AKI is very common affecting around 20% of inpatients & it is important to recognise promptly and correctly to avoid complications. In this article, we give a quick overview of the assessment and management followed by detailed information on each step.

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Quick Overview

Severity: Graded by the extent of creatinine rise from baseline or the fall in urine output

Causes: May be classified as pre-renal, intrinsic renal or post-renal. Prerenal causes include anything which reduces glomerular perfusion, most commonly systemic hypotension or hypovolaemia but also includes reduced or disrupted renal blood flow. Intrinsic renal causes are insults that directly damage the kidneys, including specific renal diseases, infections and nephrotoxic medications. Post-renal causes are any cause of obstruction of the renal or urological tracts.

History: A careful clinical history will help differentiate between potential causes of AKI and help guide management.

Examination: Should include an end of bed inspection, peripheral perfusion, CRT, skin turgor, pulse, mucous membranes, JVP, chest examination, abdominal examination, catheter, oedema, skin changes/rashes and any further specific examination for suspected causes e.g. sepsis.

Investigations: ALWAYS perform a urine dipstick.

You should also review the observation chart, drug chart, fluid balance status, patient daily weights if applicable, recent blood tests and recent imaging.

Mnemonic for management of AKI:
A – address medications
B – boost blood pressure
C – calculate fluids
D – dipstick urine
E – exclude obstruction

Escalate: If uncertain about the cause of AKI, your patient is not responding to treatment or if the AKI is severe.

Introduction

You are bleeped at 3am in the morning by a concerned nurse, informing you that a patient hasn’t passed urine for the last 7 hours. When you arrive on the ward, the patient is unknown to you and sound asleep and the nurse is busy caring for another patient.

Take a moment to consider what you might include in your assessment of this patient. What should your physical examination include? What are the common causes of this presentation?

A potential and serious cause of low urine output is acute kidney injury. It represents a deterioration in renal function. Even after treatment it can lead to a long term reduction in kidney function for the patient and is a significant cause of in-hospital morbidity and mortality. It is therefore important that it is prevented, where possible, and treated correctly and promptly.

Definition of AKI

It is clinically defined in stages that correlate with both severity and risk of the patient requiring renal replacement therapy.

Stage 1

• Serum creatinine rise of 1.5-1.99 times baseline within 7 days, OR
• Serum creatinine rise of 26micromol or more within 48 hours, OR
• Urine output <0.5ml/k/h for more than 6 hours

Stage 2

• Serum creatinine rise of 2.00-2.99 times baseline within 7 days, OR
• Urine output <0.5ml/kg/hour for more than 12 hours

Stage 3

• Serum creatinine rise of 3.00 or more times baseline within 7 days, OR
• Serum creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days, OR
• Urine output <0.3mL/kg/hour for 24 hours or anuria for 12 hours

The patient should be classified according to the criterion which shows the most severe stage.
This article considers acute kidney injury in adults only – it does not cover paediatric assessment or prescribing.

Causes of AKI

In the majority of cases, AKI occurs due to systemic illness rather than direct renal injury. There are multiple potential causes for AKI and in any individual patient, there may be multiple concurrent renal insults. There is a multitude of potential causes of AKI – the list below will not be exhaustive. It is worth knowing the common causes in-depth and being aware of the types of rarer causes so they can be recognised if they do arise. In all cases, a careful history and examination will be required to narrow down the differential.

Pre-Renal

Pre-renal causes of AKI include anything which might reduce blood flow to the glomerular capillaries. Causes include:

• Systemic causes
  • Volume depletion
    • Renal loss – diureses secondary to medications, diseases e.g. diabetic ketoacidosis
    • Extrarenal loss – haemorrhage, vomiting, diarrhoea, burns, sweating, dehydration, liver cirrhosis, third space fluid losses (e.g. pancreatitis, bowel obstruction, oedema, ascites).
  • Shock (cardiogenic, hypovolaemic, neurogenic, septic, anaphylactic)
  • Drugs with antihypertensive effects
• Causes affecting the renal blood supply
  • Renal artery disease
  • Drugs – particularly NSAIDS and ACE-inhibitors, sympathomimetics
  • Hepatorenal syndrome
  • Cardiorenal syndrome
  • Abdominal compartment syndrome
  • Hypercalcaemia

Intrinsic Renal

Causes where the kidneys are subject to direct damage include:

• Glomerular (causes of acute glomerulonephritis)
• Interstitial (causes of acute tubulointerstitial nephritis)
  • Autoimmune (sarcoidosis, lupus, Sjogren’s disease)
  • Infection
    • Bacterial – Streptococcus, Legionella, Tuberculosis
    • Viral – Epstein-Barr virus, cytomegalovirus, HIV
    • Fungal – candidiasis, histoplasmosis
  • Medication (including penicillins and other antibiotics, diuretics, NSAIDS, antiretrovirals, antivirals, phenytoin, PPIs)
• Tubular (causes of acute tubular necrosis)
  • Ischaemia (any of the pre-renal causes can lead to ischaemia and lead to overlapping pre-renal and intrinsic renal disease)
  • Nephrotoxics
    • Endogenous (pigment nephropathy – haemoglobinuria e.g. haemolysis or myoglobinuria e.g. rhabdomyolysis; myeloma, tubular crystals, tumour lysis syndrome)
    • Exogenous (NSAIDs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aminoglycosides (e.g. gentamicin), radiological contrast, platinum drugs, amphotericin, methotrexate, ethylene glycol)
• Vascular
  • Vasculitis
  • Renal vein thrombosis
  • Renal atheroembolic disease
  • Renal infarction
  • Thrombotic microangiopathies (primary causes include haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura; secondary causes include malignant hypertension, pre-eclampsia, autoimmune such as scleroderma renal crisis)
  • Renal infarction

Post-Renal

Post renal causes of AKI involve obstruction of the renal or urological system preventing usual drainage of urine. It is helpful to think of post-renal causes by categorising them further into 3 categories, based on their anatomical location:

• Intraluminal obstruction (obstruction within the lumen of the renal/urological system)
  • Kidney stones
  • Tumours
  • Clot retention
  • Sloughed papilla (e.g. post acute tubular necrosis, acute pyelonephritis, diabetes, sickle cell anaemia, analgesic nephropathy, amyloid, renal TB)
  • Crystals (acyclovir, indinavir)
• Intramural obstruction (obstruction due to the walls of the renal/urological system)
  • Drugs e.g. anticholinergics
  • Tumours
  • Strictures
  • Reflux
  • Adynamic urethral segments
• Extrinsic compression of the renal/urological system
  • Benign and malignant tumours anywhere along or near the renal or urological system including abdominal, pelvic and genital. These notably include bladder cancer, cervical cancer, prostate cancer, benign prostatic hyperplasia.
  • Gravid uterus
  • Retroperitoneal fibrosis
  • Neurogenic bladder

Clinical Assessment

Start by checking the patient’s observations and an “end of the bed” check. If they are acutely unwell, start with a full A-E assessment, correcting physiological deficits as you undertake it. If the patient is stable, you may wish to start by reviewing the notes or taking a history.

History

Important parts of the history include why the patient is in hospital and the course of their present illness, any acute changes to their condition.

Regarding AKI, consider direct questions to methodically explore prerenal, renal and post-renal causes. Because there is a huge range of possible causes of AKI, the questions you ask are likely to be slightly different depending on the patient in front of you and your clinical suspicion.

Consider as a minimum asking about oral intake, symptoms of thirst, abdominal pain, difficulties passing urine/LUTS, and consider asking about renal colic/symptoms of a pelvic mass. A systems review should include evidence of sources for infection or sepsis. Don’t forget to ask about possible fluid losses such as excessive urination, diarrhoea, vomiting, stoma losses, NG output. Assess medication causes – for a new admission ask about all medications taken at home including illicit, over the counter and herbal remedies, and for an inpatient also consider asking about any recent medications/drugs beyond those on the drug chart. Consider the possibility of rhabdomyolysis in patients who have had a crush injury, prolonged immobility e.g. from a fall or prolonged surgery or other risk factors.

Clinical Examination

The purpose of the clinical examination is to assess the fluid status and potential causes of AKI. A systematic approach would as a minimum include:

• End of bed inspection – does the patient look generally well or unwell, are they connected to any drips/medications, is there an NG in situ, are they receiving additional fluid/electrolytes e.g. via an IV feed.
• Peripheral stigmata -warm/cool peripheries, capillary refill time, skin turgor, pulse (volume, rhythm), mucous membranes, JVP.
• Chest – evidence of pulmonary oedema
• Abdomen – with particular attention to organomegaly, palpable kidneys, ascites, evidence of urinary retention e.g. palpable bladder. If there is a stoma in situ, check the output and type.
• Catheter – is there a catheter in situ? Most recent hourly measurement, colour, presence of debris.
• Presence of peripheral oedema.
• Throughout the examination look for skin changes or rashes.
• In case of specific clinical suspicion e.g. sepsis, the examination should be extended appropriately.
• You should always perform a urine dipstick.

Clinical Measurements

Observation Chart
In a patient who is volume deplete, they are likely to be tachycardic and may also be hypotensive. Be aware however that tachycardia may also result from other factors such as underlying disease process, pain or arrhythmia.

Pyrexia suggests possible infective causes and sepsis may be causing an AKI. If the patient is septic ensure they receive urgent full management for this as well as their AKI.
Orthostatic hypotension can be a helpful measure of volume depletion in an otherwise stable patient – you can detect this by performing a lying/standing blood pressure.

Drug charts
Carefully look through current medications. Don’t neglect one-off doses, fluid prescriptions and as required doses. See the management section below for more information on managing medications in AKI.

Fluid balance status
Calculate 24-hour inputs and output and total fluid balances. Inputs may commonly include oral fluids, IV fluids, IV flushes, IV medications, IV feeds, NG input. Outputs may commonly include urine output, stool, stoma outputs, NG output. Don’t forget that each patient will also have additional unmeasured insensible losses including perspiration, expiration, transdermal diffusion. In a normal adult, the loss is approximately 800mls/day with 400mls a day unmeasured water production from metabolism – so approximately 400mls additional water loss compared with the measurable inputs and outputs. Be aware that insensible losses may increase in unwell patients e.g. if the patient has skin disruption such as from burns, a fever, is in a hot ward, or if the patient has a fast respiration rate. Some patient may also have “third space fluid losses” where the patient loses significant quantities of water into the interstitial space – causes of this include pancreatitis, bowel obstruction causing loss of fluid into the gut, and extravasation in the case of sepsis. These patients, therefore, need a more careful assessment of fluid status and may require more aggressive fluid resuscitation.

Weights
In patients with considerable oedema, such as those with heart failure, daily weights can be an incredibly useful tool when monitoring fluid status. 1l water equivalates to 1kg weight loss, and in day to day measurements this is too short a period for loss of body fat or protein to contribute greatly.

Blood results
If there is not an up to date set of blood results, the patient as a minimum should have urea, electrolytes and creatinine checked. Other useful bloods, depending on the clinical situation may include full blood count, liver function, CRP, blood cultures. Have a low threshold for rechecking renal function as worsening function may show the patient is in AKI or a higher stage of AKI that thought.

AKI may be complicated by hyperkalaemia. Always ensure you have an up to date potassium result, and if the patient is hyperkalaemic, this requires emergency treatment. If the patient is refractory to medical management of their hyperkalaemia, the presence of poor renal function and refractory hyperkalaemia may be an indication for dialysis – seek early senior support and renal involvement if appropriate.

Recent imaging
Check if there is any relevant recent imaging – particularly useful are chest X-rays/CT thorax, for gauging fluid overload/pulmonary oedema; any previous renal ultrasounds or cross-sectional imaging of the abdomen/pelvis for previous evidence of obstruction or potential causes.

Management of AKI

A useful memory aid for AKI management is ABCDE. This represents all the steps that should be considered in every patient with AKI. Ensure that where an underlying cause of the AKI is identified this is urgently managed concurrently with managing the AKI e.g. sepsis and special consideration may be needed for treatment of some of the intrinsic and post-renal causes.

A – address medications
B – boost blood pressure
C – calculate fluids
D – dipstick urine
E – exclude obstruction

A – address medications

Review the patient’s drug charts. Identify medications which are directly nephrotoxic, which may cause hypotension, which may cause hypovolaemia, and which are affected by renal impairment.

Common culprits include, but are not limited to:

• Nephrotoxics: NSAIDs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aminoglycosides (e.g. gentamicin), radiological contrast, platinum drugs, amphotericin.
• Risk of reduced renal perfusion: antihypertensives, antianginals, diuretics, sympathomimetics
• Risk of urinary retention: anticholinergics and drugs with anticholinergic side effects
• Affected by renal impairment: metformin (increased risk of lactic acidosis), digoxin (can increase levels and cause toxicity), lithium (can increase levels and cause toxicity), opiates (decreased renal clearance may cause toxicity)

Consider reducing, holding or stopping medications which risk worsening AKI or causing side effects. Occasionally medications may need to be given at risk of worsening renal function – for example occasionally a scan with contrast may be deemed to be so important for immediate management that the benefit outweighs the risk of worsening renal function. These decisions should be made by a senior clinician, the risks and benefits should be discussed with the patient and family if appropriate, the patient’s conditions should be optimised prior (for example some hospitals have policies on giving fluids prior to nephrotoxic contrast where there is a risk of AKI – check your hospital policy or ask a senior), and they should be carefully monitored before and after. This also holds true of decisions to continue to give regular medications which may be nephrotoxic or toxic in renal failure – the risks and benefits should be carefully explored and the patent should be optimised otherwise to reduce the risk of worsening renal function.

For any medication you are unsure about in AKI or renal failure, check the BNF or seek senior support.

B – Boost blood pressure

If the patient is thought to have a prerenal or renal cause of AKI, careful administration of IV fluids is often the mainstay of treatment. Depending on the patient’s clinical condition and causes they may need fluid resuscitation, replacement or maintenance.

In patients who have clinical evidence or risk factors for fluid overload or oedema, fluid administration may need to be more cautious. If you are unsure discuss with a senior – some of the most difficult decisions to judge clinically can be fluid administration in a patient who is intravascularly fluid deplete but also extravascularly fluid overloaded. In these cases, the risk of AKI is weighed against that of pulmonary oedema, both of which can be fatal. Under the guidance of a senior, you may find these patients be treated anywhere from aggressively being given fluids, cautiously given fluids, or aggressively diuresed depending on the greatest risk to them clinically at that time. In most of these tricky situations, patients will be either given fluids cautiously or kept euvolaemic, often guided by close monitoring of urine output. If you are unsure about why seniors have made certain decisions around this ask them – these can be really helpful learning opportunities.

Think carefully about the types of fluid being given and the electrolytes. Patients with AKI may have electrolyte derangements and care must be taken not to exacerbate these. Be cautious around potassium either added to fluids or as part of the fluid make up (e.g. Hartmann’s) as declining renal function may precipitate hyperkalaemia. Severely dehydrated patients may be hypernatraemic, requiring careful fluid replacement, consider using 5% dextrose. Excessive 0.9% NaCl may itself cause hypernatraemia. Try to avoid rapid shifts in electrolytes, hyper- or hypo- natraemias should be corrected slowly to avoid complications.

In high monitoring areas such as ITU additional tools may be available for boosting blood pressure such as inotropes – this should be led by a senior clinician.

C – Calculate fluids

As discussed in the clinical assessment ensure there is an up to date measurement of fluid inputs and outputs to help guide your diagnosis and management.

It may be helpful to place a urinary catheter to ensure accurate measurement of urine output, especially in more severe AKI, to aid assessment and management decisions. This must be weighed against risks e.g. increased risk of urinary tract infection.

D – Dipstick urine

A urinalysis should always be performed as a simple but helpful assessment tool. It may flag a source of sepsis (UTI, pyelonephritis), haematuria from some obstructive causes of AKI (stones, masses) and underlying inflammatory processes causing nephrotic or nephritic syndrome. It will also indicate glucosuria in patients with uncontrolled diabetes who are at risk of high fluid losses passing urine. Note that a urine dipstick from a catheter sample is not reliable for detection of UTI, as normal bacterial colonisation of the catheter may give a false-positive result.

E – Exclude obstruction

All patients with a likely obstructive cause of AKI and any patients for whom a cause of AKI has not been identified should have an urgent renal ultrasound within 24 hours. If there is suspicion of pyelonephritis with hydronephrosis (pyonephrosis) the ultrasound should occur within 6 hours as the patient may need emergency urological intervention.

If the patient is thought to have a pre-renal or renal cause of AKI but doesn’t respond to appropriate supportive treatment then have a very low threshold for a renal ultrasound.

Escalation

Patients with AKI have increased morbidity and mortality even after recovery. If you feel uncertain when assessing/managing the patient or are worried the patient is not responding to management as you would expect, it is important you seek a senior opinion to ensure the patient is being managed optimally. Begin by escalating within your team, if they feel more specialist help is required they may request advice from or referral to general medicine or the renal team. Out of hours the same advice broadly applies regarding the on-call teams for those specialties.

The patient should be urgently discussed with your seniors and the renal team in the presence of Stage 4 or 5 CKD, if the patient may require renal involvement for specific underlying conditions e.g. vasculitis, glomerulonephritis, myeloma, if they have a renal transplant, if there are complications requiring urgent management or that may require renal replacement therapy if refractory to medical management e.g. acidosis, hyperkalaemia, pulmonary oedema, severe uraemia (particularly if causing pericarditis or encephalopathy).

Follow-up

Patients with AKI should be followed up routinely with the aim of monitoring renal function and preventing further episodes of AKI:

• Monitor serum creatinine – choose an appropriate frequency during admission and for post-discharge based on the degree of renal dysfunction and stability of creatinine measurements
• Consider referral to the renal team if the eGFR is 30ml/min/1.73m2 or less.
• Refer the patient to the renal team if they have a background of chronic kidney disease and develop AKI, even if the renal function returns to baseline
• After an episode of AKI consider risks and benefits of medications and use this to guide whether they should be restarted, dose changed, or stopped.
• It should be clearly documented in the patient’s medical notes and discharge letter that they have suffered AKI.
• The patient should be informed that they have had AKI and offered written information about what this means for them.

Some common pitfalls

Be aware that there may be a delay in creatinine rise in a patient with worsening renal function– urine output responds more quickly to acute kidney injury. GFR is not a tool for measuring acute kidney injury – it is derived from an equation that has only been validated for chronic kidney disease, so do not rely on it in the acute setting.

Not all the reasons for a patient not passing urine are pathological. If the patient doesn’t have a catheter in, they are likely to go for longer periods without passing urine, but should still be urinating regularly during the day. Patients with a catheter in should be passing continuous urine, which will be regularly measured by the nursing staff. More unwell patients may need more frequent measurements.

If the patient has a catheter in, always consider having the catheter flushed before assuming the patient is not passing urine, especially if they don’t have another clear cause – blocking of the catheter with debris or blood clots can be an easily fixed, but also easily missed, cause of reduced urine. You can ask the nursing staff to do this whilst you are en route to the ward to aid in your assessment (and occasionally fix the problem before you arrive!) Also check the patient hasn’t been bypassing the catheter (urine leaking from around it).

Written by Dr Briony Adams FY3