Acute Kidney Injury Flashcards

1
Q

Definition

A

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.

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2
Q

KDIGO classification

A

o Increase in serum creatinine > 26 mmol/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

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3
Q

Aetiology - Pre-Renal (90%)

A

Hypovolaemia (eg haemorrhage, severe vomiting)
Heart failure
Cirrhosis
Nephrotic syndrome
Hypotension (eg shock, sepsis, anaphylaxis)
Renal hypoperfusion (eg NSAIDs, ACE inhibitors, ARBs, renal artery stenosis/thrombosis)

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4
Q

Aetiology - Intrinsic Renal

A

Glomerular (glomerulonephritis, haemolytic uraemic syndrome)
Tubular (acute tubular necrosis)
Interstitial (acute intersitial nephritis (NSAIDs, autoimmune))
Vasculitides (Wegener’s granulomatosis)
Eclampsia

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5
Q

Aetiology - Post-Renal

A

Due to obstruction (calculi, urethral stricture, prostatic hypertrophy or malignancy, bladder tumour)

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6
Q

Risk Factors

A
Age (>75)
Pre-existing chronic kidney disease
Comorbidities (eg heart failure, liver disease)
Sepsis
Hypovolaemia 
Hypotension
Use of nephrotoxic medications (eg NSAIDs, gentamicin)
Emergency surgery
Diabetes mellitus
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7
Q

Epidemiology

A

15% of adults admitted to hospital will develop an AKI

Most common in the elderly

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8
Q

Presenting Symptoms

A
· Depends on underlying CAUSE
· Oliguria/anuria (NOTE: abrupt anuria suggests post-renal obstruction)
· Nausea/vomiting
· Dehydration
· Confusion
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9
Q

Signs on Physical Examination

A

· 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)

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10
Q

Investigations

A
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 (obstruction)
Look for hydronephrosis

Other Imaging:
CXR - pulmonary oedema
AXR - renal stones
ECG - can show hyperkalaemia

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11
Q

Management Plan

A
Treat the cause
4 MAIN components:
1 - protect patient from hyperkalaemia (calcium gluconate)
2 - optimise fluid balance
3 - stop nephrotoxic drugs
4 - consider for dialysis

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

Renal replacement therapy IF:
Hyperkalaemia refractory to medical management
Pulmonary oedema refractory to medical management
Severe metabolic acidaemia
Uraemic complications

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12
Q

Possible Complications

A
· Pulmonary oedema
· Acidaemia
· Uraemia
· Hyperkalaemia
· Bleeding
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13
Q

Prognosis

A

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

AKI is potentially reversible whereas CKD is not

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