Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

Rapid loss of glomerular filtration/renal function over hours-days following injury to the kidney, involving retention of urea and creatinine

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2
Q

What is the NICE criteria for AKI?

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours

Rise in creatinine of ≥ 50% in 7 days

Urine output of < 0.5ml/kg/hour for > 6 hours

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3
Q

What are the 3 classifications of acute kidney injury causes?

A

Pre-Renal

  • Inadequate blood supply to the kidney, reducing blood filtration

Renal/Intrinsic

  • Damage to renal parenchyma causing reduced filtration of blood

Post-Renal

  • Obstruction to urine outflow from the kidney causing back-pressure into the kidney
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4
Q

What are the pre-renal causes of AKI?

A

HF

Haemorrhage

Sepsis

Hypotension/shock

Vomiting and diarrhoea

Dehydration

Renal artery stenosis

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5
Q

What are the renal causes of AKI?

A

Glomerulonephritis

Vasculitis

Radiocontrast

Myeloma

Rhabdomyolysis

Toxins

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6
Q

What toxins can cause AKI?

A

(stop the damn drugs)

NSAIDS

Gentamicin/Aminoglyosides

ACEI and ARBS

Diuretics

Metformin

(Lithium and Digoxin increase risk of toxicity but does not cause AKI itself)

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7
Q

What are the post-renal causes of AKI?

A

Tumours

Prostate disease

Kidney stones

Ureter strictures

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8
Q

Give risk factors for AKI

A

Consider AKI in patient’s suffering from an acute illness or post surgery

Age >65

Previous AKI

HF

Liver disease

CKD

DM

Vascular disease

Cognitive impairment

Nephrotoxic medications

Contrast medians for CT

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9
Q

How does AKI present?

A

Oliguria

Oedema, pulmonary and peripheral

Arrythmias/palpitations, secondary to hyperkalaemia

Features of uraemia, such as pericarditis and encephalopathy

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10
Q

What investigations are used in AKI diagnosis?

A

Urinalysis

  • Leucocytes and nitrites
  • Protein and blood
  • Glucose

U&E

  • Increased creatinine and urea

ABG

  • Metabolic acidosis
  • Increased bicarbonate

US within 24 hours if no identifiable cause

  • Exclude obstruction

Renal biopsy

ECG

  • Hyperkalaemia changes

Myeloma screen

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11
Q

How is AKI managed?

A

Treat cause

Sepsis protocol

  • Blood culture
  • Hourly urine output of urea and creatinine
  • IV fluids
  • IV antibiotics

Medication review and stop nephrotoxic drugs

Fluid balance

  • Volume resuscitation/fluid restriction
  • IV fluids if necessary
  • Catheter to monitor fluid outgoing

Hyperkalaemia management

Optimise BP

Renal replacement therapy/haemodialysis

  • Indicated when patient is not responding to medical treatment of complications
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12
Q

How is hyperkalaemia managed?

A

IV calcium gluconate to stabilise myocardium

Shift K+ intracellularly via nebulised salbutamol and insulin-Dextrose infusion

Removal via diuretics, dialysis or anion exchange renins such as calcium resonium orally or enema

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13
Q

Give indications for dialysis

A

Pulmonary oedema

K+ >6.5mmol/l

pH<7.2

Pericarditis

Encephalopathy

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14
Q

Give indications for referral to a nephrologist?

A

Renal transplant

ITU patient with unknown cause of AKI

Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma

AKI with no known cause

Inadequate response to treatment

Complications of AKI

Stage 3 AKI

CKD stage 4 or 5

Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)

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15
Q

Describe AKI stage 1

A

1.5-1.9x baseline serum creatinine or

>26.5 umol/l increase in creatinine or

<0.5ml/kg/h urine for 6-12 hours

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16
Q

Describe AKI stage 2

A

2.0-2.9x baseline serum creatinine or

<0.5ml/kg/h urine for >12 hours

17
Q

Describe AKI stage 3

A

3.0x baseline serum creatinine or

>354 umol/l creatinine or

Initiation of replacement therapy or

<3.0ml/kg/h for >24 hours or

Anuria for >12 hours

18
Q

Give complications of AKI

A

Metabolic acidosis

Electrolyte imbalance

  • Hyperkalaemia

Fluid overload

  • HF
  • Pulmonary oedema

Uraemic complications

  • Encephalopathy
  • Pericardial rub with pericarditis
19
Q

What is the most common cause of AKI?

A

Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) seen in clinical practice

20
Q

What causes ATN?

A

Ischaemia

  • Shock
  • Sepsis

Nephrotoxins

  • Aminoglycosides
  • Myoglobin secondary to rhabdomyolysis
  • Radiocontrast agents
  • Lead
21
Q

How does ATN present?

A

Features of AKI

Muddy brown casts in urine

22
Q

Describe the test results in pre-renal causes of AKI

A

Decreased urine Na (<20)

Increased urine osmolaity (>500)

Good response to fluid challenge

Raised serum urea:creatinine ratio

Normal urine

23
Q

Describe the test results in intra-renal causes of AKI/acute tubular necrosis

A

Increased urine Na (>40)

Decreased urine osmolaity (<350)

Poor response to fluid challenge

Normal serum urea:creatinine ratio

Brown granular casts in urine

Proteinuria

24
Q

Describe the U&E results in dehydration specifically

A

Urea is porportionally higher than the rise in creatinine

25
Q

Describe the U&E results in ATN specifically

A

Proportionate rise in both urea and creatinine

26
Q

What are the causes of rhabdomylosis?

A

Seizure

Collapse/coma

Ecstasy

Crush injury

McArdle’s syndrome

Drugs

  • Statins (especially if co-prescribed with clarithromycin)
27
Q

Describe the investigation results in rhabdomylosis specifically

A

disporportionally raised creatinine

Increased urate

28
Q

What causes acute interstitial nephritis?

A

Drugs

  • Penicillin
  • Rifampicin
  • NSAIDs
  • Allopurinol
  • Furosemide

Systemic disease

  • SLE
  • Sarcoidosis
  • Sjögren’s syndrome

Infection

29
Q

What are the features of acute interstitial nephritis?

A

Fever

Rash

Arthralgia

Eosinophilia casts

Mild renal impairment

HTN
Sterile pyuria

White cell casts

30
Q

Difference between ATN and AIN?

A

ATN is more dying tubular cells whereas AIN is allergic/immune response

31
Q

What can develop in young females who develop AKI after initation of an ACEI?

A

Fibromuscular dysplasia

32
Q

Give absolute indications for renal replacemet therapy

A

K+ level of 6.9 with minimal response to insulin and dextrose treatment