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Urinary > AKI > Flashcards

AKI Flashcards

1
Q

Define AKI

A
  1. increase in serum creatinine by 26.5 micromol/L within 48 hours
  2. increase in serum creatinine by 1.5x basline within 7 days
  3. urine volume <0.5ml/kg/hour for 6 hours
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2
Q

what are the 3 mechanisms leading to AKI?

A

pre-renal failure
intrinsic renal failure
post-renal failure

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3
Q

what is pre-renal AKI caused by?

A

reduction in renal perfusion

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4
Q

what causes AKI?

A

when responses: myogenic response (afferent & efferent arterioles) & tubular glomerular (NaCl in DCT) feedback are overwhelmed

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5
Q

what happens to myogenic response & tubular glomerular feedback in hypoperfusion? (pre-renal)

A

dilation of afferent arterioles with some constriction of efferent

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6
Q

what are the main causes of pre-renal AKI?

A

reduced extracellular fluid volume

impaired renal autoregulation

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7
Q

what are the main causes of reduced extracellular fluid volume leading to pre-renal AKI?

A

hypovolaemia
cardiac failure
systemic vasodilation

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8
Q

what are the main causes of impaired renal autoregulation leading to pre-renal AKI?

A

afferent constriction

efferent dilation

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9
Q

what are causes of hypovolaemia?

A

dehydration

massive blood loss

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10
Q

what are causes of cardiac failure?

A

dysfunction of left ventricle

valve disease

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11
Q

what is a cause of systemic vasodilation?

A

sepsis

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12
Q

what are causes of afferent constriction leading to impaired renal autoregulation, and therefore pre-renal AKI? (decrease GFR)

A

sepsis (hypoperfusion of main organs)
hypercalcaemia (vasoconstrict vascular SM)
NSAIDS (block prostaglandins COX pathway)

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13
Q

what is a cause of efferent dilation leading to impaired renal autoregulation and therefore pre-renal AKI? (decreases GFR)

A

ACE-inhibitors (normally AT-II potent vasoconstrictor, also breaksdown bradykinin - vasodilator)

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14
Q

When does (ATN) acute tubular necrosis develop?

A

ATN occurs when pre-renal AKI not treated with fluids rapidly (most pre-renal AKI & ATN reversible)

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15
Q

what is ATN?

A

not strictly necrosis, but cellular damage that leads to inability to absorb NaCl (nephron) and so reduced water reabsorption and therefore volume depletion

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16
Q

what is a risk of aggressive fluid resuscitation?

A

volume overload risk

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17
Q

what are the main tubular sites of injury in ATN?

A

zone between cortex and medullar (susceptible to hypoxia) - especially S3 of PCT and TaL (and also high O2 demand)

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18
Q

what happens in pre-renal AKI due to decrease in renal blood flow??

A

actual GFR decreases
no cell damage, kidneys work hard (acidly reabsorb NaCl & H2O via RAAS & ADH release) to try and restore blood flow

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19
Q

how do you treat pre-renal AKI?

A

fluid resuscitation (increase blood volume to try and increase perfusion to increase GFR)

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20
Q

who are more likely to develop ATN?

A

patients who develop AKI who are also taking a nephrotoxic agent

21
Q

what are nephrotoxins?

A

damage to epithelial cells lining tubules

leading to cell death which sheds in the lumen

22
Q

what are the different types of nephrotoxins?

A

endogenous & exogenous

23
Q

what are examples of endogenous nephrotoxins?

A

myoglobin
nitrate
bilirubin

24
Q

what are examples of exogenous nephrotoxins?

A

endotoxin
x-ray contrast
drugs (ACE-I / NSAIDS)
other poisons (weed killers / antifreeze)

25
Q

what is rhabdomyolysis?

A

endogenous nephrotoxin
muscle necrosis from crush injury (trauma to muscle)
releases myoglobin which is filtered at glomerulus & is toxic to tubule cells

26
Q

Aside from nephrotoxins, what are other causes of intrinsic AKI?

A
  1. acute tubulo-interstitial nephritis

2. glomerular & arteriolar disease (acute glomerulonephritis)

27
Q

what is acute glomerulonephritis (glomerular & arteriolar disease)?

A

immune disease affecting glomeruli

28
Q

what are the causes of acute glomerulonephritis?

A

primary - only affects kidney

secondary - kidneys affected as part of systemic process

29
Q

what is an example of primary acute glomerulonephritis?

A

IgA nephropathy (intrinsic AKI)

30
Q

what are examples of secondary acute glomerulonephritis?

A

SLE

vasculitis (destroy blood vessels by inflammation)

31
Q

what is acute tubulo-interstitial nephritis?

A

inflammation of the interstitium surrounding the filtration apparatus

32
Q

what are causes of acute tubulo-interstitial nephritis?

A

infection

toxins

33
Q

what is an infection cause of acute tubulo-interstitial nephritis?

A

acute pyelonephritis (sudden and severe kidney infection, causes the kidneys to swell and may permanently damage them) - intrinsic AKI

34
Q

what does acute tubulo-interstitial nephritis look like under the microscope?

A

lots of infiltration of cells between glomerulus

35
Q

what is a toxic cause of acute tubulo-interstitial nephritis?

A

drugs e.g. antibiotics (gentamicin), NSAIDS, PPI

36
Q

what is the pathophysiology of post-renal failure?

A

(both kidneys blocked / only 1 functioning kidney)
obstruction of urine outflow tract with continuous urine production, leading increase intraluminal pressure (within urinary tubes) –> dilation of renal pelvis (hydronephrosis), decreasing renal function

37
Q

what are classifications of causes of post-renal AKI?

A

within the lumen
within the wall
pressure from outside

38
Q

what are causes of post-renal AKI from within the lumen?

A

kidney, ureter, bladder

e.g. stones, blood clot, tumour

39
Q

what are causes of post-renal AKI from within the wall?

A

stricture (post TB), congenital megaureter

usually CKD

40
Q

what are causes of pressure from outside leading to post-renal AKI?

A

enlarged (hypertrophy) prostate
tumour
aortic aneurysm
ligation of ureter (tying of ureter)

41
Q

how do renal & ureteric stones cause post-renal luminal AKI? (location of stones)

A

stone in BOTH renal pelvis / ureters
obstructing 1 kidney
neck of bladder
urethra

42
Q

stones of which size won’t pass through urinary tract?

A

> 10mm

43
Q

how do patients with renal & ureteric stones present?

A

pain

haematuria

44
Q

which age group is post-renal AKI more common in?

A

elderly (think about prostate enlargement)

45
Q

what are causes of pre-renal failure? (leading to decrease in blood supply via renal artery to kidneys afferent arterioles)

A

HF
cirrhosis
volume depletion

46
Q

what are causes of renal AKI?

A

renal artery / vein occlusion

47
Q

what are causes of renal parenchymal AKI?

A
  1. intrarenal vascular (segmental, interlobar, arcuate, interlobular, afferent, efferent, vasa rectar / peritubular capillaries)
  2. glomerulonephritis
  3. acute tubular necrosis (toxic / ischaemia)
  4. interstitial disease (tissue of kidney)
  5. intrarenal obstruction (struvite stone)
48
Q

what is the main cause of post renal AKI?

A

urinary tract obstruction

e.g. stones, tumour, hypertrophic prostate

49
Q

why is it dangerous for hypertensive patients to be measured against out normal kidney functioning range?

A

hypertensive patient’s baroreceptors are set to a higher setting from prolonged hypertension (>140/90), so their kidney functioning range set to a higher BP

Urinary (13 decks)

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