Acute kidney injury (AKI)

Question 1

Define AKI

Answer 1

An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.

NOTE: this can occur in patients with previously normal kidneys or in patients with pre-existing renal disease

KDIGO Classification of AKI
Increase in serum creatinine > 26μmol/L within 48 hrs
Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
Urine volume < 0.5 ml/kg/hr for 6 hour

Question 2

Explain the aetiology/risk factors of Pre-renal AKI

Answer 2

(90% of all AKI are pre-renal)
Hypovolaemia,
Heart failure
Cirrhosis
Nephrotic syndrome
Hypotension (e.g. shock, sepsis, anaphylaxis)
Renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis)

Question 3

Explain the aetiology/risk factors of Intrinsic Renal AKI

Answer 3

Glomerular - glomerulonephritis, haemolytic uraemic syndrome

Tubular - acute tubular necrosis

Interstitial- acute interstitial nephritis (e.g. NSAIDs, autoimmune)

Vasculitides - (e.g. Wegener’s granulomatosis)
Eclampsia

Question 4

Explain the aetiology/risk factors of Post-Renal AKI

Answer 4

Post-Renal (due to obstruction)
Calculi
Urethral stricture
Prostatic hypertrophy or malignancy
Bladder tumour

Question 5

Summarise the epidemiology of AKI

Answer 5

15% of adults admitted to hospital will develop an AKI

Most common in the ELDERLY

Question 6

Recognise the presenting symptoms of AKI

Answer 6

Depends on underlying CAUSE

Oliguria/anuria (NOTE: abrupt anuria suggests post-renal obstruction)

Nausea/vomiting

Dehydration

Confusion

Question 7

Recognise the signs of AKI on physical examination

Answer 7

Hypertension

Distended bladder

Dehydration-postural hypotension

Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema

Pallor, rash, bruising (vascular disease)

Question 8

Identify appropriate investigations for AKI

Answer 8

Urinalysis
Blood-suggests nephritic cause
Leucocyte esterase and nitrites - UTI
Glucose, Protein, Urine osmolality

Bloods - FBC, Blood film, U&Es, Clotting, CRP

Immunology - Serum immunoglobulins and protein electrophoresis for multiple myeloma. Also check for Bence-Jones proteins in the urine

ANA - associated with SLE, Also check anti-dsDNA antibodies (high in active lupus). Complement levels -low in active lupus

Anti-GBM antibodies - Goodpasture’s syndrome

Antistreptolysin-O antibodies - high after Streptococcal infection

Virology- check for hepatitis and HIV

Ultrasound - Check for post-renal cause, Look for hydronephrosis

Other Imaging
CXR-pulmonary oedema
AXR-renal stone

Question 9

Generate a management plan for AKI

Answer 9

Treat the cause

FOUR main components to management:
Protect patient from hyperkalaemia (calcium gluconate)
Optimise fluid balance
Stop nephrotoxic drugs
Consider for dialysis

Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrology if intrinsic renal disease is suspected

Renal Replacement Therapy (RRT) considered if:
Hyperkalaemia refractory to medical management
Pulmonary oedema refractory to medical management
Severe metabolic acidaemia
Uraemic complication

Question 10

Identify possible complications of AKI

Answer 10

Pulmonary oedema
Acidaemia
Uraemia
Hyperkalaemia
Bleeding

Question 11

Summarise the prognosis for patients with AKI

Answer 11

Inpatient mortality varies depending on cause and comorbidities

Indicators of poor prognosis:
Age
Multiple organ failure
Oliguria
Hypotension
CKD

Patients who develop AKI are at increased risk of developing CKD