Session 9 - Acute Kidney Injury Flashcards

1
Q

Give 2 clinical methods for defining AKI

A
  • Increase in serum creatinine by >26.5 umol/L within 48 hours OR
  • Increase in serum creatinine by >1.5 times baseline within 7 days OR
  • Urine volume <0.5 ml/kg/h for 6 hrs - oligouria
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2
Q

What are the 3 main types of AKI?

A

1) Pre-renal 2) Renal 3) Post-renal

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3
Q

What is pre renal AKI? What causes pre renal AKI?

A
  • Reduction in renal perfusion
  • Is a physiological response to renal hypoperfusion

Pre-renal failure can also be caused by a reduction in the effective ECF volume such as in hypovolemia due to blood loss, systemic vasodilation as in anaphylaxis and sepsis, or in cardiac failure.

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4
Q

How can the autoregulatory mechanisms of the renal system be overcome to cause pre renal AKI?

A

o NSAIDS – prevent vasodilation of afferent arteriole

o ACE inhibitors – prevents vasoconstriction of efferent arteriole

o Disease of afferent arteriole – diabetes mellitus, hypertension etc.

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5
Q

What happens in acute tubular necrosis? What is it caused by?

A
  • Ischemia
  • Nephrotoxin
  • Sepsis

ATN – Renal cells damaged, cannot be immediately reversed. Damaged cells cannot reabsorb salt and water efficiently or expel excess water

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6
Q

How would you differentiate between pre renal and ATN? Why does this method work?

A
  • Na+ reabsorbed in pre-renal AKI to restore volume but reduced in renal AKI due to tubular cell damage
  • Can therefore use sodium reabsorption to tell what stage the AKI is in.
  • Fractional Sodium Excretion = (urine Na+/Plasma Na+) / (urine Creatinine / plasma creatinine) x 100
  • In pre-renal the FENa is <1%. In ATN the FENa is >1%.
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7
Q

What is a nephrotoxin?

A

Damage the epithelial cells lining the tubules and cause cell death and shedding into the lumen. Can be endogenous or exogenous e.g. drugs

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8
Q

Give 2 examples of an endogenous nephrotoxin

A

myoglobin, urate, bilirubin

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9
Q

Give 2 examples of an exogenous nephrotoxin

A

drugs (e.g. ace inhibitors, NSAIDs, gentamicin), x-ray contrast, other poisons.

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10
Q

What is rhabdomyolysis and how does it cause AKI? In whom does it occur?

A
  • Muscle necrosis results in large release of myoglobin.
  • Can occur from drug users, elderly, wars, natural disasters
  • Results in AKI
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11
Q

What is acute glomerulonephritis? What forms can it take?

A

o Immune disease affecting the glomeruli

o Can be primary (only affecting kidneys) or secondary (systemic)

o Secondary e.g. systemic lupus erythematosis

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12
Q

How does endothelium damage lead to RBC destruction?

A

o Endothelium damage results in platelet thrombus, which results in partial obstruction of small arteries and the destruction of RBCs

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13
Q

Give the pathology of a post-renal AKI

A

1) Obstruction with continuous urine production results in rise in intraluminal pressure
2) Results in dilatation of renal pelvis
3) Which produces a decrease in renal function

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14
Q

Give the 3 types of post renal AKI

A

1) Obstruction within the lumen
2) Obstruction within the wall
3) Obstruction by pressure from the outside

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15
Q

Give 2 things that can cause an obstruction in the lumen of the ureters

A
  • Stones
  • Blood clots
  • Papillary necrosis – sloughed papillae following infection and ischaemia
  • Tumour of renal pelvis, ureter, bladder
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16
Q

Give 2 causes of post renal AKI within the wall of the ureters

A

Congenital causes:

  • Pelviureteric neuromuscular dysfunction
  • Megaureter – Dilated ureter
  • Neurogenic bladder – lack of bladder control

Non congenital:

• Ureteric stricture e.g. post-TB

17
Q

Give 3 causes of post renal AKI due to pressure from the outside

A
  • Prostatic hypertrophy
  • Tumours
  • Aortic aneurysm
  • Diverticulitis
  • Accidental ligation of ureter
18
Q

What indications in serum biochemistry would occur in AKI?

A

Increased urea and creatinine in all causes of AKI

19
Q

Fill in

A
20
Q

What is a RBC cast?

A

Cylindrical structure in urine made up of RBC

21
Q

How would you treat pre renal AKI?

A
  • Immediate infusion of IV fluids to increase renal perfusion
  • Avoid nephrotoxins
  • Can force alkaline diuresis to remove myoglobin – use a drug to make the urine alkaline to draw out myoglobin
22
Q

How would you treat ATN?

A
  • Prevent volume overload by restricting dietary NA and water intake (<1L per day)
  • Prevent hyperkalaemia – restrict dietary K, Ca gluconate, dextrose and insulin (uptake of K into cells),
  • Prevent acidosis – Protein restriction, sodium bicarbonate infusion
23
Q

When would you use dialysis for ATN?

A
  • Metabolic acidosis where sodium bicarbonate infusion is not appropriate
  • Fluid overload refractory to diuretics
  • Presence of dialyzable nephrotoxin
  • High K+ refractory to treatment (not treatable with treatment due to refractory period)
24
Q

What are the 3 main types of proteinuria? Define them

A

1) Glomerular proteinuria – An increase in the permeability of the glomerulus to protein due to damage of the bowman’s capsule
2) Tubular proteinuria – Tubulointersitial disease impairs reabsorption of low molecular weight proteins at the PCT
3) Overflow proteinuria – Overproduction of smaller proteins leads to a rate of filtration that exceeds the transport maximum for reabsorption at the PCT.

25
Q

Define nephrotic syndrome

A

Defined as proteinuria sufficient to cause hypoalbuminaemia and hence peripheral oedema. Proteinuria needs to exceed 5g/24hr.

26
Q

Describe how lowered oncotic pressure can lead to oedema in 2 ways

A

1) Lowered oncotic pressure –> oedema
2) Hypovolemia results which stimulates RAS –> increase in aldosterone production
3) Aldosterone stimulates salt and water retention –> increased oedema.

27
Q

What is nephrological and urological haematuria?

A

Nephrological haematuria – results from glomerular inflammation and bleeding

Urological haematuria – Due to renal stones, renal cell carcinoma, tubular cell carcinoma

28
Q

What features would suggest nephrological as opposed to urological haematuria? Give 3 things

A

o Abnormal renal function

o Proteinuria

o Salt and water retention

o Hypertension

o Young age (uroepithelial malignancy unlikely)

29
Q

What 2 urinary features would you find in glomerulonephritis?

A
  • Dysmorphic red cells
  • Red cell cast