pathophys of AKI - amboss Flashcards
define AKI
sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen BUN
three main causes of AKI
decreased renal perfusion (prerenal)
direct damage to kidneys (intrarenal/intrinsic)
inadequate urine drainage (post renal)
diagnosis of AKI is made based on
increase in serum creatinine concenration and/or decrease in urine output
prerenal causes of AKI
decreased blood flow into kidneys may be due to
- absolute loss of fluid: haemorrhage, vomiting, diarhoea, severe burns, poor oral intake, diuretics
- relative loss of fluid: hypotension, distributive shock, congestive heart failure
- local to the renal artery: renal artery stenosis, embolus
pathophysiology of prerenal AKI
less blood is pumped to glomeruli
less blood filtered
decreased glomerular filtration rate (GFR)
azotaemia
high levels of nitrogen containing compounds in the blood
signs of prerenal AKI
oliguria - low urine
azotaemia - high urea and creatinine in blood
BUN:creatinine ratio of >20:1
concentrated urine
intrarenal AKI is due to
damage to the tubules, glomerulus or interstitium
eg.
- acute tubular necrosis via ischaemia (usually due to a prerenal decrease in blood flow) or via nephrotoxins
- glomerulonephritis
- acute interstitial nephritis
- vascular diseases
causes of acute tubular necrosis
ischaemia eg. due to prolonged hypotension
nephrotoxic drugs:
aminoglycosides (antibiotics)
cisplatin, methotrexate
radiocontrast dye
poisons:
lead
ethylene glycol
endogenous toxins:
uric acid (tumour lysis syndrome)
haemoglobin in intravascular haemolysis
myoglobin released from damaged muscles n rhabdomyolysis
glomerulonephritis
inflammation of the glomerulus
often caused by antigen antibody complexes causing inflammation and damage
cells lining glomerulus
podocytes
signs of intrarenal AKI
proteinuria and haematuria due to damaged podocytes
decreased GFR due to fluid leakage causing. reduced pressure difference
oliguria
more fluid in the blood: oedema and. hypertension
azotaemia
acute interstitial nephritis
infiltration of immune cells
canbe caused by NSAIDs, diuretics, penecillin
oliguria and eosinophiluria
failure to cease medications causing acute interstitial nephiritis may lead to
renal papillary necrosis
where the renal papillae are destroyed
how common in prerenal
60% of AKIs
cardiorenal syndrome
a spectrum of conditions affecting cardiac and renal systems when dysfunction in one organ results in dysfunction of the other
eg. congestive heart failure causing poor renal perfusion
hepatorenal syndrome
kidney injury in patients with cirrhosis
abdominal compartment syndrome
high abdominal pressure associated with organ dysfunction or failure
causes of decreased circulating volume
cardiorenal syndrome
hepatorenal syndrome
abdominal compartment syndrome
nephrotic syndrome
acute pancreatitis
how common is intrinsic acute kidney injury
35% of cases of AKI
infections causing acute interstitial nephritis
bacterial: legionella, strep
fungi: candida, histoplasma
viral: hepatitis C virus, cytomegalovirus, HIV
infiltrative diseases eg. sarcoidosis, amyloidosis
vascular diseases causing intrarenal AKI
haemolytic uraemic syndrome
thrombotic thrombocytopaenic purpura
hypertensive emergency
vasculitis, scleroderma renal crisis
renal vein thrombosis, renal atheroemboli, renal infarction
post renal acute kidney injury
any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra
how common is post renal kidney injury
5% of AKI
causes of acquired obstructions
benign prostatic hyperplasia BPH
iatrogenic eg. catheter associated injuries
tumours eg. bladder, prostate, cervical, metastases
stones
bleeding with subsequent blood clot formation
causes of post renal acute kidney injury
acquired obsructions
neurogenic bladder
congenital malformations
serum creatinine levels in patients with unilteral ureteral obstruction
typically remain normal as long as the contralateral kidney remains in tact
pathophysiology of prerenal kidney injury
decreased blood supply to the kidneys due to hypovolaemia, hypotension, or renal vasoconstriction
failure of renal vascular autoregulation to maintain renal perfusion
decreased GFR
activation of renin angiotensin system
increased aldosterone release
increased resorption of Na+, H2O
increased urine osmolality
secretion of anti diuretic hormone
increased reabsorbtion H2O and urea
creatinine is still secreted inthe proximal tubules, so the blood BUN:creatinine ratio increases
BUN:creatinine ratio in prerenal kidney injury
increases
creatinine is still secreted in the proximal tubules but there is increased resorbtion of urea
pathophysiology of intrinsic kidney injury
damage to a vascular or tubular component of the nephron
necrosis or apoptosis of tubular cells
decreased resorption capacity of electrolytes (eg. Na, water and/or urea)
increased Na and H20 in the urine
decreased urine osmolality
pathophysiology of post renal kidney injury
bilateral urinary outflow obstruction eg. stones, BPH, neoplasia, congenital anomalies
increased retrograde hydrostaticpressure within renal tubules
decreased GFR and compression of the renal vasculature
acidosis, fluid overload, and increased BUN, Na and K
GFR in post renal kidney injury
remains normal as long as one kidney is functioning normally
anuria
<50ml/24 hours
complications of oliguric/anuric phase of kidney injury
fluid retention (pulmonary oedema)
hyperkalaemia
metabolic acidosis
uremia
lethargy
asterixis
phases of AKI
initiating event
oliguric or anuric phase
polyuric/diuretic phase
recovery phase
clinical features of AKI
oliguria or anuria
signs of volume depletion - reduced skin turgor, orthostatic or frank hypotension and tachycardia
signs of fluid overload (from Na and H2o retention)
signs of uremia
signs of renal obstruction
fatigue, confusion, and lethargy
in severe cases: seizures or coma
affected individuals have a higher risk of secondary infection throughout all phases
signs of fluid overload
peripheral or pulmonary oedema
hypertension
heart failure
shortness of breath
signs of uremia
anorexia
nausea
encephalopathy, asterixis
pericarditis
platelet dysfunction
signs of renal obstruction
distended bladder
incomplete voiding
pain over the bladder or flanks
what happens during intrinsic aki
dead podocytes block the tubules
decreases glomerular filtration rate
less urea and creatinine get filtered out
potassium and metabolic acids build up in the blood because they are not excreted by dead podocytes
membrane permeability in intrarenal damage
large molecules can get through causing proteinuria and haematuria
clinical features of intrarenal AKI
azotemia
more circulating fluid - hypertension and edema
lower GFR
causes of postrenal AKI
compression - BPH, intra abdominal tumours
blackage - kidney stones
