruction, although this may not be the case in the early stages (first 8 hours).
Repeat the ultrasound after 24 hours if:
There is a high index of suspicion for hydronephrosis (as it may take several hours for this to develop due to initial non-compliance of the pelvi-caliceal system)
The patient has oliguric acute tubular necrosis with superimposed obstruction (because urine is needed to dilate the kidneys).
Ultrasound may demonstrate small (sometimes scarred) kidneys consistent with advanced CKD (such changes are unlikely to be seen in less severe CKD).
Be aware that an ultrasound finding consistent with CKD does not exclude the possibility of AKI on a background of CKD.
Consider requesting a CT or MRI if obstruction is suggested on ultrasound (e.g., possible masses or stones).
These are not routinely needed - the decision will depend on the degree of obstruction.
Be cautious with intravenous iodinated contrast CT scans in patients with AKI. MRI is preferred (although note that gadolinium may be needed for MRI enhancement).
Nuclear renal flow scans can sometimes be useful to evaluate for obstruction in cases of mild hydronephrosis, when the diagnosis of mechanical obstruction is uncertain.
The scan is performed before and after a dose of loop diuretic.
Impaired tracer excretion is suggestive of acute tubular necrosis.
Poor blood flow is suggestive of obstructed blood supply.
Normal blood flow and tracer excretion with tracer accumulation in the collecting system is suggestive of obstruction of the urine outflow tract.
Anti-nuclear antibodies (ANA) and anti-DNA antibody (lupus nephritis).
Complement (lupus nephritis, post-infectious glomerulonephritis).
Anti-glomerular basement membrane antibodies (Goodpasture syndrome, anti-glomerular basement membrane syndrome).
Anti-neutrophil cytoplasmic antibodies (ANCA-associated vasculitis).
Serum/urine electrophoresis and urinary Bence Jones protein (myeloma).
Serum electrophoresis will show a paraprotein (monoclonal immunoglobulin).
Urine electrophoresis will detect Bence Jones proteins (free light chains) which are not detected on urinalysis.
Acute hepatitis profile: hepatitis B, C, and D (glomerulonephritis).
HIV test (glomerulonephritis or drug-induced AKI).
Complement mutations (haemolytic uraemic syndrome).
Anti-streptolysin O titres (post-streptococcal glomerulonephritis).
May be performed to diagnose rarer forms of AKI (e.g., interstitial nephritis, glomerulonephritis, or vasculitis).
May be requested to identify the cause of obstructive AKI (e.g., ureteric stenosis, bladder tumour).
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