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Urinary > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

Sudden deterioration of renal function over hours or days

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2
Q

What is oliguria?

A

Production of small amounts of urine
100-400ml

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3
Q

What is anuria?

A

Failure of kidneys to produce urine
<100ml

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4
Q

Three categories of causes of acute kidney injury

A

Pre renal
Intrinsic renal
Post renal

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5
Q

Risk factors of AKI

A
  • older age >65
  • sepsis
  • CKD
  • heart failure
  • diabetes
  • liver disease
  • cognitive impairment > leading to reduced fluid intake
  • meds e.g. diuretics, ACE inhibitors, NSAIDs
  • radiocontrast agents
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6
Q

Causes of pre renal cute kidney injury

A
  • Sepsis
  • Hypovolaemia
  • Shock
  • Renal artery stenosis
  • NSAIDs
  • Congestive cardiac failure
  • ACE inhibitors
    . generally cause a decreased blood supply to kidneys
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7
Q

Causes of intrinsic renal acute kidney injury

A

Acute tubular necrosis
Acute interstitial nephritis
Glomerulonephritis
Rhabdomyolysis
Haemolytic uraemic syndrome

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8
Q

Causes of post renal acute kidney injury

A

Obstruction of urine
Bilateral calculus of ureters
Ureteric/urethra stricture
Tumour
Retro-peritoneal fibrosis
Benign prostatic hyperplasia

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9
Q

Diagnosis of AKI

A
  • rise in creatinine for >25mmol/L in 48 hours
  • rise in creatinine of >50% in 7 days
  • urine output <0.5nl/kg/hr over >6 hours
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10
Q

Complications of acute kidney injury

A
  • Metabolic acidosis
  • Hyperkalaemia
  • Ureamia > encephalopathy + pericarditis
  • Volume overload > heart failure + pulmonary oedema
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11
Q

Urine volume in oliguria

A

100-400ml a day

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12
Q

Urine volume in anuria

A

<100ml a day

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13
Q

Staging of acute kidney injury

A

Stage 1
- serum creatinine: 1.5-1.9 times baseline
- urine output: <0.5ml/kg/h for 6-12 hours

Stage 2
- serum creatinine: 2-2.9 times baseline
- urine output: <0.5 ml/kg/h for >12 hours

Stage 3
- serum creatinine: 3 times baseline
- urine output: <0.3ml/kg/h for >24hours or anuria for >12 hours

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14
Q

Stage 1 AKI

A
  • serum creatinine: 1.5-1.9 x baseline
  • urine output: 0.5ml/kg/h for 6-12 hours
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15
Q

Stage 2 AKI

A
  • serum creatinine: 2-2.9 x baseline
  • urine output: <0.5ml/kg/h for >12 hours
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16
Q

Stage 3 AKI

A
  • serum creatinine: 3 x baseline
  • urine output: <0.3ml/kg/h for >24hours or anuria for >12 hours
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17
Q

Treatment of pre-renal AKI

A

Treat the cause

  • IV fluids for hypovolaemia
  • stop potentially nephrotoxic meds e.g. NSAIDs, ACEi
  • diuretics
18
Q

Treatment of intrinsic renal AKI

A
  • correct electrolytes
  • renal replacement therapy (dialysis)
  • call nephrology
19
Q

Treatment of post renal AKI

A
  • urinary or supra-pubic catheter
  • ureteric stents
  • nephrostomy
20
Q

Management of AKI

A
  • stop nephrotoxic agents
  • treat underlying cause
  • fix any electrolyte imbalances
  • ensure volume status + perfusion pressure (IV fluids if dehydrated | diuretics if overloaded)
  • monitor urine output + daily bloods
21
Q

How can AKI cause metabolic acidosis?

A

Unable to make more bicarbonate in intercalated cells or glutamine

22
Q

Symptoms of a patient with failing kidneys?

A
  • palpitations
  • deceased urine output
  • fatigue
  • vomiting (to resolve acid base imbalance)
  • oedema (volume overload)
  • confusion (end stage)
23
Q

What meds do you want to stop if a patient has an AKI?

A

Stop the DAMN meds

Diuretics
ACE inhibitors
Metformin
NSAIDs

24
Q

What is acute tubular necrosis?
What is it due to?

A

Damage + necrosis of the epithelial cells of renal tubules due to:
- ischaemia due to hypoperfusion
- nephrotoxins e.g. gentamicin, radiocontrast agents

25
Q

What is used to confirm acute tubular necrosis?

A

Muddy brown casts on urinalysis
Renal tubular epithelial cells may also be seen

26
Q

What is acute interstitial nephritis?
What is it due to?

A

Acute inflammation of the interstitium due to an immune reaction assocaited with:
- drugs e.g NSAIDs
- infection e.g. E.coli, HIV
- autoimmune conditions e.g. SLE, sarcoidosis

27
Q

Management of acute interstitial nephritis

A

Treat underlying cause
Steroids can reduce inflammation + improve recovery

28
Q

Are ACEi nephrotoxic?

A
  • No but they should be stopped during an AKI as they reduce filtration pressure
  • They have a protective effect on the kidneys long term
29
Q

Investigations of AKI

A
  • urine dipstick
  • daily FBCs, U&Es, LFTs, bone profile (phosphate + Ca) + CRP
  • urine PCR
  • USS KUB - to rule out obstruction
30
Q

Indications for renal replacement therapy in AKI

A
  • hyperkalaemia refractory to medical therapy
  • metabolic acidosis refractory to medical therapy
  • fluid overload refractory to diuretics
  • uraemic pericarditis
  • uraemic encephalopathy
31
Q

What further investigations are needed if protein + blood are detected on urine dipstick in patient with AKI and why?

A
  • c-ANCA + p-ANCA - vasculitis
  • anti-GBM, ANA, C3 + C4 - lupus nephritis
  • serum immunoglobulins + electrophoresis - myeloma
32
Q

What is haemolytic uraemic syndrome?
What is it due to?
What is the classic triad?

A
  • Involves thrombosis in small blood vessels in the body due to shiga toxins from E.coli or shigella.
    .
    Triad of:
  • microangiopathic haemolytic anaemia
  • acute kidney injury
  • thrombocytopenia
33
Q

How can haemolytic uraemic syndrome cause the classic triad?

A
  • formation of blood clots uses platelets > thrombocytopenia
  • the thrombi partially obstructs small blood vessels + damage RBCs > microangiopathic haemolytic anaemia
  • the thrombi reduces kidney perfusion + damage the RBCs > acute kidney injury
34
Q

Presentation of haemolytic uraemic syndrome

A
  • E. coli + shigella cause gastroenteritis > bloody diarrhoea
  • fever
  • pallor or jaundice
  • bruising
  • abdominal pain
  • oliguria
  • lethargy
  • confusion
35
Q

Management of haemolytic uraemic syndrome

A
  • stool culture to establish causative organism
  • blood transfusion
  • IV fluids
  • anti hypertensive meds
  • haemodialysis
36
Q

What does muscle cell death release?

A

Myoglobin
Potassium
Phosphate
Creatine kinase

37
Q

Causes of Rhabdomyolysis

A
  • prolonged immobility
  • extremely rigorous exercise beyond person’s fitness level
  • crush injuries
  • statins
  • seizures
38
Q

Presentation of Rhabdomyolysis

A
  • muscle pain, swelling + weakness
  • oliguria
  • red-brown urine (Myoglobinuria)
  • fatigue
  • N+V
  • confusion
39
Q

Investigations of Rhabdomyolysis

A
  • Creatine kinase levels
  • U&Es
  • potassium levels + ECG
  • urine dipstick for presence of blood (for myoglobin in urine)
40
Q

Management of Rhabdomyolysis

A
  • IV fluids
  • treatments of hyperkalaemia
    .
    Possible options but have risks:
  • IV sodium bicarbonate to increase urinary pH
  • IV mannitol to increase urine output + reduce oedema

Urinary (24 decks)

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