Acute Kidney Injury

Question 1

What is acute kidney injury (AKI)?

Answer 1

Akidney injury (AKI) is a term covering a spectrum of injury to the kidneys which can result from a number of causes. It is a clinical syndrome rather than a biochemical diagnosis.

Question 2

Differentiate between pre-renal, renal and post-renal causes of AKI

Answer 2

Pre-renal (most common): due to reduced perfusion of the kidneys and leading to a decreased glomerular filtration rate (GFR). It is usually reversible with appropriate early treatment

Intrinsic renal: a consequence of structural damage to the kidney, for example, tubules, glomeruli, interstitium, and intrarenal blood vessels. It may result from persistent pre-renal or post-renal causes damaging renal cells.

Post-renal (least common, accounting for around 10% of acute kidney injury): due to acute obstruction of the flow of urine resulting in increased intratubular pressure and decreased GFR.

Question 3

Give examples of pre-renal causes of AKI

Answer 3

Hypovolaemia (e.g. inability to maintain hydration without help from others, haemorrhage, gastrointestinal losses, renal losses, burns).

Reduced cardiac output (e.g. cardiac failure, liver failure, sepsis, drugs).

Drugs that reduce blood pressure, circulating volume or renal blood flow (e.g. ACE inhibitors, ARBs, NSAIDs, loop diuretics).

Question 4

Give examples of renal causes of AKI

Answer 4

Toxins and drugs (for example antibiotics, contrast, chemotherapy).

Vascular (e.g. vasculitis, thrombosis, athero/thromboembolism, dissection).

Glomerular (e.g. glomerulonephritis).

Tubular (e.g. acute tubular necrosis, rhabdomyolysis, myeloma).

Interstitial (e.g. interstitial nephritis, lymphoma infiltration).

Question 5

Give examples of post-renal causes of AKI

Answer 5

Obstruction (e.g. renal stones, blocked catheter, enlarged prostate, genitourinary tract tumours/masses, neurogenic bladder).

Question 6

What are the risk factors for AKI?

Answer 6

• People aged 65 years or over
• A history of acute kidney injury
• Chronic kidney disease
• Symptoms or history of urological obstruction or conditions which may lead to obstruction
• Chronic conditions such as heart failure, liver disease and diabetes mellitus
• Use of a contrast medium such as during CT scans
• Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer)
• Sepsis
• Hypovolaemia
• Oliguria
• Nephrotoxic drug use within the last week

Question 7

Give examples of nephrotoxic drugs

Answer 7

• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin II receptor antagonists (ARBs)
• Diuretics

Question 8

What are the signs of AKI?

Answer 8

• Hypotension
• Volume overload (e.g. crackles, tachypnoea)
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Question 9

What are the symptoms of AKI?

Answer 9

• Nausea and vomiting, or diarrhoea, evidence of dehydration
• Reduced urine output or changes to urine colour
• Confusion, fatigue and drowsiness

Question 10

What investigations should be ordered for AKI?

Answer 10

• Basic metabolic panel (including urea and creatinine)
• Serum potassium
• FBC
• CRP
• Blood culture
• Urinanlysis
• Urine culture
• Urine output monitoring
• CXR
• ECG

Question 11

According to NICE, what criteria must be met to diagnose AKI?

Answer 11

• Rise in creatinine of ≥ 25 micromol/L in 48 hours
• Rise in creatinine of ≥ 50% in 7 days
• Urine output of < 0.5ml/kg/hour for > 6 hours

Question 13

Why investigate urea and creatinine?

Answer 13

AKI is diagnosed based on an acute rise in serum creatinine and/or a sustained reduction in urine output.

1. A rise in serum creatinine of 26 micromol/L or greater within 48 hours
2. A 50% or greater rise in serum creatinine (more than 1.5 times baseline) known or presumed to have occurred within the past 7 days
3. A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours (if it is possible to measure this, for example, if the person has a catheter)

Question 14

Why investigate serum potassium?

Answer 14

Ensure close monitoring of serum potassium.

Hyperkalaemia is a common complication of AKI.

Question 15

Why investigate FBC?

Answer 15

May show anaemia, leukocytosis and/ or thrombocytopenia.

Question 16

Why investigate CRP?

Answer 16

Request in all patients.

Elevated in infection and also in vasculitis.

Question 17

Why investigate using blood culture?

Answer 17

Request if infection is suspected.

Sepsis is a common cause of AKI.

Question 18

Why investigate using urinanalysis?

Answer 18

Perform urine dipstick testing for specific gravity, blood, protein, leucocytes, nitrites and glucose as soon as AKI is suspected or diagnosed.

Question 19

Why investigate urine culture?

Answer 19

Send urine culture if clinical features of urinary tract infection are present and/or urinalysis is positive for blood, protein, leukocytes, or nitrites.

May show bacterial growth with antibiotic sensitivity.

Question 20

Why investigate via measuring urine output?

Answer 20

Start urine output monitoring in any patient diagnosed with AKI (hourly if catheterised, 4-hourly if not).

Confirm a diagnosis of AKI if urine output <0.5 ml/kg/hour for at least 6 consecutive hours (at least 8 hours in children/young people).

Question 21

Why investigate using CXR?

Answer 21

Request a chest x-ray. It may demonstrate signs of:

• Infection
• Pulmonary oedema
• Haemorrhage (e.g., ANCA-associated vasculitis, Goodpasture syndrome [pulmonary haemorrhage, rapidly progressive glomerulonephritis, and anti-glomerular basement membrane antibodies])
• Cardiomegaly

Question 22

Why investigate using ECG?

Answer 22

An ECG is important to assess for hyperkalaemia.

Hyperkalaemia is a common complication of AKI.

Question 23

What changes can be seen on an ECG with hyperkalaemia?

Answer 23

ECG changes associated with hyperkalaemia:

• Peaked T waves
• Increased PR interval
• Widened QRS
• Atrial arrest
• Deterioration to a sine wave pattern

Question 24

When should renal ultrasound be used to diagnose AKI?

Answer 24

If pyonephrosis (an infected/obstructed renal tract) is suspected, ensure the patient has an ultrasound - and if indicated a nephrostomy - within 6 hours due to the risk of septic shock.

Renal tract ultrasound is not routinely required. Only request it if no obvious cause for the AKI can be found or if obstruction, pyelonephritis, or pyonephrosis is suspected.

Question 25

Briefly describe the treatment for AKI

Answer 25

In most patients, successful management consists of:

• 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)

Question 26

How is volume status managed in AKI?

Note: hypovolaemia

Answer 26

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.[62][64]
Prompt correction of volume depletion can reverse or improve AKI.

If the patient is hypovolaemic, start immediate intravenous fluid resuscitation to improve kidney perfusion - but take care to avoid volume overload.

• Give a 500 mL bolus of intravenous fluid over 15 minutes.
• Use a wide bore cannula to allow adequate fluid resuscitation.
• A crystalloid fluid is preferred
• Reassess haemodynamic status after the initial fluid bolus and consider whether further 250 to 500 mL boluses are required

Question 27

What fluids can be used for fluid resuscitation?

Note: non-hyperkalaemia and hyperkalaemia present

Answer 27

Use a balanced crystalloid unless hyperkalaemia is suspected or confirmed. Balanced crystalloid options include Hartmann’s solution, Ringer’s acetate, or Plasma-Lyte 148®.

Use normal saline (0.9% sodium chloride) instead if hyperkalaemia is present (potassium >5.5 mmol/L) or suspected (e.g., rhabdomyolysis).

Question 28

Why are balanced crystalloids not suitable for fluid resuscitation with hyperkalaemia?

Answer 28

This is because balanced crystalloids all contain potassium.

Question 29

What are the complications of AKI?

Answer 29

• Hyperkalaemia
• Fluid overload, heart failure and pulmonary oedema
• Metabolic acidosis
• Uraemia (high urea) can lead to encephalopathy or pericarditis
• End-stage kidney disease

Question 30

What differentials should be considered for AKI?

Answer 30

1. Chronic kidney disease
2. Drug side effect

Question 31

How does AKI and chronic kidney disease differ?

Answer 31

Differentiating signs and symptoms:

• Reduced kidney function with elevation of creatinine is chronic (>3 months), although there may be acute on chronic kidney disease

Differentiating investigations:

• An acutely elevated serum creatinine is diagnostic of AKI and indicative of reduced clearance
• The clinical context is important in differentiating AKI from a progression of CKD at initial presentation if there are no recent comparison creatinine values available for the patient
• Features that favour a diagnosis of CKD (although do not exclude AKI) include hypocalcaemia, hyperphosphataemia, anaemia, and small kidneys (sometimes scarred) on ultrasound

Question 32

How does AKI and drug-side effect differ?

Answer 32

Differentiating signs and symptoms:

• Certain medicines such as cimetidine or trimethoprim may lead to an elevation of creatinine that is minor and non-acute

Differentiating signs and symptoms:

• Discontinuing the medicine should result in normalising of the serum creatinine
• Twenty-four-hour urine study for creatinine clearance should demonstrate normal function