Acute kidney injury (AKI)

Question 1

What are the functions of the kidneys?

Define acute kidney injury.

Answer 1

Acute decline in renal function, leading to a rise in serum creatinine and a decrease in urine output.

• The kidneys therefore cannot carry out their functions of:
  
  1. Water homeostasis
  2. Electrolyte balance
  3. Acid-base homeostasis
  4. Endocrine function: RAS, EPO, Vit D
  5. Clearance of waste products

Question 2

What is the most common form of AKI? What are the top 5 causes of in-patient AKI?

Answer 2

Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in 19% of ICU patients

Top 5 causes of in-hospital AKI:

1. Decreased renal perfusion
2. Medications
3. Radiographic contrast media
4. Postoperative
5. Sepsis

Source: In-hospital AKI. Nash 2002

Question 3

What is the aetiology of pre-renal AKI?

Answer 3

Pre-renal causes:

1. Reduced renal perfusion e.g. hypovolaemia, haemorrhage, sepsis, renal artery stenosis
2. Exogenous toxins e.g. immunoglobins, myoglobin
3. Endogenous toxins e.g. ACEi. NSAIDs

Question 4

What is the aetiology of post-renal AKI?

Answer 4

1. Renal obstruction
2. Ureteric obstruction
3. Urethral obstruction
4. Catheter obstruction

Question 5

What is the aetiology of intrinsic renal AKI?

Answer 5

1. Vascular Disease e.g. vasculitis
2. Glomerular Disease e.g. glomerulonephritis
3. Tubular Disease e.g. ATN
4. Interstitial Disease e.g. analgesic nephropathy

Question 6

What is the pathophysiology of renal AKI?

Answer 6

Most commonly ATN (acute tubular necrosis) due to…

1. impaired renal perfusion –> tissue hypoxaemia –> severe ischaemia –> increased ROS and reduced adenosine triphosphate* –> cellular dysfunction/death –> microvascular endothelial injury (most severe in early proximal tubule and outer medullary segments)

Question 7

What is oliguria?

Answer 7

A urine output of less than 400-500mL per 24 hours in adults

(Normal urine output for an adult is 0.5ml/kg/hr and for children 1ml/kg/hr on average)

Question 8

What are the risk factors for AKI?

Answer 8

Risk factors for AKI include:

• CKD
• chronic disease e.g. heart failure, liver disease, DM
• history of AKI
• nephrotoxic medications (e.g. NSAIDs, aminoglycosides, ACEi, ARBs and diuretics) within the past week
• use of iodinated contrast agents within the past week
• age 65 years or over

Question 9

What are the KDIGO criteria for diagnosing AKI?

Answer 9

• Increase in serum creatinine by ≥26.5 micromol/L (≥0.3 mg/dL) within 48 hours; or
• Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
• Urine volume <0.5 mL/kg/hour for 6 hours.

Question 10

Is there genetic predisposition to AKI?

Answer 10

There is preliminary evidence that a genetic predisposition for AKI may exist, especially with apolipoprotein E (APO-E) genes.

Question 11

Summarise RAS response to reduced circulating volume.

Answer 11

1. Central baroreceptors are activated
2. RAS activation
3. Vasopressin release
4. Sympathetic system activation
5. Vasoconstriction, renal sodium retention, increase in CO

*Angiotensin II stimulates aldosterone release promoting water and sodium reabsorption at collecting duct

*Low BP also promotes ADH release and increased tubular water re-absorption concentrating the urine

Question 12

What two main ix are used to define severity of AKI?

Answer 12

Serum creatinine

Urine output (or eGFR)

Question 13

What is the pathophysiology of post-renal AKI?

Answer 13

Obstruction –> increased intratubular pressure –> ischaemia and atrophy of renal tubules

Probably due to influx of monocytes and macrophages releasing cytokines, free radicals, proteases and TNF-beta which cause irreverisble injury and fibrosis.

Question 14

Recognise the presenting symptoms of acute kidney injury (AKI).

Answer 14

Often asymptomatic and diagnosed by laboratory tests.

General symptoms:

• N&V
• Uraemia
• Altered mental status

Question 15

Recognise the signs of acute kidney injury (AKI) on physical examination

Answer 15

Hypotension, hypertension, pulmonary oedema, peripheral oedema. Asterixis. Altered mental status

Patients with…

• fluid loss, sepsis, or pancreatitis may have hypotension along with other signs of circulatory collapse.
• glomerular disease typically present with hypertension and oedema, proteinuria, and microscopic haematuria (nephritic syndrome).
• rash, petechiae, or ecchymoses may suggest an underlying systemic condition such as vasculitis, thrombotic microangiopathy, or glomerulonephritis.
• after haemorrhage, sepsis, drug overdose, surgery, cardiac arrest, or other conditions associated with hypotension and prolonged renal ischaemia –> ATN
• renovascular disease may have an underlying abdominal bruit
• prostatic obstruction may present with abdominal distension from a full bladder.

Question 16

Identify appropriate investigations for acute kidney injury (AKI)

Answer 16

Diagnosed based on reduced UO and rising sCr.

Bloods: U&E, VBG, FBC, urinalysis and culture, urinalysis, serological (if AI suspected then ESR, anti-streptolysin O, anti-nuclear antibodies, anti-DNA, complement, anti-glomerular BM antibodies, hepatitis profile, HIV test ect)

Scans: renal USS. CXR, ECG. Later CT, MRI

Invasive: cystoscopy*,

Question 17

What acronym is used for management of AKI?

Answer 17

STOP AKI

Sepsis - urgent septic screen within 1hr

Toxins - identify and stop e.g. NSAIDs, aminoglycoside abx, contrast

Optimise volume and BP - fluids, vasopressors in ICU

Prevent harm - check reversible causes e.g. U&Es, obstruction, meds

Question 18

What is the management of pre-renal, renal and post-renal acute kidney injury (AKI)?

Answer 18

Pre renal -

• volume expansion/red blood cell transfuision - crystalloids (Ringer’s lactate/saline)/colloids (only for severe hypoalbuminaeamia). HES not reccommended.
• vasopressor -adrenaline(1microg/min IV), dopamine(1microg/kg/min), to keep MAP >60mmHg.
• diuretic - e.g. furosemide (40-80mg IV)
• RRT - for 4-6hrs

Intrinsic -

• treat underlying condition
• diuretic - furosemide (40-80mg) for volume control
• volume expansion - as above
• RRT

Obstructive -

• bladder catheterisation
• relief of obstruction above bladder neck (e.f. ureteral stenting, lithotripsy, exploratory laparotomy, percutaneous nephrostomy)
• diuretic
• RRT

Question 19

Identify the possible complications of acute kidney injury (AKI) and its management

Answer 19

hyperphosphataemia - give phosphate binders like calcium acetate/carbonate.

uraemia –> lethargy, confusion, obtundation

volume overload (pulmonary and peripheral oedema)

hyperkalaemia - from impaired excretion of potassium, cell lysis or tissue breakdown

metabolic acidosis - may be managed by oral bicarbonate solutions

Question 20

Question 21

Which class of drugs may predispose patients to developing pre-renal AKI? Explain each.

• A.NSAIDs
• B.Calcineurin inhibitors
• C.ACEi or ARBs
• D.Diuretics
• E.All of the above

Answer 21

All of the above:

• NSAIDs - decrease afferent flow
• Calcineurin inhibitors - decrease afferent flow
• ACEi or ARBs - increase efferent flow so decrease filtration
• Diuretics – affect tubular function, decrease preload

Question 22

When do you refer for emergency RRT?

Answer 22

1. Refractory HYPERKAL (potassium >6.5 mmol/L)
2. Refractory metabolic ACIDOSIS (pH <7.15)
3. Refractory volume OVERLOAD with or without pulmonary oedema
4. End-organ complications of URAEMIA (e.g., pericarditis, encephalopathy, uraemic bleeding) or other end-organ involvement (e.g., neuropathy, myopathy)
5. Severe AKI and POISONING/drug overdose (e.g., ethylene glyc

Question 23

What are the KIDGO stages of AKI?

Answer 23

AKI Stage 1:

• sCr : x1.5- 1.9 the reference OR rise of ≥26 µmol/L
• UO: <0.5ml/kg/hr for 6-12 hrs

AKI Stage 2:

• sCr : x2.0-2.9 the reference
• UO: <0.5ml/kg/hr for _>_12hrs

AKI Stage 3:

• sCr : x≥3 the reference OR or rise of ≥354 µmol/L
• UO: <0.3ml/kg/hr for _>_24hrs OR anuria for _>_12 hours

Question 24

What is the RIFLE criteria for AKI?

Answer 24

RIFLE (Risk, Injury, Failure, Loss of kidney function, and Endstage kidney disease):

Severity groups:

1.Indicates risk:

• Serum creatinine increased 1.5 times; or
• Urine production of <0.5 mL/kg body weight for 6 hours

2. Indicates injury:

• Creatinine increased 2.0 times; or
• Urine production of <0.5 mL/kg for 12 hours.

3.Indicates failure:

• Creatinine increased 3.0 times; or
• Urine output <0.3 mL/kg for 24 hours or anuria for 12 hours.

4.Indicates loss:

• Persistent AKI for more than 4 weeks; complete loss of kidney function.

5.Indicates ESRD:

• ESRD (loss >3 months).