AKI Flashcards
AKI definition
acute drop in kidney function.
diagnosis: measuring the serum creatinine (waste product that is filtered by kidneys into the urine)
1. Rise in creatinine of ≥ 25 micromol/L in 48 hours
2. Rise in creatinine of ≥ 50% in 7 days
3. Urine output of < 0.5ml/kg/hour for > 6 hours
e. g 60kg patient producing <30mls of urine per hour for more than 6 hours
risk factors for AKI
acute illness (infection/surgical operation)
Chronic kidney disease (CKD)
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment (less likely to take fluid in)
Nephrotoxic medications such as NSAIDS and ACE inhibitors
*iatrogenic - Use of a contrast medium such as during CT scans
causes of AKI
- pre renal
- renal
- post renal
pre-renal AKI (azotemia)
azotemia= high levels of nitrogen in the blood
inadequate blood supply to the kidneys, reducing the filtration of blood (hypo-perfusion)
- dehydration (d+v)
- haemorrhage
- sepsis
- hypotension (shock)
- heart failure (LV failure, reduced kidney perfusion)
- ACEi, NSAIDs
- vomiting, diarrhoea, severe burns
- distributive shock
- renal artery stenosis
- emobuls
loss of haemodynamic control
(Afferent arteriole vasoconstriction- NSAIDs)
(efferent arteriolar vasodilation ACEi, ARB’s)
less blood filtered = less urea and creatinine filtered out so more in the blood (high levels in the blood) and less urine (oligouria)
kidneys stimulate the RAAS to reabsorb sodium to increase BP= more urea absorbed.
BUN: creatinine ratio >20:1
intra-renal AKI
damage to the glomerulus, tubules or interstitial
intrinsic disease inside the kidney so filtering blood poorly
tubules:
1. glomerulonephritis
2. interstitial nephritis
3. acute tubular necrosis. epithelial cells necrose (die) via ischaemic. usually caused by a pre-renal AKI
4. nephrotoxins (amino glycoside abx, heavy metals like lead, myoglobin from damaged muscles, ethylene glycol anti freeze, radio contrast die, uric acid (waste product when cells die in cancer= tumour lysis syndrome)
causes plugging= high pressure so filter is less
= oliguria
= azotemia (high levels of nitrogen containing compounds in the blood)
= hyperkalaemia, metabolic acidosis. brown granular cast in urine.
post renal AKI
obstruction to outflow (travelling through the ureters- bladder- urethra) back pressure into kidney.
(obstructive uropathy)
obstruction to the outflow of the kidneys, causing back-pressure into the kidney and reduced kidney function
'obstructive uropathy' kidney stones masses- abdomen, pelvis cancer ureter or ureteral strictures enlarged prostate or prostate cancer
bladder outlet
bilateral urteric obstruction
- compression (intra abdominal tumor)
- benign prostatic hyperplasia
- blockage inside (kidney stones)
- urethral strictures
if one ureter obstructed= unilateral and the other kidney can preserve kidney function
if urethra is obstructed= bad
back up causes increases in pressure which messes up the gradient (high pressure to higher pressure!) this lowers the GFR. less urea and creatinine is filtered= more in blood. azotemia and oliguria.
BUN:creatinine ratio
>15:1
increased pressure damages the epithelial cells responsible for reabsorption so now more urea will be excreted. this causes the BUN to fall <15:1
AKI investigations
bedside:
1. urinalysis for leukocytes, nitrites (infection) protein, blood (acute nephritis / infection)
glucose (diabetes)
- clinical assessment- fluid balance
bloods:
3. serum creatinine
imaging:
4. ultrasound - look for obstruction (renal USS, renal biopsy)
management of AKI
prevention
avoid nephrotoxic meds
ensure adequate fluid if unwell patients
include IV fluids
- fluid rehydration with IV fluids (cautious if in heart failure)
- stop nephrotoxic meds (NSAIDs, antihypertensives because these reduce filtration pressure of the kidney e.g. ACEi)
- relieve obstruction (post renal AKI) insert, catheter e.g retention from enlarged prostate.
if severe= input from renal specialist
if persist/severe= dialysis
AKI complications
Hyperkalaemia (can’t filter out K+)
Fluid overload, heart failure and pulmonary oedema (cannot filter out fluid so it builds up in lungs, circulation and around body)
Metabolic acidosis (kidneys aren’t doing their role in acid base balance by producing bicarbonate)
Uraemia (high urea) can lead to encephalopathy or pericarditis (confusion and reduced brain function)
stages of AKI
stage 1:
Increase in Cr by more than 27umol/l
>150% increase in baseline Cr
Urine output less than 0.5 ml/kg per hour > 6 hours
stage 2:
200 to 300% increase in Cr
Urine output less than 0.5 ml/kg per hour for >12 hours
stage 3:
Increase in serum creatinine > 300% from baseline
Urine output less than 0.3 ml/kg per hour for 12 hours
Anuria for 6 hours
intra-renal AKI (tubual)
damage to the glomerulus, tubules or interstitial
tubules:
1. acute tubular necrosis. epithelial cells necrose (die) via ischaemic. usually caused by a pre-renal AKI
2. nephrotoxins (amino glycoside abx, heavy metals like lead, myoglobin from damaged muscles, ethylene glycol anti freeze, radio contrast die, uric acid (waste product when cells die in cancer= tumour lysis syndrome)
causes plugging= high pressure so filter is less
= oliguria
= azotemia (high levels of nitrogen containing compounds in the blood)
= hyperkalaemia, metabolic acidosis. brown granular cast in urine.
intra renal AKI
glomerulus
glomerulonephritis
caused by antigen-antibody complex depositing in the glomerulus tissue. this activates the complement tissue which attracts macrophages and neutrophils to site= releases lysosomal enzymes to the site= damage to the podocytes.
podocytes usually prevent large molecules through. so now membrane permeability has decreased =proteinuria, haematuria. fluid leakage= eGFR drops.
more fluid in blood (oedema)
less urine (oligouria)
hypertension
azotemia (high nitrogen in blood)
infrarenal AKI (interstitial)
acute interstitial nephritis
inflammation of the nephritis over days-weeks
infiltration of immune cells (neutrophils, eosinophils)
type I or IV hypersentivity
in response to meds- NSAIDS, penicillin, diuretics.
oligouria, eosinophiluria.
fever, rash
renal papillary necrosis
(can cause more haematuria, flank pain) *chronic use of anaglesic, diabetes, sickle cell disease, pyelonephritis
kidneys cannot filter blood proplery- damaged- reabsorption and secretion is impaired.
urea is not absorbed. less urea stays in blood relative to creatinine.
BUN : creatinine <15:1
Na+ >40 (cannot reabsorb sodium)
management of complications
hyperkalaemia (insulin + glucose+ calcium gluconate) uraemia (GCS) (encephalitis) acidotic (sodium bicarbonate IV) hyponatraemia fluid overlaod (pulmonary oedema)
examples of nephrotoxic drugs
hyperkalaemia (insulin + glucose+ calcium gluconate) uraemia (GCS) (encephalitis) acidotic (sodium bicarbonate IV) hyponatraemia fluid overlaod (pulmonary oedema)
