Acute Kidney Injury

Question 1

What are the common U&E reference ranges?

Answer 1

Na 135-145
K 3.5-5.5
Urea 2.5-7.8
Creat 49-90
eGFR >90

Question 2

What are the AKI scoring criteria?

Answer 2

AKI Grade 1:

• Creatinine rise of >26 or 50-99% of baseline (i.e. 1.50-1.99x greater than baseline)
• <0.5 ml/kg/hr urine for 6-12 hours

AKI Grade 2:

• Creatinine rise of 100-199% of baseline (2.00-2.99x baseline)
• <0.5 ml/kg/hr urine for 12+ hours

AKI Grade 3:

• Creatinine rise of >200% (3x baseline); or serum creatinine >354, with an acute rise of at least 26
• <0.3 ml/kg/hr for urine >24hrs or anria for 12 hours.

Question 3

What symptoms or signs may lead you to suspect AKI?

Answer 3

Nausea and vomiting, diarrhoea

Evidence of dehydration (fluid losses > fluid intake; peripheral perfusion/CRT; mucous membranes and skin turgor)

Reduced urine output
- less than 0.5 ml/kg/hour for more than 6 hours.

Confusion, fatigue, drowsiness

Acute illness/lower urinary tract symptoms/sepsis

Creatinine
- Rise of 26 micromol/L or greater within 48 hours

Question 4

What is the role of urinalysis in assessing AKI?

Answer 4

Dipstick testing may suggest the source of the AKI:

AKI with -ve urinalysis usually indicates a pre-renal cause, but drugs should also be considered.

AKI with protein++ and blood++ may suggest glomerular disease.

Leucocytes are non-specific but may suggest infection or interstitial nephritis

Question 5

What is the earliest marker of a deterioration in renal function?

A) Urinalysis
B) Urine output
C) Serum creatinine

Answer 5

B) Urine output

Question 6

Why is serum creatinine helpful for assessing renal function?

Answer 6

Creatinine is almost solely excreted by the kidneys.

Question 7

Why is urine output an earlier marker of renal function than creatinine?

Answer 7

Creatinine is a product of creatine - a compound found in muscles and released into the blood when muscle is broken down.

Not a lot of muscle is broken down on a normal day, but a small amount of creatine is released each day. Because of the time taken for creatine levels to rise and for this to be converted to creatinine, there is roughly a day’s lag between renal function deterioration and the rise in serum creatinine.

Urine output is affected almost immediately by reduced renal function. Therefore, if a patient’s renal function drops today, you might expect to see a rise in their creat tomorrow.

Question 8

True or false: ACE inhibitors commonly cause a reduction in renal function, sometimes leading to AKI.

Answer 8

True.

ACE inhibitors, such as ramipril, cause efferent vasodilation and subsequent reduction in glomerular filtration.

Question 9

What is the role of ECG in assessing a patient with AKI?

Answer 9

ECG changes may show features hyperkalaemia, a serious sequelae of AKI.

The classic hyperkalaemic ECG change is tall, tented T waves (i.e. T wave larger than R wave in 2+ leads).

Other ECG changes:

• Flattened p-waves
• Broad, bizarre QRS
• Sloping ST
• Sine wave (S and T wave merging)
• Any arrhythmia

Question 10

What is the role of VBG in assessing a patient with AKI?

Answer 10

Metabolic acidosis is a common sequelae of AKI.

Question 11

If your patient with AKI develops hyperkalaemia, what is the recommended treatment?

Answer 11

Protect the myocardium by giving 30mls of 10% calcium gluconate

• IV bolus over 10 mins
• Repeat every 5 mins if ECG changes present
• Repeat every 30 mins if K still 6.5

AND

Shift potassium into cells using 50mls 50% dextrose and 10 units of actrapid IV over 20 minutes

So, treat hyperkalaemia with calcium gluconate and insulin dextrose.

Question 12

What are prerenal causes of AKI?

Answer 12

One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.

Examples

• hypovolaemia secondary to diarrhoea/vomiting
• renal artery stenosis

Question 13

What are post renal causes of AKI?

Answer 13

This group relates to problems after the kidneys. This is where there is an obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.

Examples

• kidney stone in ureter or bladder
• benign prostatic hyperplasia
• external compression of the ureter

Question 14

When is a renal ultrasound indicated for investigation of AKI?

Answer 14

If patients have no identifiable cause for the deterioration (rising creat, falling urine output) or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.

Question 15

Which one of the following should be stopped in AKI?

A) Aspirin 75 mg od
B) Atorvastatin
C) Ibruprofen
D) Lithium
E) Warfarin

Answer 15

C) Ibruprofen

NSAIDs should be stopped (except aspirin at cardio protective dose, e.g. 75 mg od)

Lithium may have to be stopped as it increases the risk of toxicity, but doesn’t usually worsen AKI itself.

Common drugs that are usually safe to continue in AKI include:

• Paracetamol
• Warfarin
• Statins
• Aspirin (at a cardio protective dose of 75mg od)
• Clopidogrel
• Beta-blockers

Drugs that should be stopped in AKI:

• NSAIDs
• Aminoglycoside
• ACEi’s
• ARBs
• Diuretics

Drugs that may need to be stopped, but not necessarily:

• Metformin
• Lithium
• Digoxin

Question 16

How is AKI managed?

Answer 16

Supportive care is based on the status of the patient.

• If clinically hypovolaemic, give fluid bolus.
• If patient euvolaemic but requires electrolyte replacement, decide if they can meet needs orally. If not, you may need to start parenteral replenishment.
• Seek expert help where needs are complex or symptoms are refractory.