Acute kidney injury Flashcards

1
Q

Define acute kidney injury (AKI)

A

Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output. [1] The change in terminology emphasises that kidney injury presents as a disease spectrum from mild renal impairment to severe renal failure.

Kidney Disease: Improving Global Outcomes (KDIGO) definition of AKI [1]
Any of the following:

  • Increase in serum creatinine by ≥26.5 micromol/L (≥0.3 mg/dL) within 48 hours; or
    Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
    -Urine volume <0.5 mL/kg/hour for 6 hours.
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2
Q

Explain the aetiology / risk factors of acute kidney injury (AKI)

A

Risk factors for aki include pre-existing ckd, age, male sex, and comorbidity (dm, cardiovascular disease, malignancy, chronic liver disease), complex surgery).
R

FORMAT OF STUFF BELOW TO BE CHANGED
1.Explain the aetiology / risk factors of acute kidney injury (AKI)
Aetiology can be divided according to site (table 7.4) as:
Pre-renal: failure due to impaired renal perfusion, with an appropriate renal response.
Intrinsic: failure due to direct injury to renal parenchyma.
Post-renal: failure due to obstruction of urinary outflow.

Pathologies with examples of conditions that lead to them fir each category is show below
Pre-renal

Reduced vascular volume( e.g. Haemorrhage, D&V(DIARRHOEA AND VOMITING), burns, pancreatitis)
Reduced cardiac output (e.g. Cardiogenic shock, MYOCARDIAL INFARCTION)
Systemic vasodilation (Sepsis, drugs)¬
Renal vasocontriction (NSAIDs, ACE-i, ARB, hepatorenal syndrome)

Renal
Glomerular(Glomerulonephritis, ATN (prolonged renal hypo-perfusion causing intrinsic renal damage)
Interstitial(Drug reaction, infection, infiltration (eg sarcoid))
Vessels(Vasculitis, HUS, TTP, DIC)
Post-renal
Within renal tract(Stone, renal tract malignancy, stricture, clot)
Extrinsic compression(Pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis)

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3
Q

Summarise the epidemiology of acute kidney injury

A

aki is common, occurring in up to 18% of hospital patients and ~50% of icu patients

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4
Q

Recognise the signs of acute kidney injury (AKI) on physical examination

A

Hypotension, hypertension, pulmonary oedema, or peripheral oedema may be present. There may be asterixis or altered mental status when uraemia is present.

Patients with fluid loss, sepsis, or pancreatitis may have hypotension along with other signs of circulatory collapse.

Patients with glomerular disease typically present with hypertension and oedema, proteinuria, and microscopic haematuria (nephritic syndrome).

The presence of rash, petechiae, or ecchymoses may suggest an underlying systemic condition such as vasculitis, thrombotic microangiopathy, or glomerulonephritis.

Patients with ATN may present after haemorrhage, sepsis, drug overdose, surgery, cardiac arrest, or other conditions associated with hypotension and prolonged renal ischaemia.

An underlying abdominal bruit may support renovascular disease.

The patient with prostatic obstruction may present with abdominal distension from a full bladder.

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5
Q

Recognise the presenting symptoms of acute kidney injury (AKI)

A
reduced urine production
vomiting
dizziness
orthopnoea
paroxysmal nocturnal dyspnoea
orthostatic hypotension
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6
Q

Identify appropriate investigations for acute kidney injury (AKI) and interpret the results

A

FROM BMJ BEST PRACTICE(where more detail can be viewed):
Initial work-up should include basic metabolic profile (including urea and creatinine), venous blood gases, full blood count, urinalysis and culture, urine chemistries (for fractional excretion of sodium and urea), renal ultrasound (when appropriate by history or examination), chest x-ray, and ECG. Urine osmolality is rarely ordered but, if high, suggests pre-renal azotemia (in the absence of contrast dyes). Urinary eosinophil counts have low sensitivity and specificity for acute interstitial nephritis, but may be of some use in patients with pyuria. [78]

Chest x-ray may reveal pulmonary oedema or cardiomegaly.

ECG may demonstrate arrhythmias if hyperkalaemia is present.

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7
Q

Generate a management plan for acute kidney injury (AKI)

A

• Treat the cause
• FOUR main components to management:
o Protect patient from hyperkalaemia (calcium gluconate)
o Optimise fluid balance (if there is too much or too little?)
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
• Renal Replacement Therapy (RRT) considered if:
o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications

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8
Q

Identify the possible complications of acute kidney injury (AKI) and its management

A
  • Pulmonary oedema
  • Acidaemia
  • Uraemia
  • Hyperkalaemia
  • Bleeding
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9
Q

Summarise the prognosis for patients with acute kidney injury (AKI)

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
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