AKI in Cirrhosis by Dr. Dhingra

Jagmeet S Dhingra
45 yo hispanic male with long standing cirrhosis due to
HepC and Alcohol
Multiple admissions for hepatic encephalopathy
Diuretic resistant ascites with therapeutic paracentesis
every 2 months
Physical examination suggestive of volume overload
with peripheral edema and ascites
Acute rise in Cr to 2.9 in 5 days from a baseline of 1.01.2 found on outpatient labs
Baseline BP 90-100’s
On lactulose at home.
Last LVP 1 week ago with 10 liter removal
What to do and Whats going on. Options
I cant believe I am having another crappy
Do a detailed history and exam
Start normal saline at 150cc/hour-he is likely
intravascularly depleted
Do a diagnostic paracentesis
Send of UA, urine lytes along with chemistries
Call the renal fellow
AKI is a relatively frequent problem, occurring
in approximately 20% of hospitalized patients
with cirrhosis
Renal dysfunction (creatinine and blood urea
nitrogen/azotemia) both powerful predictors
of death in decompensated cirrhosis.
Higher serum creatinine consistently portends
worse survival
Hospitalized cirrhotic patients 20% present
with AKI at admission
70 % develop with AKI during Admission
Patients admitted with SBP 41-56% have AKI
5-6% develop AKI after TIPS
Annals of Hepatology 2012 11(3) 301-310
During the history you obtain while trying to
stay awake, he mentions he has been taking
Ibuprofen for knee pain and has also been
having some abdominal discomfort. Hasn ’ t
noticed increased stool output on lactulose but
they were black yesterday. Abdomen on exam
is not tense but does have some generalized
What next
Why couldn’t he come to hospital earlier in the
day and why do I get all the train wrecks
Start normal saline at 150/hour. He is likely GI
Do a diagnostic paracentesis. This is likely
Its probably the ibuprofen.
Send of labs and urine studies and start
Call the renal fellow
Nonsteroidal antiinflammatory drugs may also
cause renal failure in patients with cirrhosis,
since their kidney function is extremely
dependent on renal prostaglandin synthesis.
Patients who have ascites, particularly those
with hyponatremia, bacterial infections,
gastrointestinal bleeding, or severe sodium
retention, are at high risk for renal failure, as
are all patients hospitalized for acute
decompensation of cirrhosis
Creatinine is derived from creatine, mostly
synthesized by the liver.
Patients with liver disease tend to have lower
creatine synthesis and consequently, lower
serum creatinine values for any given level of
These lower values are compounded by the
loss of muscle mass that is common in patients
with progressive chronic liver disease.
Also have a degree of creatinine dilution
caused by the accumulation of peripheral
edema and ascites.
Clinical chemistry laboratories typically
measure serum creatinine by a modified Jaffe
colorimetric assay, which depends on a color
change that can be influenced by noncreatinine
chromogens such as bilirubin, particularly with
serum bilirubin concentrations >10 mg/dl. This
effect of bilirubin reduces the measured
creatinine value. Alternative is to measure it
Serum creatinine and estimated GFR calculated
using serum creatinine overestimate actual
kidney function.
Likewise, an increase in serum creatinine
concentration of 0.3 mg/dl (i.e., corresponding
to Acute Kidney Injury Network stage 1 AKI)
represents a much greater decrease in kidney
function in cirrhotic patients compared with
others who develop AKI
Electrolytes and protein should be measured
(preferably in 24-hr urine samples) in all
patients with renal failure;
protein/day) and urine-sediment abnormalities
usually indicate parenchymal renal disease.
A renal biopsy is helpful when parenchymal
renal disease is suspected because of
proteinuria, hematuria, or both and
is also helpful in deciding on simultaneous
kidney transplantation in candidates for liver
Intra-abdominal pressure may be increased in
patients with cirrhosis because of the presence of
tense ascites.
Although a typical compartment syndrome
causing AKI may be associated with intraabdominal pressures of 18 mmHg or greater, lower
pressures can cause renal dysfunction, especially
in the setting of systemic hypoperfusion or sepsis.
Renal perfusion has been reported to improve after
drainage of ascites.
Overzealous removal of ascites, even with colloid
hypovolemia and ischemic AKI; Be careful with
His stool hemoccult turns out to be negative.
He forgot to tell you he had also just started
iron pills
His paracentesis suggests markedly elevated
white count with high amount of polys
His urine sodium is less than 10 with a bland
UA and no proteinuria
It cant be 7 A.M soon enough
Start antibiotics and Albumin infusions
This is HRS due to the low urine sodium. Start
midodrine and octreotide right away
He is septic. Given him 2 liter saline bolus and
hold his diuretics
Transfer him to ICU for norepinephrine
infusion for HRS
Call the renal fellow.
HRS is a specific form of volume-unresponsive
kidney injury in patients with progressive
cirrhosis and ascites
Only around 50% of patients treated for HRS
with vasoconstrictive agents respond to
treatment with a reduction in serum creatinine
1-year and 5-year probabilities of developing
HRS in patients with ascites are approximately
20% and 40%,
Highest in patients with more marked sodium
and water retention and marked activation of
vasoconstrictive systems.
HRS is divided into two types (1 and 2) based
on prognosis and clinical characteristics.
Survival of patients with HRS-1 is shorter than
that of patients with HRS-2 (median survival
1.0 versus 6.7 months)
Bacterial infection
GI losses
GI bleeding
NSAIDs including COX-2
ACE inhibitors
Presence of ascites is a prerequisite for the
diagnosis of HRS because the same
mechanisms that lead to ascites formation lead
to HRS
HRS have advanced liver disease, as evidenced
by the median Child-Pugh score in these
patients being 11.2, and their low MAP
(median, 74 mmHg), and low serum sodium
(median, 127 mEq/L), findings that are
consistent with the presence of vasodilatation
(low MAP), sodium retention (ascites), water
retention (dilutional hyponatremia), and renal
vasoconstriction (HRS)
Baseline SCr is a predictor of HRS reversal
The probability of HRS reversal decreases by
39% for each 1-mg/dL increase in baseline
OLT is the only definitive therapy for HRS,
only therapy associated with improvement in
Important to try reverse HRS because
improving renal function pretransplantation is
associated with improved posttransplantation
Vasoconstrictors used in the treatment of HRS
for periods greater than 3 days are associated
with increases in MAP, GFR, and serum
sodium and decreases in SCr and plasma renin
Noradrenaline, in continuous infusion, has also
been shown to ameliorate the hemodynamic
/renal abnormalities in HRS as has the
combination of midodrine.
They almost always require co administration
of albumin
Method to adjust the dose of vasoconstrictors is
by monitoring MAP (an indirect indicator of
vasodilatation), a method that has been used
for adjusting the dose of midodrine plus
octreotide, an alternative to terlipressin (not
available in the US)
The doses of octreotide and midodrine were
titrated to obtain an increase in mean arterial
pressure of at least 15 mm Hg.
Octreotide was administered subcutaneously at
an initial dose of 100 μg three times daily and
then, if necessary,increased to 200 μg three
times daily.
Midodrine was administered orally at an initial
dose of 7.5 mg three times daily and then, if
need be, increased to 12.5 mg three times daily.
In addition, an amount of 20 to 40 g/d of
albumin was infused.
Albumin is administered together with the
The maintenance dose, once the diagnosis of
HRS is established and vasoconstrictors are
initiated, is 25 to 50 g/day.
Albumin may be discontinued if serum
albumin concentration is greater than 4.5
mg/dL and should be withdrawn in case of
pulmonary edema.
In addition to serving as an intravascular
volume expander, albumin also has binding
sites for free radicals and toxins, and hence, in
patients with liver failure, albumin infusions
may help by increasing the capacity to bind
such toxins
Although intravenous infusion of crystalloid
solutions can usually be safely given to patients
with cirrhosis because of their systemic
vasodilatation, any fluid bolus that initially
subsequently distribute to expand the entire
extracellular space, worsening peripheral
edema and ascites.
Overzealous fluid administration can also
precipitate cirrhotic cardiomyopathy with heart
hepatopulmonary syndrome.
Treatment can be stopped if SCr does not
decrease by at least 50% after 7 days at the
highest dose, or if there is no reduction in
creatinine after the first 3 days.
In patients with early response, treatment
should be extended until reversal of HRS
(decrease in creatinine below 1.5 mg/dL) or for
a maximum of 14 days.
Vasoconstrictor therapy should be restarted if
HRS recurs after discontinuation of therapy.
Once creatinine normalizes, TIPS should be
considered, particularly if transplantation is
not foreseeable in the near future and the
patient has refractory ascites
Patient is started on albumin infusions and
antibiotics. He does not respond to albumin
and renal consult is called for worsening
A smart renal fellow ( now attending) starts the
patient on midodrine octreotide with gradual
uptitration of dose without much improvement
Transplant surgery and hepatology say patient
not a transplant candidate due to active alcohol
When do I get off service. This guy is a rock.
He will be here forever
Discuss with nephrology about initiating
dialysis with worsening volume status
Family meeting and palliative care consult
Discuss with hepatology about TIPS
In a large study involving 129 cirrhotic patients
with varying degrees of baseline renal function,
TIPS has been shown to improve renal
Patients with pre-treatment serum creatinine
levels between 1.2 and 1.9 mg/dL had reduced
mean levels of creatinine, from 1.5 to 1.1
mg/dL, and those with pre-TIPS creatinine
levels > 2.0 mg/dL showed a reduction from
2.8 to 1.5 mg/dL.
The prognosis for patients with cirrhosis and
renal failure is poor.
The overall survival rate is approximately 50%
at 1 month and 20% at 6 months.
Survival rates can differ according to the type
of renal failure.
HRS is associated with the worst prognosis.
Type 1 HRS mortality 80% at 2 weeks with 10%
3 month survival
MELD score median survival 1 month if Meld
20 or more and 8 month if Meld less than 20
The risk of the hepatorenal syndrome is
substantial in patients with cirrhosis and
spontaneous bacterial peritonitis but may be
markedly reduced with the intravenous
administration of albumin (1.5 g per kilogram
of body weight at diagnosis and 1.0 g per
kilogram 48 hours later).
The mechanism by which albumin prevents the
understood but may be related to albumin’s
positive effects on circulatory function and
other effects, such as its antioxidant properties
Patients with ascitic fluid that contains less
than 15 g of protein per liter and who have
associated impairment of liver function, renal
function, or both (a bilirubin level above 3 mg
per deciliter, a Child–Pugh score greater than
10, a serum sodium level below 130 mmol per
liter, or a serum creatinine concentration above
1.2 mg per deciliter, the long-term
administrationof oral norfloxacin (400 mg per
day) reducesthe risk of the hepatorenal
syndrome and improves survival
After informing the patient about his prognosis
and outcome and that dialysis will not change
his outcome due to his severe liver disease,
patient and family decide to go with hospice
care. Patient expired 1 week after discharge
All AKI in Cirrhosis is not HRS
Look for a precipitating cause
Use volume judiciously
Avoid nephrotoxic agents
If starting vasoconstrictors, adjust doses based
on repsonse. Do not leave patient on single
fixed dose
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