Lecture 13: Acute Kidney Injury

Question 1

KDIGO definition for acute kidney injury

Answer 1

• increase in serum creatine >/= 26.5umol/l within 48hrs or
• increase in serum creatinine >/= 1.5x the baseline within the last 7 days or
• urine volume < 0.5ml/kg/hr for 6 hours

Question 2

AKI epidemiology

Answer 2

AKI affects 10-20% of all hospitalised patients and up to 50% of critically ill patients in intensive care

Question 3

AKI pre-renal causes

Answer 3

• cardiac failure
• haemorrhage
• sepsis
• vomiting and diarrhoea

Question 4

renal causes of AKI

Answer 4

• Acute tubular necrosis (can happen due to dehydration, shock, heart failure or toxins such as gentamicin, radiocontrast agents or cisplatin)
• Glomerulonephritis
• Acute interstitial nephritis
• Haemolytic uraemic syndrome
• Rhabdomyolysis

Question 5

AKI signs and symptoms

Answer 5

• rapid rise in serum creatinine levels and urea
• decrease in urine output (< 0.5ml/kg/h for 6hrs)
• fluid overload signs (e.g., oedema, hypertension, pulmonary oedema)
• signs related to underlying cause (e.g., sepsis, rashes in vasculitis)
• signs of uraemia in severe cases (e.g., fatigue, anorexia, nausea, pruritus, altered mental status)

Question 6

To diagnose AKI, the following investigations may be used:

Answer 6

• Bloods: Full blood count (FBC), urea and electrolytes (U&Es), liver functions tests (LFTs), glucose, clotting, bone profile, creatine kinase (CK), C-reactive protein (CRP).
• Venous blood gas (VBG)/arterial blood gas (ABG): For acidosis, hypoxia, urgent potassium level.
• Urine tests: Dipstick (looking for blood and protein), microscopy, culture & sensitivity (MC&S; to exclude infection), biochemistry (electrolytes, osmolality), urine protein:creatinine ratio (uPCR; to quantify proteinuria).
• ECG: To look for hyperkalaemia.
• Chest X-ray (CXR): To identify pulmonary oedema.
• Renal ultrasound: To evaluate renal size (normal is 10–13 cm) and echotexture, hydronephrosis, structural kidney disease.

in cases where the cause is unclear, an acute ‘renal screen’ may be necessary

Question 7

indication for acute dialysis or haemofiltration

AEIOU

Answer 7

• Acidosis (severe metabolic acidosis with pH of < 7.2
• Electrolyte imbalance (resistant hyperkalaemia)
• Intoxication (drug overdose, poisoning)
• Oedema (refractore pulmonary oedema)
• Uraemia (encephalopathy or pericarditis)

Question 8

management of AKI

Answer 8

• ABCDE approach
• adress immediate threats: acidosis, hypovolaemia, hypekalaemia, sepsis and pulmonary oedema.
• identify and treat underlying cause
• monitor patient: regular observations of fluid status, including measurements of urine output and U&Es.
• medication review: suspend nephrotoxic drugs and those that may worsen AKI (NSAIDs, aminoglycosides, ACEis/ARBs)

Question 9

post-renal causes of AKI

Answer 9

• tumours
• prostate disease
• stones

Question 10

STOP AKI prevention steps

Answer 10

• Sepsis: if suspected screen and treat promptly - SEPSIS 6
• Toxins: avoid e.g. gentamicin, NSAIDs IV iodinated contrast
• Optimise BP and volume status: avoid/correct hypovolaemia, review BP medications
• Prevent harm: daily U&Es, fluid balance and medication review

Question 11

When you are unwell with any of the following:
- Vomiting or diarrhoea (unless minor)
- Fevers, sweats and shaking

Then STOP taking the following medications:

Answer 11

• ACEis
• ARBs
• NSAIDs
• diuretics
• metformin

Question 12

AKI response SHOUT

Answer 12

• Suspect sepsis: treat as per local guidance (consider avoiding gentamicin)
• hypovolaemia: assess and document fluid status, consider fluid resuscitation, fluid balance chart, urinary catheter and hourly volumes
• Obstruction: consider bladder scan and/or US
• Urinalysis: is there blood or protein?
• Toxins: consider stopping antihypertensives, NSAIDs, gentamicin, contrast, metformin etc.

Question 13

what is the earliest ECG change in hyperkalaemia

Answer 13

• peaked T waves (usually the earliest signs of hyperkalaemia) tall tented T waves

Question 14

what is the treatment for hyperkalaemia?

Answer 14

• stabilise (myocardium): calcium gluconate
• shift (K+ intracellularly): salbutamol, insulin-dextrose
• remove with: diuresis, dialysis, anion exchange resins

Question 15

how can NSAIDs cause acute kidney injury in relation to the afferent (blood in) arteriole?

Answer 15

• prostaglandins normally dilate the afferent arteriole to maintain glomerular perfusion.
• NSAIDs block prostaglandin leading to the contstrictions of the afferent arteriole and decreased perfusion.

Question 16

how can NSAIDs cause acute kidney injury in relation to the efferent (blood out) arteriole?

Answer 16

• when renal perfusion is low, angiotensin II causes constriction of efferent arteriole to maintain glomerular filtration.
• therefore blocking angiotensin II can lead to acute fall in GFR if perfusion is low e.g. when used with a NSAID.