Week 9 - Acute kidney injury Flashcards

1
Q

What is acute kidney injury?

A
  • Clinical syndrome
  • Abrupt decline in actual GFR
  • – Upset of ECF volume, electrolyte and acid/base homeostasis
  • – Accumulation of nitrogenous waste products
  • Defined by:
  • – Increase in serum creatinine by >= 26.5 μmol/L within 48 hours
  • – Increase in serum creatinine by >= 1.5 times baseline within 7 days
  • – Urine volume
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2
Q

How can pre-renal failure cause AKI?

A
  • Volume depletion, heart failure, cirrhosis, etc.
  • Mechanism:
  • – Actual GFR reduced due to decreased renal blood flow
  • – No cell damage so kidneys work harder to restore blood flow
  • – Lots of reabsorption of salt and water
  • Responds well to fluid resuscitation
  • In mild hypoperfusion:
  • – Autoregulation ensures renal blood flow is preserved
  • If compensatory mechanisms are overwhelmed, AKI occurs
  • – May be due to disease of the afferent arteriole can lead to too great or too little response to these stimuli
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3
Q

What are some causes of pre-renal failure?

A
  • Reduced effective extracellular fluid volume
  • – Hypovolaemia (due to blood loss, fluid loss)
  • – Cardiac function (due to LV dysfunction, valve disease, tamponade)
  • – Systemic vasodilatation (due to sepsis, cirrhosis, anaphylaxis)
  • Impaired renal autoregulation
  • – Preglomerular vasoconstriction (due to sepsis, hypercalcaemia, hepatorenal syndrome, drugs [NSAIDS])
  • – Postglomerular vasodilatation (due to ACEi, AIIR antagonists)
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4
Q

What are some causes of intrinsic renal failure?

A
  • Intrarenal vascular
  • Glomerulonephritis
  • – Immune disease affecting the glomeruli
  • – Can be primary (only affects kidney) or secondary (a systemic process)
  • Ischaemic ATN (acute tubular necrosis)
  • Toxin ATN
  • Interstitial disease
  • Intrarenal obstruction
  • Haemolytic uraemic syndrome
  • Malignant hypertension
  • Pre-eclampsia
  • Acute tubulo-interstitial nephritis
  • – Infection: acute pyelonephritis
  • – Toxin induced: many drugs, most common = antibiotics, NSAIDs, PPIs
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5
Q

What are some causes of post-renal failure?

A
  • Within the lumen (kidney, ureter, bladder)
  • – E.g. stones, blood clot, tumours
  • – Stones must be in both renal pelves or ureters, neck of the bladder or urethra
  • Within the wall
  • – E.g. congenital megaureter, stricture post TB
  • Pressure from outside
  • – E.g. enlarged prostate, tumour, aortic aneurysm, ligation of ureter
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6
Q

What are some causes of acute tubular necrosis?

A
  • Ischaemia
  • Nephrotoxins
    — Damage the epithelial cells lining the tubules
    — Cause cell death and shedding into the lumen
    — Endogenous = e.g. myoglobin (due to rhabdomyolysis), urate, bilirubin
    • Rhabdomyolysis: release of myoglobin due to muscle necrosis, crush injury
    • Myoglobin is filtered at the glomerulus and is toxic to tubule cells
    — Exogenous = e.g. endotoxin, s-ray contrast, drugs (ACEi, NSAIDs), other poisons (e.g. weedkillers, antifreeze)
    — ATN is much more likely if there is reduced perfusion and a nephrotoxin
  • Sepsis
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7
Q

What would you expect to see in blood tests for suspected AKI?

A
  • Increased urea
  • Increased creatinine
  • May or may not be present:
  • – Hyperkalaemia
  • – Hyponatraemia
  • – Hypocalcaemia and hyperphosphataemia
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8
Q

What would you look for on an ECG for AKI?

A

To check for signs of hyperkalaemia

  • Tall T waves
  • Small or absent P waves
  • Increased P-R interval
  • Wide QRS complex
  • Sine wave pattern
  • Asystole
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9
Q

What signs are there if blood volume is depleted?

A
  • Cool peripheries
  • Increased pulse
  • Low BP/postural hypotension
  • Low JVP
  • Reduced skin turgor
  • Dry axillae
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10
Q

What signs are there if blood volume is overloaded?

A
  • Gallop rhythm
  • BP (may be high, low or normal)
  • Raised JVP
  • Pulmonary oedema
  • Peripheral oedema
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11
Q

What are some signs of sepsis?

A
  • Pyrexia and rigors
  • Vasodilatation, warm peripheries
  • Bounding pulse
  • Rapid capillary refill
  • Hypotension
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12
Q

What would you see upon urine testing for AKI?

A
  • Detection of blood, protein, leucocytes
  • – Intrinsic renal disease = lots of blood and/or protein
  • – Pre-renal AKI = normal urinalysis, normal microscopy
  • – Glomerulonephritis = proteinuria, haematuria
  • – ATN = normal urinalysis
  • Culture urine if dipstick is positive
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13
Q

If the AKI is due to a urinary tract obstruction, what would you discover from the history and find on examination?

A
  • History: (suspect obstruction in patients with: )
  • – Anuria
  • – Single functioning kidney
  • – Loin pain or suprapubic pain
  • – History of renal stones
  • – History of prostatism or previous pelvic or abdominal surgery
  • Examine for:
  • – Palpable bladder
  • – Pelvic or abdominal masses
  • – Enlarged prostate in men – rectal examination
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14
Q

What are some susceptibilities for AKI?

A
  • Advanced age
  • CKD
  • Heart disease
  • Liver disease
  • Diabetes mellitus
  • Cancer
  • Neurological impairment
  • Previous AKI
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15
Q

What are some exposures for AKI?

A
  • Dehydration or volume depletion
  • Sepsis
  • Critical illness
  • Burns/trauma
  • Cardiac surgery
  • Emergency surgery
  • Neprotoxins
  • Radio-iodinated contrast in last week
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16
Q

How can you prevent AKI?

A
  • Identify risk factors
  • Monitor ‘at risk’ patients closely
  • Ensure adequately hydrated
  • Avoid nephrotoxins
  • Detect early and identify cause
17
Q

How can you manage AKI?

A
  • Volume overload:
  • – Restrict dietary Na
  • – Restrict water (
18
Q

What are some causes of microscopic haematuria?

A
  • Urinary infection
  • Polycystic kidneys
  • Renal stones
  • Renal/bladder tumours
  • Arteriovenous malformations
  • As well as kidney/glomerular disease
19
Q

What is macroscopic haematuria?

A
  • Episodic macroscopic haematuria associated with glomerular disease is often brown or smoky in colour
  • Clots are very unusual in glomerular haematuria
  • Ask about relationship to urinary stream
  • Needs to be distinguished from other causes of red or brown urine:
  • – Haemoglobinuria
  • – Myoglobinuria
  • – Consumption of food dyes
  • Usually painless in glomerular haematuria
  • Commonest glomerular cause is IgA nephropathy
  • – Macroscopic haematuria typically occurs within 24 hours of upper respiratory tract infection
20
Q

What are some symptoms of proteinuria if it is heavy enough?

A
  • Frothy urine
  • Reduced plasma oncotic pressure
  • – Oedema
  • Loss of immunoglobulins
  • – Infection
  • Imbalanced regulators of coagulation cascade
  • – Thromboembolic risk increased
21
Q

How can asymptomatic kidney disease be detected?

A

Detected incidentally by dipstick urinalysis

  • Well person check
  • Employment medical
  • Life insurance medical
  • Etc.
22
Q

What would you find/see in nephrotic syndrome?

A
  • Classic triad of symptoms:
    — Proteinuria
    — Hypoalbuminaemia
    — Oedema
    — + hyperlipidaemia
  • Pathognomonic of glomerular disease
  • Requires renal biopsy for diagnosis
    — To determine the type of glomerular disease
  • Clinical presentation:
    — Muehrcke’s bands
    — Xanthelasma
    — Fat bodies in urine
    o— Oedema/swelling
23
Q

How can nephritic syndrome present?

A
  • Rapid onset
  • Oliguria
  • Hypertension
  • Generalised oedema
  • Haematuria with smoky brown urine
  • Normal serum albumin
  • Variable renal impairment
  • Urine contains blood protein and red cell casts
24
Q

What is nephritic syndrome?

A
  • The classic nephritic syndrome is that which accompanies post-streptococcal glomerulonephritis
  • Can be as a result of other glomerulonephritides
  • Often self-limiting
  • Renal biopsy required for diagnosis
25
Q

What is rapidly progressive glomerulonephritis?

A
  • A clinical situation in which glomerular injury is so severe that renal function deteriorates over days
  • Patients may present as a uraemic emergency with evidence of extrarenal disease
  • Associated with crescenteric glomerulonephritis
  • Anti-neutrophil cytoplasmic antibodies
  • Anti-glomerular basement membrane antibodies
  • Often associated with systemic vasculitis
  • Renal biopsy required for diagnosis