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Week 12 - Nephrology and urology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is the definition of AKI from the UKRA guidelines?

A

Decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatinine

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2
Q

How can you classify the severity of AKI?

A

AKI-KDIGO
•Stage 1
•Stage 2
•Stage 3

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3
Q

What is stage 1 AKI?

A

Serum creatinine >/1.5 and <2 times the AKI baseline or >/26.0micro mol/l increase above the AKI baseline

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4
Q

What is stage 2 AKI?

A

Serum creatinine >/2 and <3 times the AKI baseline

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5
Q

What is stage 3 AKI?

A

Serum creatinine >/3 times the AKI baseline or >/354 micro mol/l increase above the AKI baseline

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6
Q

Define oliguria

A

Urine output that is less than 1mL/kg/h in infants, less than 0.5mL/kg/hour in children and less than 400mL or 500mL per 24 hours in adults

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7
Q

Explain what AKI e-alerts are

A
  • They highlight AKI using lab data algorithm
  • Serum creatinine >/1.5 times higher than the median of all creatinine values 8-365 days ago
  • Serum creatinine >/1.5 times higher than the lowest creatinine within 7 days
  • Serum creatinine >26micromol/l higher than the lowest creatinine within 48 hours
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8
Q

What are the diagnostic classifications of AKI?

A
  • Pre renal = circulatory failure
  • Renal
  • Post renal = obstruction
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9
Q

What are the pre renal causes of acute kidney injury?

A

•Hypovolaemia and hypotension due to:

  • diarrhoea/vomiting
  • inadequate fluid intake
  • blood loss through trauma
  • third space fluid losses

•Reduced effective circulating volume

  • circulating volume
  • cardiac failure
  • septic shock (vasodilation so effective perfusion decreases)
  • cirrhosis

•Drugs (in setting of hypovolaemia)

  • NSAIDs
  • ACEi

•Renal artery stenosis

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10
Q

What are the renal causes of AKI?

A
  • Glomerular - glomerulonephritis
  • Tubular (obstruction and dysfunction)
  • ischaemic ATN
  • nephrotoxic ATN
  • myeloma cast nephropathy

•Tubulointerstitial

  • drugs
  • myeloma
  • sarcoid
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11
Q

What are the post renal causes of AKI?

A 
Anything between the renal pelvis and urethral meatus which obstructs the flow of urine 
•Renal papillary necrosis 
•Kidney stones 
•Retroperitoneal fibrosis 
•Carcinoma of the cervix 
•Prostatic hypertrophy/malignancy 
•Tumours: ureter, bladder, prostate, cervix, ovarian, cna be extrinsic 
•lymph nodes 
•Urethral strictures
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12
Q

What two key things are needed for the kidneys to make urine?

A
  • A blood supply

* An un-obstructed collecting system to ensure urine can be excreted

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13
Q

What will you see on ultrasound of an obstructed kidney?

A

Dilated renal pelvis surrounded by renal cortical tissue

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14
Q

If a man presents with an obstructive cause of AKI, what is the first thing to rule out?

A

Prostate

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15
Q

If a woman presents with obstructive causes of AKI, what is the first thing to rule out?

A

Gynaecological tumour

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16
Q

What are the categories of acute tubular necrosis?

A
  • ischaemic

* Toxic

17
Q

What is the most common intrinsic AKI cause?

A

Acute tubular necrosis

18
Q

What drug can affect the glomeruli causing an AKI?

A

Gentamicin

19
Q

What are the tubular renal causes of AKI?

A
  • Tubulo-interstitial nephritis

* Rhabdomyolysis

20
Q

What is the cause of acute tubular necrosis?

A
  • Any pre-renal cause of AKI if severe/of sufficient duration
  • Under perfusion of the tubules and/or direct toxicity
  • Hypotension
  • Sepsis
  • Toxins
  • Can be all 3 of above
21
Q

What is the prognosis of acute tubular necrosis?

A
  • It is usually reversible
  • 10-15% won’t recover renal function
  • A further 10-15% will have chronic renal impairment following ATN putting them at risk of progressive kidney disease
22
Q

Describe the histology of acute tubular necrosis

A
  • Focal loss of tubular epithelial cells
  • Partial occlusion of tubular lumens by cellular debris
  • In recovery phase: multiple mitoses indicative of regenerating tubular cells
23
Q

What are the exogenous toxins causing ATN?

A
  • Drugs (e.g. NSAIDs, gentamicin, ACEi)
  • Contrast
  • Poisons (e.g. metals, anti-freeze)
24
Q

What are the endogenous toxins causing AKI?

A
  • Myoglobin e.g. rhabdomyolysis
  • Haemoglobin
  • Immunoglobins
  • Calcium
  • urate
25
Q

Explain how glomerular perfusion is maintained in a state of hypovolaemia

A
  • Blood pressure drops
  • Afferent arteriole dilates in response to prostaglandins
  • Efferent arteriole constriction under regulation of angiotensin II
26
Q

Which medications should you stop and why in cases of reduced glomerular filtration pressure in a state of hypovolaemia

A
  • ACEi/ARBs as they inhibit angiotensin II which constricts the efferent arteriole
  • NSAIDs as they inhibit prostaglandins which dilate the afferent arteriole
27
Q

What should you measure to manage AKI?

A
  • Bloods - U+Es
  • Potassium - if elevated worry about cardiac arrest
  • Urine output
  • Assess fluid status: BP, JVP, oedema, heart sounds
28
Q

Explain the treatment of AKI

A

•Commence immediately
•Airway and breathing
•Circulation- shock, restore renal perfusion
- hyperkalaemia, pulmonary oedema
•Remove the causes: drugs, sepsis
• Exclude obstruction and consider the renal causes (are the pre-renal causes sufficient to account for AKI?)

29
Q

Describe the diagnostic process of AKI?

A
  • History and examination (sepsis, rash, haemoptysis, rhabdomyolysis)
  • Drugs
  • Urinalysis - look for blood/protein
  • Renal ultrasound to look for obstruction and size of kidney
  • GN screen - ANCA, ANA, immunoglobulins+EP, aGBM, Urine bench jones protein
  • Other: blood film, LDH, CK, check viral status etc.
30
Q

What are the signs of chronic kidney disease on ultrasound?

A
  • Small kidneys

* loss of corticosteroids-medullary differentiation

31
Q

Describe the effects of potassium on treatment in AKI

A
  • K<6: abnormal but no immediate concern
  • K= 6-6.4: risk of arrhythmia, needs treatment urgently especially if ECG changes
  • K>6.5 is a medical emergency
32
Q

What is the treatment of hyperkalemia?

A
  • Reduce absorption from the gut - calcium resonium 15g 4x day orally
  • Insulin 10-15 units actracpid and 50ml 50% dextrose to move potassium into the cells (risk of hypoglycaemia, watch blood glucose)
  • Calcium glutinate 10ml 10% as cardiac membrane stabiliser
33
Q

What should you do in a patient with raised potassium and lowered HCO3

A

if HCO3<16 it is worth bicarb supplementation: IV NaBicarb 1.26&

34
Q

What are the two absolute indications for dialysis?

A
  • Refractory potassium >/6.5mmol/l

* Refractory pulmonary oedema

35
Q

What are the relative indications for dialysis?

A
  • Acidosis (pH<7.1)
  • Uraemia (esp if urea >40)
  • Toxins (lithium, ethylene glycol etc)
36
Q

Describe the recovery period from acute tubular necrosis

A
  • Often a polyuric phase for 48-72 hours
  • May be up to 6l of urine a day
  • Often subsequent low K, Ca, Mg as low quality urine
  • Tubules fail to concentrate urine

Week 12 - Nephrology and urology (14 decks)

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