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SA urinary > S10) Acute Kidney Injury > Flashcards

S10) Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A
  • AKI is a clinical syndrome wherein there is an abrupt decline in actual GFR (days to weeks)
  • urea and creatine rise rapidly
  • associated with oliguria (no urine) or anuria (no urine)
  • usually reversible but not always
  • This disrupts homeostasis (ECF volume, electrolyte and acid-base) and leads to an accumulation of nitrogenous waste products
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2
Q

In terms of laboratory findings, provide three definitions of AKI

A
  • 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 <0.5 ml/kg/h for 6 hours
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3
Q

Define Stage 1 AKI in terms of serum creatinine and urine output

A
  • Serum Cr criteria: ↑ Cr ≥ 1.5- 2x from baseline
  • Urine output criteria: <0.5 mL/kg/hr for >6 h
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4
Q

Define Stage 2 AKI in terms of serum creatinine and urine output

A
  • Serum Cr criteria: ↑ Cr > 2-3x from baseline
  • Urine output criteria: <0.5 mL/kg/h for >12 h
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5
Q

Define Stage 3 AKI in terms of serum creatinine and urine output

A
  • Serum Cr criteria: ↑ Cr >3x from baseline or initiated on RRT
  • Urine output criteria: <0.3 mL/kg/h for 24 h or anuria for 12 h
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6
Q

Identify the three causes of AKI

A
  • Pre-renal failure (volume responsive)
  • Intrinsic renal failure
  • Post-renal failure
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7
Q

Describe the epidemiology of AKI in high income countries in terms of:

  • Typical patients
  • Location
  • Causes
  • Treatment
A
  • Patients: older people
  • Location: hospital-acquired AKI
  • Causes: dehydration and hypotension
  • Treatment: dialysis withheld most commonly due to futility
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8
Q

Describe the epidemiology of AKI in low income countries in terms of:

  • Typical patients
  • Location
  • Causes
  • Treatment
A
  • Patients: younger people (often children)
  • Location: community-acquired AKI
  • Causes: dehydration, hypotension, obstetric causes, snake and insect bites
  • Treatment: dialysis withheld due to lack of resources
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9
Q

In 6 steps, outline the pathophysiology of pre-renal AKI

A

⇒ Decreased renal blood flow

⇒ Reduced actual GFR

⇒ Kidneys work hard to restore blood flow (no cell damage)

⇒ Reabsorb Na+ & H2O (aldosterone, ADH release)

⇒ If mild hypoperfusion, autoregulation preserves renal blood flow

⇒ If overwhelmed compensatory responses, AKI occurs

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10
Q

Explain how prescription drugs can affect renal perfusion

A
  • NSAIDS and ACEi can override intrinsic autoregulatory mechanisms
  • Disease of the afferent arteriole (BP, DM) can result in too great or too little a response to these stimuli
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11
Q

Describe the causes of pre-renal AKI in terms of:

  • Reduced effect arterial blood volume
  • Impaired renal autoregulation
A
  • Reduced effective arterial blood volume:

I. Hypovolaemia

II. Systemic vasodilation – sepsis, cirrhosis, anaphylaxis - too low a blood pressure

III. Cardiac failure

- Impaired renal autoregulation:

I. Pre-glomerular vasoconstriction – sepsis, NSAIDs

II. Post-glomerular vasodilatation – ACEi, ARBs

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12
Q

Acute tubular necrosis is volume unresponsive AKI.

Identify three of its causes

A
  • Ischaemia (depletion of cellular ATP)
  • Nephrotoxins
  • Sepsis
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13
Q

Describe the pathophysiology of ATN (acute tubular necrosis)

A

⇒ Death of tubular epithelial cells

⇒ Damaged cells cannot reabsorb / expel excessive H2O efficiently

⇒ Aggressive fluid resuscitation risks fluid overload

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14
Q

Describe the course of renal blood flow

A
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15
Q

Identify the sites of tubular injury in ATN

A
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16
Q

Compare and contrast the urinary biochemistry of Pre-renal AKI and ATN in terms of:

  • Specific gravity
  • Osmolality
  • Urinary Na+
A
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17
Q

ATN is much more likely if there is reduced perfusion and a nephrotoxin.

What do nephrotoxins do?

A

Nephrotoxins damage the epithelial cells lining the tubules and cause cell death

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18
Q

Nephrotoxins can be endogenous or exogenous.

Identify some examples of each

A
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19
Q

What is rhabdomyolysis?

A
  • Rhabdomyolysis is a serious syndrome due to a direct or indirect muscle injury e.g. crush injury
  • Muscle necrosis cases releases of myoglobin into the bloodstream
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20
Q

When is rhabdomyolysis likely to occur?

A
  • AKI in wars / natural disasters (earthquakes)
  • Drug users (unconscious so don’t move)
  • Elderly (fall & can’t get up)
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21
Q

Explain the association of rhabdomyolysis with AKI

A
  • Released myoglobin is filtered at the glomerulus and toxic to tubule cells
  • Released myoglobin can also cause renal obstruction
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22
Q

What is myoglobinuria and how does it present?

A

Myoglobinuria is the presence of myoglobin in the urine usually associated with rhabdomyolysis or muscle destruction

23
Q

Besides ATN, identify two other intrinsic renal causes of AKI

A
  • Thrombotic microangiopathy
  • Acute (tubule)-interstitial nephritis
24
Q

Identify 4 clinical conditions which present with thrombotic microangiopathy

A
  • Haemolytic uraemic syndrome
  • Malignant hypertension
  • Scleroderma
  • Pre-eclampsia
25
Q

In 5 steps, explain how thrombotic microangiopathy leads to microangiopathic haemolytic anaemia

A

⇒ Endothelial damage

⇒ Platelet thrombi

⇒ Partial obstruction of small arteries

⇒ Destruction of RBC’s

⇒ Microangiopathic haemolytic anaemia occurs

26
Q

Identify and describe the two causative mechanisms of acute interstitial nephritis

A
  • Toxin induced: antibiotics, NSAID’s, PPI’s
  • Infections: due to inflammatory response (not direct effect of infection)
27
Q

Post-renal failure accounts for 5 - 10% of AKI cases.

How does it occur?

A
  • Occurs commonly in elderly
  • Obstruction must block both kidneys or a single functioning kidney
28
Q

Describe the pathophysiology of post-renal AKI

A

⇒ Obstruction with continuous urine production

⇒ Rise in intraluminal pressure

⇒ Dilatation of renal pelvis (hydronephrosis)

⇒ Decrease in renal function

29
Q

Identify and describe the three different causes of post-renal AKI

A
  • Within the lumen (kidney, ureter, bladder) – stones, blood clot, tumours
  • Within the wall (usually cause CKD rather than AKI) – congenital megaureter, post-TB stricture
  • Pressure from outside – enlarged prostate, tumour, aortic aneurysm
30
Q

Identify 5 clinical signs in serum biochemistry which are indicative of AKI

A
  • Metabolic acidosis
  • Hyperkalaemia
  • Hyponatraemia
  • Hypocalcaemia
  • Hyperphosphataemia
31
Q

In 3 steps, describe how metabolic acidosis occurs in AKI

A

⇒ Reduction in GFR

⇒ Impaired reabsorption & regeneration of HCO3-

⇒ Impaired acid excretion

32
Q

Identify and describe 4 causes of hyperkalaemia

A
  • Excessive intake
  • Movement out of cells (acidosis / tissue damage)
  • Reduced urine loss (reduced GFR, reduce distal deliver of Na+, reduced secretion)
  • Drugs (ACE-Inhibitors, spironolactone, NSAIDs, trimethoprim, amiloride)
33
Q

Can cause life-threatening cardiac arrhythmias.

Identify 5 clinical signs on an ECG that indicate hyperkalaemia

A
  • Tall T waves
  • Small/absent P waves
  • Increased P-R interval
  • Wide QRS complex
  • Asystole
34
Q

Identify and describe the 5 investigations used for AKI

A
  • Urinalysis (blood, protein, leucocytes)
  • Urine microscopy
  • CXR (fluid overload ± infection)
  • Ultrasound scan (only for obstruction – within 24 hours)
  • Kidney biopsy (systemic inflammatory symptoms/ igns)
35
Q

In terms of volume overload and hyperkalaemia, outline the management of AKI

A
  • Volume overload – restrict dietary Na+ / water < 1L/day
  • Hyperkalaemia – calcium gluconate, restrict dietary K+, stop K+-sparing diuretics, ACEi, ARB
36
Q

What are the 5 indications for dialysis?

A
  • Hyperkalaemia (refractory to treatment)
  • Fluid overload (refractory to diuretics)
  • Metabolic acidosis (NaHCO3- not appropriate)
  • Signs of uraemia (pericarditis, reduced consciousness)
  • Dialysable nephrotoxin e.g. aspirin overdose, ethylene glycol
37
Q

How can one prevent AKI?

A
  • Identify risk factors
  • Monitor ‘at risk’ patients closely
  • Ensure adequate hydration
  • Avoid nephrotoxins
  • Detect early and identify cause
38
Q

Identify 5 risk factors for AKI in terms of susceptibility

A
  • Advanced age
  • CKD
  • Heart disease
  • Liver disease
  • Diabetes Mellitus
39
Q

Identify 5 risk factors for AKI in terms of exposure

A
  • Dehydration
  • Sepsis
  • Burns / trauma
  • Cardiac surgery
  • Nephrotoxins (NSAIDS, ACE-I, ARB)
40
Q

what are the 4 main complications of an AKI

A
  • Metabolic Acidosis
  • hyperkalemia
  • volume overload
  • uraemia
41
Q

what investigation can be taken at the beside

A
  • bladder scan
  • urinalysis
  • microscopy culture and specimen
42
Q

what bloods can be taken from a patient

A
  • VBG - to show if the patient is becoming acidotic
  • CK - breakdown of muscle
    • immunology screening - see if its autoimmune
43
Q

what imaging could be done

A
  • USS KUB
  • CT

both to show is there is any post renal cause

  • CXR - to show is there is any pulmonary oedema
44
Q

what procedures can be carried out

A
  • nephrostogram
  • cystoscopy (procedure to look into the bladder)
45
Q

what is the management for pre renal hypovolemia

A
  • IV fluid replacement to correct hypovolameia and optimise renal blood flow
  • hold nephrotoxic medication
  • diuretics
46
Q

management of renal hypovolemia

A

correct electrolytes

renal replacement therapy

47
Q

management of post renal issues

A
  • urinary or supra pubic catheter
  • ureteric stents to open the ureter
  • nephrostomy - tube in renal pelvis
48
Q

what is a nephrostomy

A
  • urine is backed up in the ureter
  • so urine is drained out via a bag that is attached to the kidney
49
Q

post renal causes

A
  • calculus → renal stone
  • ureteric stricture → scarring in the ureter due to a stone
  • Benign prostatic hyperplasia → prostate gland swells so urethra gets squeezed
  • tumour - blocks
  • retro peritoneal blockage - fibrotic tissue
50
Q

left hydronephrosis

A
51
Q

pre renal causes

A

sepsis - systemic vasodilation

hypovolaemia - low blood volume so reduced perfusion

shock - low BP

renal artery stenosis - narrowing

CCF - reduced CO, so reduced blood flow to kidney

NSAIDS - inhibit prostaglandin

ACEi -

52
Q

how does ACEi cause pre renal Aki

A
  • causes vasodilation of the efferent arteriole
  • this causes low perfusion rates
53
Q

left hydronephrosis on X-ray

A

the kidney normally has some black In the middle, but here the kidney is enlarged

54
Q

what does a baseline xray of the kidneys look like

A

the grey diagonal lines coming from the pine are the two posts major muscles

this is also taken on a coronal plane

SA urinary (25 decks)

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