UptoDate: Hepatorenal
syndrome
The ideal therapy for hepatorenal syndrome is improvement of liver
function from recovery of alcoholic hepatitis, treatment of decompensated
hepatitis B with effective antiviral therapy, recovery from acute hepatic
failure, or liver transplantation. The ability of liver function to improve
with abstinence from alcohol and effective antiviral therapy of hepatitis B is
remarkable.
However, when improvement of liver function is not possible in the short
term, we recommend that medical therapy be instituted in an attempt to reverse
the acute kidney injury associated with hepatorenal syndrome.
In patients with hepatorenal syndrome who are critically ill, we suggest initial treatment with norepinephrine in
combination with albumin. Norepinephrine is given intravenously as a continuous
infusion (0.5 to 3 mg/hr) with the goal of raising the mean arterial pressure
by 10 mmHg, and albumin is given for at least two days as an intravenous bolus
(1 g/kg per day [100 g maximum]). Intravenous vasopressin may also be
effective, starting at 0.01 units/min and titrating upward as needed to raise
the mean arterial pressure.
In patients with hepatorenal syndrome who are not critically ill, where terlipressin therapy is not available, we
suggest initial treatment with a combination of midodrine, octreotide, and
albumin. Midodrine is given orally (starting at 7.5 mg and increasing the dose
at eight-hour intervals up to a maximum of 15 mg by mouth three times daily), octreotide is either given as a continuous intravenous infusion (50 mcg/hr)
or subcutaneously (100 to 200 mcg three
times daily), and albumin is given for two days as an intravenous bolus (1
g/kg per day [100 g maximum]), followed by 25 to 50 grams per day until
midodrine and octreotide therapy is discontinued.
In patients who fail to respond to the above therapies, develop severely
impaired renal function, and either are candidates for liver transplantation or
have a reversible form of liver injury and are expected to survive, we
recommend dialysis as a bridge to liver transplantation or liver recovery.
In patients treated with
norepinephrine, terlipressin, or octreotide, we usually treat for a total of two weeks. However, we and others
occasionally treat for longer durations (up to one month or more) if there is
some but not complete improvement in renal function after two weeks of therapy.
In patients who respond to therapy, we occasionally treat indefinitely with
midodrine to maintain a higher mean arterial pressure (or until liver
transplantation or resolution of liver injury). Many patients who recover from
type 1 hepatorenal syndrome continue to have refractory ascites, and midodrine
may be effective in such patients [42]. In contrast, if a patient has no improvement in renal function after two
weeks, therapy with these drugs
can be considered futile.
EASL clinical practice
guidelines on the management of ascites, spontaneous bacterial peritonitis, and
hepatorenal syndrome in cirrhosis
Management of hepatorenal syndrome
The most effective method currently available is the administration of
vasoconstrictor drugs. Among the vasoconstrictors used, those that have been
investigated more extensively are the vasopressin analogues particularly
terlipressin. The rationale for the use of vasopressin analogues in HRS is to
improve the markedly impaired circulatory function by causing a
vasoconstriction of the extremely dilated splanchnic vascular bed and
increasing arterial pressure.
Drug therapy of type 1 hepatorenal syndrome Terlipressin (1 mg/4–6 h
intravenous bolus) in combination with albumin should be considered the first
line therapeutic agent for type 1 HRS. The aim of therapy is to improve renal
function sufficiently to decrease serum creatinine to less than 133 mcmol/L (1.5
mg/dl) (complete response). If serum creatinine does not decrease at least 25%
after 3 days, the dose of terlipressin should be increased in a stepwise manner
up to a maximum of 2 mg/4 h. Median time to response is 14 days and usually depends
on pre-treatment serum creatinine, the time being shorter in patients with
lower baseline serum creatinine. A serum bilirubin less than 10 mg/dl before
treatment and an increase in mean arterial pressure of >5 mm Hg at day 3 of treatment
are associated with a high probability of response to therapy. For patients
with partial response (serum creatinine does not decrease <133 mcmol/L) or
in those patients without reduction of serum creatinine treatment should be discontinued
within 14 days. Recurrence after withdrawal of therapy is uncommon and retreatment
with terlipressin is generally effective.
In most studies, terlipressin was given in combination with albumin (1
g/kg on day 1 followed by 40 g/day) to improve the efficacy of treatment on
circulatory function.
Japan
Society of Transfusion Medicine and Cell Therapy: Evidence-based Guidelines for
the Use of Albumin Products 2017
Hepatorenal syndrome is referred to as acute renal failure in patients
with end-stage liver cirrhosis or hepatic insufficiency, such as fulminant
hepatitis, but represents functional pre-renal failure without any organic or
pathological changes in renal tissues. Hepatorenal syndrome is classified into
2 types: type 1 showing rapidly progressive symptoms of renal failure and type
2 showing slowly progressive renal failure. Patients with hepatorenal syndrome
has a low glomerular filtration rate (serum Cr >1.5 mg/dl or 24-hour CCr
<40 ml/min), resulting in oliguria. In many cases, hepatorenal syndrome progresses
in an irreversible manner, is associated with a mortality rate of ≥90%, and is one of the causes of death in
end-stage liver cirrhosis. The use of terlipressin and albumin is recommended
for the treatment of type-1 hepatorenal syndrome. Improvement of renal
impairment is also noted in 83% of patients with coadministration of
norepinephrine and albumin, which represents a beneficial treatment regimen while waiting for a liver
transplant.
Treatment with a hypertonic albumin solution and a
vasoconstrictor is effective in improving type-1 hepatorenal syndrome. Albumin
should be administered at a dose of 1 g/kg body weight on day 1 and 20 to 40
g/body weight on subsequent days, in combination with terlipressin and other
drugs (evidence grade 1A).
Guideline
|
Recommended Dosages of Human Albumin
Injection for SBP
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UptoDate
[Accessed 19 August
2019]
|
Critically
ill
For at least two days as
an intravenous bolus
(1 g/kg per day [100 g
maximum])
Not
critically ill
Given for two days as an
intravenous bolus (1 g/kg/day [100 g maximum]), followed by 25-50 g/day until
terlipressin therapy is discontinued
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Clinical Guidelines for
Human Albumin Use (NHS Scotland 2016)
|
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EASL clinical practice
guidelines on the management of ascites, spontaneous bacterial peritonitis,
and hepatorenal syndrome in cirrhosis 2010
|
1 g/kg on day 1, followed
by 40 g/day
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Evidence-based
Guidelines for the Use of Albumin Products (Japan Society of Transfusion
Medicine and Cell Therapy 2017)
|
1 g/kg body weight on
day 1 , then,
20 to 40 g/body weight
on subsequent days
|
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Guideline for the use of
human albumin solution (Guy’s and St. Thomas’ 2015)
|
Day 1: 1g/kg
Day 2 -14: 0.5g/kg
The transfusions should stopped
once patient’s condition has resolved.
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Guidelines for
Intravenous Albumin Administration at Stanford Health Care (Stanford Health
Care 2017)
|
Suspected HRS
Defined as acute renal dysfunction (serum
creatinine >1.5 mg/dL or 132.6 mcmol/L) in the presence of cirrhosis
1 g/kg/day for 2 days (max. 100 g/day) *
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Confirmed HRS
Defined as:
·
Serum creatinine >1.5 mg/dL in the
presence of cirrhosis
·
Absence of shock, ongoing bacterial
infection, and/or current treatment with nephrotoxic drugs
·
Absence of sustained improvement in
renal function after discontinuation of diuretics and a trial of albumin 1
g/kg
·
Absence of proteinuria (<500
mg/day) or hematuria (<50 red cells per high-power field)
·
Absence of ultrasonographic evidence
of obstructive uropathy or parenchymal renal disease
25-50 g* daily for a total of 72 hours
(starting 1-2 days after initial diagnostic trial of albumin, if applicable),
and consult nephrology and hepatology services to determine whether to continue
Should be used in addition to midodrine and
octreotide
|
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Albumin – Adult –
Inpatient Clinical Practice Guideline (University of Wisconsin Hospitals
2018)
|
Management
of hepatorenal syndrome (HRS) / acute kidney injury (AKI) in patients with
cirrhosis
and probable non-structural injury (i.e. pre-renal azotemia):
As fluid
challenge (UW Health low
quality evidence; strong recommendation)
Assess for resolution or
progression of AKI at 48 hours after initiating albumin therapy
|
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Treatment of
Type 1 HRS with cirrhosis (UW Health
high quality evidence; strong recommendation)
1 g/kg on day 1 (max.100
g/day), then 25 g/day
The following duration
of therapy for albumin is recommended:
1.
For
patients that respond to vasoconstrictors and albumin as evidenced by a
decrease in plasma creatinine, discontinue albumin when plasma creatinine has
returned to or is close to baseline, or has not decreased further after 3
days of treatment
2.
In
patients that do not respond to vasoconstrictors and albumin, discontinue
albumin after a maximum of 7 days
3.
Discontinue
albumin if patient is started on renal replacement therapy or the plasma
albumin level is > 3 g/dL (30 g/L).
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*Use 25%.
References:
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