AKI Flashcards
Define AKI
- increase in serum creatinine by 26.5 micromol/L within 48 hours
- increase in serum creatinine by 1.5x basline within 7 days
- urine volume <0.5ml/kg/hour for 6 hours
what are the 3 mechanisms leading to AKI?
pre-renal failure
intrinsic renal failure
post-renal failure
what is pre-renal AKI caused by?
reduction in renal perfusion
what causes AKI?
when responses: myogenic response (afferent & efferent arterioles) & tubular glomerular (NaCl in DCT) feedback are overwhelmed
what happens to myogenic response & tubular glomerular feedback in hypoperfusion? (pre-renal)
dilation of afferent arterioles with some constriction of efferent
what are the main causes of pre-renal AKI?
reduced extracellular fluid volume
impaired renal autoregulation
what are the main causes of reduced extracellular fluid volume leading to pre-renal AKI?
hypovolaemia
cardiac failure
systemic vasodilation
what are the main causes of impaired renal autoregulation leading to pre-renal AKI?
afferent constriction
efferent dilation
what are causes of hypovolaemia?
dehydration
massive blood loss
what are causes of cardiac failure?
dysfunction of left ventricle
valve disease
what is a cause of systemic vasodilation?
sepsis
what are causes of afferent constriction leading to impaired renal autoregulation, and therefore pre-renal AKI? (decrease GFR)
sepsis (hypoperfusion of main organs)
hypercalcaemia (vasoconstrict vascular SM)
NSAIDS (block prostaglandins COX pathway)
what is a cause of efferent dilation leading to impaired renal autoregulation and therefore pre-renal AKI? (decreases GFR)
ACE-inhibitors (normally AT-II potent vasoconstrictor, also breaksdown bradykinin - vasodilator)
When does (ATN) acute tubular necrosis develop?
ATN occurs when pre-renal AKI not treated with fluids rapidly (most pre-renal AKI & ATN reversible)
what is ATN?
not strictly necrosis, but cellular damage that leads to inability to absorb NaCl (nephron) and so reduced water reabsorption and therefore volume depletion
what is a risk of aggressive fluid resuscitation?
volume overload risk
what are the main tubular sites of injury in ATN?
zone between cortex and medullar (susceptible to hypoxia) - especially S3 of PCT and TaL (and also high O2 demand)
what happens in pre-renal AKI due to decrease in renal blood flow??
actual GFR decreases
no cell damage, kidneys work hard (acidly reabsorb NaCl & H2O via RAAS & ADH release) to try and restore blood flow
how do you treat pre-renal AKI?
fluid resuscitation (increase blood volume to try and increase perfusion to increase GFR)
who are more likely to develop ATN?
patients who develop AKI who are also taking a nephrotoxic agent
what are nephrotoxins?
damage to epithelial cells lining tubules
leading to cell death which sheds in the lumen
what are the different types of nephrotoxins?
endogenous & exogenous
what are examples of endogenous nephrotoxins?
myoglobin
nitrate
bilirubin
what are examples of exogenous nephrotoxins?
endotoxin
x-ray contrast
drugs (ACE-I / NSAIDS)
other poisons (weed killers / antifreeze)
what is rhabdomyolysis?
endogenous nephrotoxin
muscle necrosis from crush injury (trauma to muscle)
releases myoglobin which is filtered at glomerulus & is toxic to tubule cells
Aside from nephrotoxins, what are other causes of intrinsic AKI?
- acute tubulo-interstitial nephritis
2. glomerular & arteriolar disease (acute glomerulonephritis)
what is acute glomerulonephritis (glomerular & arteriolar disease)?
immune disease affecting glomeruli
what are the causes of acute glomerulonephritis?
primary - only affects kidney
secondary - kidneys affected as part of systemic process
what is an example of primary acute glomerulonephritis?
IgA nephropathy (intrinsic AKI)
what are examples of secondary acute glomerulonephritis?
SLE
vasculitis (destroy blood vessels by inflammation)
what is acute tubulo-interstitial nephritis?
inflammation of the interstitium surrounding the filtration apparatus
what are causes of acute tubulo-interstitial nephritis?
infection
toxins
what is an infection cause of acute tubulo-interstitial nephritis?
acute pyelonephritis (sudden and severe kidney infection, causes the kidneys to swell and may permanently damage them) - intrinsic AKI
what does acute tubulo-interstitial nephritis look like under the microscope?
lots of infiltration of cells between glomerulus
what is a toxic cause of acute tubulo-interstitial nephritis?
drugs e.g. antibiotics (gentamicin), NSAIDS, PPI
what is the pathophysiology of post-renal failure?
(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
what are classifications of causes of post-renal AKI?
within the lumen
within the wall
pressure from outside
what are causes of post-renal AKI from within the lumen?
kidney, ureter, bladder
e.g. stones, blood clot, tumour
what are causes of post-renal AKI from within the wall?
stricture (post TB), congenital megaureter
usually CKD
what are causes of pressure from outside leading to post-renal AKI?
enlarged (hypertrophy) prostate
tumour
aortic aneurysm
ligation of ureter (tying of ureter)
how do renal & ureteric stones cause post-renal luminal AKI? (location of stones)
stone in BOTH renal pelvis / ureters
obstructing 1 kidney
neck of bladder
urethra
stones of which size won’t pass through urinary tract?
> 10mm
how do patients with renal & ureteric stones present?
pain
haematuria
which age group is post-renal AKI more common in?
elderly (think about prostate enlargement)
what are causes of pre-renal failure? (leading to decrease in blood supply via renal artery to kidneys afferent arterioles)
HF
cirrhosis
volume depletion
what are causes of renal AKI?
renal artery / vein occlusion
what are causes of renal parenchymal AKI?
- intrarenal vascular (segmental, interlobar, arcuate, interlobular, afferent, efferent, vasa rectar / peritubular capillaries)
- glomerulonephritis
- acute tubular necrosis (toxic / ischaemia)
- interstitial disease (tissue of kidney)
- intrarenal obstruction (struvite stone)
what is the main cause of post renal AKI?
urinary tract obstruction
e.g. stones, tumour, hypertrophic prostate
why is it dangerous for hypertensive patients to be measured against out normal kidney functioning range?
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
