Acute kidney injury

Question 1

Define

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.

Question 2

Classification

Answer 2

any of the following:
o Increase in serum creatinine > 26 mol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for 6 hours

Question 3

Causes of AKI

Answer 3

• Pre-Renal (90%) – reduced kidney perfusion leads to falling GFR
o Hypovolaemia (e.g. haemorrhage, severe vomiting, dehydration)
o Heart failure
o Cirrhosis
o Nephrotic syndrome
o Hypotension without hypovolaemia (e.g. shock, sepsis, anaphylaxis)
o Renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, Amphotericin B, renal artery stenosis, calcineurin inhibitors)
• Intrinsic Renal
o Glomerular – glomerulonephritis (common), haemolytic uraemic syndrome, TTP, preeclampsia
o Tubular - acute tubular necrosis (most common) due to ischaemia or toxins
o Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune) (common)
o Vasculitides (e.g. Wegener’s granulomatosis)
o Eclampsia

Biochemical measures such as urine sodium can help distinguish between pre-renal causes and intra-renal causes. In prerenal, urine sodium is low (<20), whereas in intrinsic renal, >40.

• Post-Renal (due to urinary tract obstruction)
o Calculi (common)
o Urethral stricture
o Prostatic hypertrophy or malignancy (common)
o Bladder tumour
o Ascending urinary infection
o Urinary retention

Question 4

What are the risk fatcors?

Answer 4

o	Age 
o	Chronic kidney disease 
o	Comorbidities (e.g. heart failure) 
o	Sepsis 
o	Hypovolaemia
o	Use of nephrotoxic medications 
o	Emergency surgery
o	Diabetes mellitus

Question 5

Epidemiology

Answer 5

• 15% of adults admitted to hospital will develop an AKI

* Most common in the ELDERLY

Question 6

What are the presenting symptoms?

Answer 6

• Depends on underlying CAUSE
• Often asymptomatic and diagnosed by lab tests
• Oliguria/anuria
o NOTE: abrupt anuria suggests post-renal obstruction
• Nausea/vomiting and confusion (seen in later stages)
• History of trauma/ predisposing disease

Question 7

What are the signs?

Answer 7

•	Hypertension
•	hypotension (fluid loss, sepsis, pancreatits)
•	Biochemical abnormalities
o	Hyperkalaemia
o	Metabolic acidosis (unless vomiting)
o	Hyponatraemia
o	hypocalcaemia
•	pulmonary oedema
•	Uraemia
o	Weakness, fatigue
o	Nausea and vomiting
o	Mental confusion, seizures, coma
•	Asterixis (when uraemia is present)
•	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

What are the 1st investigations?

Answer 8

• Urinalysis
o Blood - suggests nephritic cause
o Leucocyte esterase and nitrites - UTI
o Glucose
o Protein
o Urine chemistries (fractional excretion of sodium and urea)
• Bloods
o FBC
o VBG
o Blood film
o U&Es
o Clotting
o CRP
o 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
o Virology - check for hepatitis and HIV
• Ultrasound
o Check for post-renal cause
o Look for hydronephrosis (swelling of kidney due to build up of urine)
• Other Imaging
o CXR - pulmonary oedema
o AXR - renal stones
• ECG (arrythmias if hyperkalaemia is present)

Question 9

How would you manage?

Answer 9

Pre-renal:
Volume expansion and/or RBC transfusion (if severe hypotension, give vasopressor/ with volume overload, diuretic/ with uraemia, met acidosis, hyperkalaemia refractory to management or volume overload unresponsive to diuretics, renal replacement therapy)

Intrinsic renal:
Treat underlying cause first. Then if volume overload, diuretic. With pre-existing pre-renal, volume expansion. With uraemia, met acidosis, hyperkalaemia refractory to management or volume overload unresponsive to diuretics, renal replacement therapy.

Post-renal:
Bladder catheterisation. Then relief of obstruction over bladder neck by ureteral stenting. If volume overload, diuretic. With uraemia, met acidosis, hyperkalaemia refractory to management or volume overload unresponsive to diuretics, renal replacement therapy.

Question 10

What are the 4 components of management?

Answer 10

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

Question 11

When is renal replacement therapy considered?

Answer 11

o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications

Question 12

What are the possible complications?

Answer 12

• Pulmonary oedema, peripheral oedema
• Metabolic acidosis
• Hyperphosphatemia
• Hyperkalaemia
• Uraemia
• Chronic progressive kidney disease
• End stage renal disease

Question 13

What’s the prognosis?

Answer 13

•	Inpatient mortality varies depending on cause and comorbidities 
•	Indicators of poor prognosis:
o	Age 
o	Multiple organ failure 
o	Oliguria
o	Hypotension 
o	CKD 
•	Patients who develop AKI are at increased risk of developing CKD