Acute Kidney injury PT1 Flashcards
2 measures of a rapid decline in renal function
- rise in serum creatinine
- decrease in urine output
laboratory findings for increase in creatinine
> 26.5 micromol/L witin 48 hours
increase in creatinine above baseline for AKI
> 1.5x within 7 days
decrease in urine for AKI
<0.5 ml/kg/h for 6 hours
3 types of AKI
pre-renal
renal
post-renal
Urea: creatinine ratio for normal and post renal AKI
40-100 : 1
Urea: creatinine ratio for pre-renal AKI
> 100: 1
Urea: creatinine ratio for intrinsic renal damage
<40: 1
what do pre-renal AKIs cause in the body
Azotemia
3 characteristics in prerenal failure
low urine Na
high urine osmolarity
high BUN:cr ratio
causes of prerenal failure (5)
- renal artery stenosis
- NSAID
- systemic hypotension
- hepatorenal syndrome
- hypercalcaemia
genetic condition that can cause renal artery stenosis
fibromusclular dysplasia
diagnostic key for renal artery stenosis
uncontrolled hypertension refractory to treatment
treatment of renal artery stenosis
angioplasty and treat LDL with statins
danger of ACEi with bilateral RAS
can lead to a very low GFR
when can NSAIDs cause prerenal failure
in patients with pre-existing renal disease
what do NSAIDs block
prostaglandins
what do prostaglandins do and therefore NSAIDs stop
dilation of the afferent arteriole
what absorption co-exists with Na reabsorption
urea reabsorption -therefore RAAS activation causes high BUN levels
more commonly what type of AKI do NSAIDs cause
intrarenal
hypoadrenalism means
low cortisol and aldosterone
low cortisol and aldosterone from addison’s means the nephron can’t______
reabsorb Na and water leading to hypotension and hypoatremia
symptoms of Addisons
salt craving weakness abdo pain syncope higher pigmentation uremia
lab results for Addison’s (5)
hypotension hyponatremia hyperkalaemia elevated BUN:cr ratio acidosis
treatment of Addison’s
cortisol replacement -hydrocortisone or prednisolone
mineralocorticoid replacement -fludrocortisone
hepatorenal syndrome=
idiopathic prerenal failure with pre-existing liver disease
symptoms of hepatorenal syndrome
jaundice
pruritis
asterixis
uremia
most common cause of intrinsic AKI
acute tubular necrosis
what happens to the epithelial cells in acute tubular necrosis
When epithelial cells become damaged, they slough off, accumulate and aggregate together in the renal tubule forming an obstruction→ high pressure behind obstruction reducing GFR
cells most affected by ischaemia in acute tubular necrosis
PCT and TAL
4 types of insult to the epithelial cells in Acute tubular necrosis
ischaemic
toxic
drugs
contrast induced
2 toxic causes of acute tubular necrosis
rhambdomylosis
heme
rhambdomylosis=
muscle injury
damaged muscle causes
-fluid sequestration in the damaged muscle induces volume depletion, activation of the sympathetic nervous system, ADH secretion and RAS activation all of which favor vasoconstriction and renal salt and water preservation
what can myoglobin from muscle injury do
myoglobin can cause direct tubular obstruction
2 drugs causing acute tubular necrosis
aminoglycosides
amphotericin B
what does contrast do to the tubules (2)
- causes vasoconstriction in nephrons
- can cause direct tubular toxicity and ischaemia
a form of inter-renal AKI caused by infiltration of neutrophils and eosinophils into the interstitium inducing inflammation
acute interstitial nephritis
presentation of acute interstitial nephritis
eosinophils
fever
rash
main cause of acute interstitial nephritis=
drug allergies
common drug allergies causing acute interstitial nephritis (4)
Beta lactams
PPIs
NSAIDs
diuretics
what type of reaction is acute interstitial nephritis
hypersensitivity reaction
treatment of acute interstitial nephritis
cessation of inflammatory inducing medications
if the hypersensitivity reaction of acute interstitial nephritis continues what is it called
renal papillary necrosis
less common cause of acute interstitial nephritis
pyelonephritis
pathology of pyelonephritis causing acute interstitial nephritis
chemokines and cytokines secreted by offending pathogens leads to inflammatory cell infiltration and direct damage to the interstitium
glomerular cause of intra-renal AKI
glomerulonephritis (inflammation of the glomerulus)
possible negative consequence of glomerulonephritis
membranous nephropathy -widespread thickening of the glomerular basement membrane
findings of glomerulonephritis (5)
- decreased GFR
- oliguria
- oedema
- hypertension
- azotemia
what is often the cause of glomerulonephritis
antigen-antibody complex in the glomerulus
what causes post-renal AKI
obstruction of the flow of urine
causes of post-renal obstruction
- BPH
- intra-abdominal tumour
- renal calculi
- kidney stone
- inflammation: stricture
- post-urethral valves
- infection: TB, schistosomiasis
what does the obstruction cause
back flow of urine causing increased pressure in the tubules reducing the pressure gradient reducing GFR .
what can high pressure in the tubules due to absorption
encourages reabsorption of Na, water and urea
what is the long term effect of high pressure in tubules from obstruction
causes the tubular epithelial cells to die impairing reabsorption and secretion
lab results of post renal AKI
azotemia
oliguria
increase BUN;cr ratio
what does the obstruction need to be to cause AKI
bilateral
