AKI Flashcards

1
Q

Define AKI

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.

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

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2
Q

KDIGO Classification of AKI

A

Increase in serum creatinine > 26 mmol/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 hours

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3
Q

Aetiology: Pre-Renal (90%)

A

Hypovolaemia (e.g. haemorrhage, severe vomiting)

Heart failure

Cirrhosis

Nephrotic syndrome

Hypotension (e.g. shock, sepsis, anaphylaxis)

Renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis)

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4
Q

Aetiology: Intrinsic Renal

A

Glomerular - glomerulonephritis, haemolytic uraemic syndrome

Tubular - acute tubular necrosis

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

Vasculitides (e.g. Wegener’s granulomatosis)

Eclampsia

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5
Q

Aetiology: Post-Renal

A

(due to obstruction)

Calculi- stone

Urethral stricture- scarring

Prostatic hypertrophy or malignancy

Bladder tumour

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6
Q

RISK FACTORS

A

Age

Chronic kidney disease

Comorbidities (e.g. heart failure)

Sepsis

Hypovolaemia

Use of nephrotoxic medications

Emergency surgery

Diabetes mellitus

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7
Q

Summarise the epidemiology of AKI

A

15% of adults admitted to hospital will develop an AKI

Most common in the ELDERLY

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8
Q

Recognise the presenting symptoms of AKI

A

Depends on underlying CAUSE

Oliguria/anuria

NOTE: abrupt anuria suggests post-renal obstruction

Nausea/vomiting

Dehydration

Confusion

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9
Q

Recognise the signs of AKI 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

Identify appropriate investigations for AKI

A

urinanalysis
bloods
ultrasound
other imaging

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11
Q

Urinanalysis

A

Blood - suggests nephritic cause

Leucocyte esterase and nitrites - UTI

Glucose

Protein

Urine osmolality

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12
Q

Bloods

A

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

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13
Q

Ultrasound

A

Check for post-renal cause

Look for hydronephrosis

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14
Q

Other Imaging

A

CXR - pulmonary oedema

AXR - renal stones

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15
Q

Generate a management plan for AKI

A

Protect patient from hyperkalaemia (calcium gluconate)

Optimise fluid balance

Stop nephrotoxic drugs

Consider for dialysis

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16
Q

Renal Replacement Therapy (RRT) considered if:

A

Hyperkalaemia refractory to medical management

Pulmonary oedema refractory to medical management

Severe metabolic acidaemia

Uraemic complications

17
Q

Identify possible complications of AKI

A

Pulmonary oedema

Acidaemia

Uraemia

Hyperkalaemia

Bleeding

18
Q

Summarise the prognosis for patients with AKI

A

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