Hepatorenal syndrome Flashcards
renal failure in liver disease causes
sepsis (chronic liver disease increases susceptibility to infection) (can lead to AKI)
hepatorenal syndrome
hypovolemia- diuretics, GI bleeding
nephrotoxic drugs
parenchymal renal disease
hepatorenal syndrome
renal failure that occurs in patients with severe liver disease in the absence of any pathological cause for the development of renal failure
People with hepatorenal syndrome have narrowed and constricted blood vessels in their kidneys in response to liver failure, which reduces blood flow to the kidneys.
cause of hepatorenal syndrome
serious complication of liver cirrhosis
functional renal failure, kidneys stop working, reduced renal blood flow and glomerular filtration rate
HRS reversibility
reversible with liver transplant
AKI
acute kidney injury
an acute significant reduction in the glomerular filtration rate
serum creatinine
biomarker of renal function
influenced by bodyweight, race, age (less muscle as u age), gender
patients with cirrhosis:
less creatinine in muscles (muscle wasting)
increased renal tubular secretion of creatinine
interference w assays for sCr by elevated bilirubin
diagnosing AKI
inc in sCr from baseline
3 stages
stage 3 requires dialysis and renal replacement
main features of hepatorenal syndrome HRS
functional renal failure (replace liver and kidney will work) caused by intra-renal vasoconstriction in patients with end stage liver disease and circulatory dysfunction
circulatory dysfunction caused by splanchnic vasodilation and insufficient cardiac output
leads to hypovolemia
spontaneous w deteriorating liver function
or secondary to precipitating event such as bacterial infection
ascites
accumulation of fluid in peritoneal cavity
causes abdominal swelling
main factors in pathogenesis of HRS
hemodynamic factors (lowering of BP)
impaired cardiac output
increased activation of sympathetic NS
increased formation of vasoactive mediators
diagnosing HRS
lowered mean arterial pressure
lowered bp
lowered renal blood flow (because ascites increases renal venous pressure, compresses renal vein)
low cardiac output (increases risk of hrs)
vasoactive mediators
can lead to intra-renal vasoconstriction
can cause mesangial / smooth muscle cell contraction and reduce glomerular filtration rate by decreasing the single nephron glomerular filtration rate
pathophysiology of low glomerular filtration rate GFR
normal:
mesangial cell relaxation
prostaglandin E2
low gfr:
mesangial cell contraction
lowered surface area
no prostaglandin E2
NSAIDS effect
NSAIDs cause renal failure in ascites
reversible inhibitor of cyclooxygenase
blocks production of prostaglandin E2
AKI
management of hrs
treat underlying precipitating cause-
fluid challenge, review drugs, culture and antibiotics
support renal function until recovery of liver failure or liver transplant
optimise bp- vasoconstrictor drugs
paracentesis for tense ascites (removing fluid)
renal support (hemofiltration or dialysis)