Acute kidney injury (URO) Flashcards

1
Q

Define acute kidney injury (AKI).

A

Acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output (dysregulation of fluid balance and electrolytes, and retention of nitrogenous waste products)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some risk factors of AKI? (8)

A
  • age >65
  • Hx of:
    • CKD
    • HF
    • liver disease
    • diabetes
    • multiple myeloma
    • contrast administration
    • NSAIDs/ACEi’s or ARBs/diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three types of AKI?

A
  • prerenal - any condition that leads to decreased renal perfusion –> low urinary sodium (anything impairing blood supply to kidney)
  • intrinsic (intrarenal) - any condition that leads to severe direct kidney damage –> high urinary sodium
  • postrenal - any condition that results in bilateral obstruction of urinary flow from renal pelvis to urethra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is prerenal AKI commonly associated with? (3)

A

Sepsis, hypovolaemia and/or hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is intrinsic AKI commonly associated with? (3)

A
  • nephrotoxins like aminoglycoside Abx (e.g. gentamicin) and NSAIDs
  • rare causes include vasculitis or interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is postrenal AKI commonly associated with?

A

Urinary outflow obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some prerenal causes of AKI? (5)

A
  • hypovolaemia - haemorrhage, diarrhoea, vomiting
  • hypotension - shock, sepsis, anaphylaxis
  • heart failure
  • renal artery stenosis (investigate with magnetic resonance angiography MRA, asymmetrical kidneys, avoid ACEi)
  • drugs - e.g. NSAIDs, ACEi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the serum urea:creatinine ratio in prerenal AKI?

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some causes of intrinsic AKI? (6 + 4)

A
  • acute tubular necrosis (most common)
  • acute interstitial nephritis (drug-induced)
  • haemolytic uraemic syndrome (vascular)
  • thrombolytic thrombocytopenia purpura (vascular)
  • glomerulonephritis
  • membranous nephropathy (adult nephrotic syndrome - proteinuria, hypoalbuminemia, hyperlipidaemia etc)
  • vasculitides, eclampsia, rhabdomyolysis, tumour lysis syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common cause of intrinsic AKI seen in clinical practice?

A

Acute tubular necrosis - damage to tubular cells due to ischaemia (shock or sepsis) or nephrotoxins (contrast or aminoglycosides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe ischaemic acute tubular necrosis (intrarenal AKI).

A

Damage to tubular cells due to prolonged and severe ischaemia:

  • shock
  • heart failure
  • renal artery stenosis
  • excessive GI fluid loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give examples of endogenous toxins that can cause acute tubular necrosis (intrarenal AKI)? (3)

A
  • myoglobin from rhabdomyolysis (raised CK)
  • uric acid from tumour lysis syndrome
  • monoclonal light chains from multiple myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give examples of exogenous toxins that can cause acute tubular necrosis (intrinsic AKI)? (5)

A
  • aminoglycosides e.g. gentamicin
  • NSAIDs
  • cisplatin
  • contrast agents
  • anti-freeze
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is seen on microscopy of acute tubular necrosis (intrinsic AKI)?

A

Muddy brown granular casts in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe urine sodium and osmolality in acute tubular necrosis (intrinsic AKI)?

A

High urine sodium
Low urine osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common drug-induced cause of intrinsic AKI?

A

Acute interstitial nephritis - caused by penicillin/Abx or NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some systemic symptoms of acute interstitial nephritis (intrinsic AKI)? (4)

A
  • fever
  • arthralgia
  • rash
  • eosinophilia (allergic-type reaction –> type IV hypersensitivity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What might you find on urinalysis, urine dip and bloods of acute interstitial nephritis (intrinsic AKI)?

A
  • urinalysis: white cell casts because an immune reaction is occurring
  • urine dip: leukocytes +++
  • bloods: raised IgE, eosinophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

List two types of vascular disease causing intrinsic AKI. (2)

A
  • haemolytic uraemic syndrome (HUS)
  • thrombotic thrombocytopenia purpura (TTP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the clinical features of haemolytic uraemic syndrome (intrinsic AKI)? (3)

A
  • haemolytic (normocytic) anaemia - jaundice, schistocytes
  • thrombocytopenia - petechiae, purpura
  • AKI following blood diarrhoeal illness - due to Shiga-toxin producing E.coli O157:H7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the management for haemolytic uraemic syndrome (HUS - intrinsic AKI)?

A

Supportive management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is thrombotic thrombocytopenia purpura (TTP -intrinsic AKI)?

A

Abnormally large and sticky multimers of VWF cause platelets to clump within vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List clinical features of thrombotic thrombocytopenia purpura (TTP - intrinsic AKI)? (3)

A
  • overlap with HUS (haemolytic anaemia, thrombocytopenia)
  • fever
  • neurological signs - headache, confusion, seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is thrombotic thrombocytopenia purpura (TTP) measured? (2)

A
  • plasmapheresis
  • rituximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the two ways that glomerulonephritis (intrinsic AKI) can present? (2)

A
  • nephrotic syndrome (proteinuria)
  • nephritic syndrome (haematuria)
26
Q

List some causes of postrenal AKI. (4)

A
  • kidney stones
  • BPH
  • external compression of ureter e.g. due to tumour
  • neurogenic bladder due to MS, spinal cord lesions or peripheral neuropathy
27
Q

What is the criteria used to stage AKI?

A

KIDIGO criteria

  • stage 1:
    • creatinine rise of 1.5x baseline OR
    • creatinine rise of >=26pmol/L in 48h OR
    • urine output <0.5ml/kg/hour for 6 hours
  • stage 2:
    • creatinine rise of 2x baseline OR
    • urine output <0.5ml/kg/hour for 12 hours
  • stage 3:
    • creatinine rise of 3x baseline OR
    • urine output <0.3ml/kg/hour for 24 hours OR
    • anuria for 12 hours OR
    • serum creatinine >354 pmol/dl
28
Q

What are the clinical features of AKI? (6)

A
  • decreased urine output –> oliguria (reduced) or anuria (absence)
  • signs of volume depletion (prerenal AKI) - hypotension, tachycardia, reduced skin turgor, orthostatic hypertension, thirst
  • signs of fluid overload (Na+ and H2O retention) - peripheral/pulmonary oedema, hypertension, HF, SOB
  • signs of uraemia (due to failure of kidneys to excrete urea) - anorexia, nausea, encephalopathy, asterixis, pericarditis
  • signs of renal obstruction (postrenal AKI) - distended bladder (suprapubic distension), lower urinary tract symptoms due to incomplete voiding, pain over bladder or flanks, haematuria
  • arrhythmias due to hyperkalaemia (–> muscle weakness, paraesthesia)
29
Q

What are the clinical signs of volume depletion in prerenal AKI? (5)

A
  • hypotension
  • tachycardia
  • reduced skin turgor
  • orthostatic hypotension
  • thirst
30
Q

What are the clinical signs of fluid overload in AKI? (4)

A
  • peripheral or pulmonary oedema
  • hypertension
  • HF
  • SOB
31
Q

What are the clinical signs of uraemia in AKI? (5)

A
  • anorexia
  • nausea
  • encephalopathy
  • asterixis
  • pericarditis
32
Q

What are the clinical signs of renal obstruction in postrenal AKI? (4)

A
  • distended bladder (suprapubic distension)
  • incomplete voiding –> overload –> lower urinary tract symptoms
  • pain over bladder or flanks
  • haematuria
33
Q

What arrhythmia can occur in AKI and what are some clinical features of this? (1 + 2)

A

Hyperkalaemia

  • muscle weakness
  • paraesthesia
34
Q

In AKI, what can fever, rash and arthralgia be a sign of?

A

Small-vessel vasculitis or (acute) interstitial nephritis - intrinsic AKI

35
Q

What are the 1st line investigations for AKI? (8)

A
  • U&Es
  • creatinine
  • LFTs
  • serum potassium
  • FBC
  • bicarbonate
  • urinalysis (dipstick)
  • VBG/ABG
36
Q

What will investigations generally show if AKI? (3)

A
  • increase in serum creatinine
  • decrease in urine output
  • hyperkalaemia
37
Q

When is hyperkalaemia considered severe? (2)

A
  • if K+>6.5 OR
  • ECG changes:
    • tall tented T-waves
    • loss of P waves
    • broad QRS complexes
38
Q

What does blood on urinalysis indicate (AKI)?

A

Nephritic cause

39
Q

What does leukocyte esterase and nitrites on urinalysis indicate?

A

UTI

40
Q

What does glucose on urinalysis indicate?

A

Osmotic diuresis

41
Q

What does protein on urine dipstick indicate?

A
  • rules out prerenal and postrenal causes of AKI
  • indicates intrinsic cause - glomerular disease
42
Q

What will acute ischaemic necrosis show on a urine dipstick?

A

Leukocytes +++

43
Q

What does glomerulonephritis show on urine dipstick?

A

Positive blood

44
Q

What do you see on blood film in haemolytic uraemic syndrome?

A

Schistocytes

45
Q

What do you do after initial investigation if no obvious cause of AKI can be found?

A

Renal ultrasound to look for obstruction in postrenal AKI

46
Q

What can VBG/ABG show in suspected AKI?

A

An anion gap metabolic acidosis is seen in AKI due to impaired excretion of non-volatile acids

47
Q

What can cause false positive creatinine rises? (2)

A
  • use of trimethoprim
  • serum creatinine falls during pregnancy so rise after recent delivery may be false +ve
48
Q

What are some differential diagnoses for AKI?

A
  • CKD (hypocalcaemia, small kidneys US)
  • HUS (AKI+haemolytic anaemia+thrombocytopenia)
  • rhabdomyolysis (falls, seizures)
  • pre-renal uraemia
  • acute tubular necrosis
  • nephritic syndromes (sudden onset haematuria, oliguria, hypertension, oedema)
  • nephrotic syndrome (proteinuria, hypoalbuminemia, oedema, no haematuria)
  • increased muscle mass
  • drug side effects (cimetidine, trimethoprim)
  • orthostatic proteinuria
49
Q

What is the general 1st line management plan for AKI? (5)

A
  • stop nephrotoxic substances
  • manage volume status (hypovolaemia or hypervolaemia)
  • treat hyperkalaemia
  • patient may require catheterisation if postrenal AKI
  • identify and treat underlying cause of AKI
50
Q

What nephrotoxic substances are stopped in AKI? (4)

A

DAMN substances:

  • diuretics
  • ACEi & aminoglycosides (gentamicin)
  • metformin if eGFR<45 (does not worsen AKI but can accumulate –> lactic acidosis)
  • NSAIDs
51
Q

What NSAID can be continued in AKI?

A

Aspirin at cardio-protective doses i.e. 75mg to prevent cardiovascular events

52
Q

How can we manage hypovolaemic (pre-renal) AKI?

A
  • immediate IV fluid resuscitation with 500mL bolus IV fluid over 15mins
  • if hyperkalaemia >5.5 or suspected (e.g. rhabdomyolysis): normal saline at 0.9% NaCl
  • if still hypotensive: vasopressors (IV norepinephrine)
53
Q

How can we manage hypervolaemic AKI?

A
  • loop diuretic e.g. furosemide
  • sodium and fluid restriction
  • renal replacement therapy (dialysis) if these do not work
54
Q

How can we manage different stages of hyperkalaemia in AKI?

A
  • mild (5.5-5.9mmol/L): identify and treat underlying cause, CONSIDER cation-exchange resin/polymer
  • moderate (6.0-6.4 and normal ECG): PLUS insulin (Actrapid)+dextrose to drive K+ into cells
  • severe (>6.5 or ECG changes): PLUS calcium chloride/gluconate (IV gluconate 10% 30mL to stabilise cardiac membrane) PLUS salbutamol
55
Q

What can remove potassium from the body in hyperkalaemia (AKI)?

A

Calcium resonium

56
Q

What do we consider in patients with AKI and metabolic acidosis?

A

Sodium bicarbonate

57
Q

How do we manage hypervolaemic AKI with pulmonary oedema? (3)

A
  • upright position
  • high-flow oxygen
  • glyceryl trinitrate (GTN)
58
Q

What are the indications for renal replacement therapy (haemodialysis) in AKI? (5)

A
  • refractory metabolic acidosis
  • refractory hyperkalaemia
  • refractory pulmonary oedema
  • refractory hypervolaemia
  • uraemia (complications e.g. pericarditis/encephalopathy)
  • (NB refractory = non-responsive to treatment)
59
Q

What is an acronym we can use that indicates whether referral for renal replacement therapy in AKI is needed?

A

AEIOU BLAST

  • Acidosis (pH<7.2 or HCO3<10)
  • Electrolyte (persistent hyperkalaemia i.e. >7mmol/L)
  • Intoxication (OD of Barbiturates, Lithium, Alcohol, Salicylates, Theophylline)
  • Oedema (pulmonary that is refractory)
  • Uraemia (urea>40 or complications e.g. encephalitis)
60
Q

What are some complications of AKI? (5)

A
  • hyperkalaemia
  • hyperphosphatemia
  • uraemia
  • chronic progressive kidney disease
  • end-stage kidney disease
61
Q

What can cause AKI in elderly patients?

A

A ‘long lie’ following a fall = prolonged immobility –> rapid breakdown of muscles –> myoglobulin products that are toxic to glomerulus –> AKI

Raised CK = rhabdomyolysis

62
Q

What is an electrolyte difference between AKI and CKD?

A

Both can have hyperkalaemia (due to impaired K+ excretion) but CKD often has hypocalcaemia too (lack of 1-a-hydroxylase)