2. INTRODUCTION
PRE-RENAL type of renal failure
seen in patients of liver disease
(mostly cirrhosis, sometimes acute)
ALTERED HAEMODYNAMICS
FUNCTIONAL
Renal Histology NORMAL
3.
DEFINITION BY
INTERNATIONAL ASCITES
CLUB:-
Hepatorenal syndrome is a
clinical condition that develops
in patients with chronic/acute
liver disease and advanced
hepatic failure and portal
hypertension.
4. Characterized by impaired renal
function and marked
abnormalities in the arterial
circulation and activity of the
endogenous vasoactive systems.
11. Cirrhosis with ascites
Serum creatinine level ≥
1.5 mg/dL
No or insufficient
improvement in serum
creatinine level (remains
≥1.5 mg/dL) 48 hr after
diuretic withdrawal and
adequate volume expansion
with intravenous albumin
12. Absence of shock
No evidence of recent use
of nephrotoxic agents
Absence of intrinsic renal
disease
13. Major Criteria
Low GFR indicated by S.creatinine > 1.5 mg/dL
or creatinine clearance < 40 ml/min
Absence of shock, ongoing bacterial
infection, current treatment with
nephrotoxic drugs
No sustained improvement in renal function
(decrease in serum creatinine to 1.5mg/dL or
increase in creatinine clearance to 40 ml/min)
after diuretic withdrawal & expansion of
plasma volume with 1.5 L of a plasma expander
Proteinuria < 500 mg/ dL & no USG evidence
of obstructive uropathy or parenchymal renal
disease
15. NOTE:
Decrease muscle mass in
CLD, in turn result in
reduced serum creatinine
and blood urea nitrogen
levels- delaying recognition
of HRS.
16. Diuretics, lactulose may
influence intravascular
volume status & renal
perfusion.
HRS in 20 to 30% of SBP
patients. Low threshold for
evaluating cirrhotic patients
with ascites for the presence
of SBP needed.
17. CLINICAL FEATURES
Due to liver disease
Due to complications of
cirrhosis
Decreased urine output
(Note: Oliguria may not be
present initially in all cases
of HRS)
18. HRS diagnosed in an
individual at risk on basis
of the results of
laboratory tests, in the
exclusion of other
causes.
21. Acute viral hepatitis
Drug-induced liver injury
(acetaminophen, idiopathic
drug-induced hepatitis)
Flare of chronic hepatitis B
virus infection by an
emergent resistant viral
strain or withdrawal of
antiviral therapy or
superimposed acute delta
virus hepatitis.
22. Risk Factors for developing
HRS
Previous episodes of ascites
Poor nutritional status
High plasma renin activity (>4
ng/mL per h)
Low mean arterial pressure
(<85 mm Hg)
25. UNOS has made the following
modifications to the score:
If the patient has
been dialyzed twice within the last
7 days, then the value for serum
creatinine used should be 4.0
Any value less than one is given a
value of 1 (i.e. if bilirubin is 0.8,
a value of 1.0 is used)
26. MELD scores of about 10 is
associated with an 8% and 11% risk
of HRS at 1 and 5
years, respectively.
If the MELD score approaches
18, nearly 40% of patients develop
HRS within 1 year..!!
27. TYPES OF HRS
Type 1 : Cirrhosis with rapidly
progressive acute renal failure
Type 2 : Cirrhosis with sub-acute
renal failure
Type 3 : Cirrhosis with types 1 or 2
HRS superimposed on CKD or AKI
Type 4 : Fulminant liver failure
with HRS
28. TYPE 1
Creatinine level doubles to
greater than 2.5 mg/dL
within 2 weeks
Rapid progression & high
mortality
Median survival - 1 to 2
weeks
TRIGGERS
29. TYPE 2
Creatinine increases slowly and
gradually (several weeks or
months )
Reciprocal gradual reduction in
GFR.
Median survival - 6 months
Without triggers
May transform to type 1 if
trigger
30.
31. TYPE 3
85% of end-stage cirrhotics have
intrinsic renal disease on renal
biopsy
Patients with pre-existing renal
disease do not meet traditional
diagnostic criteria for HRS
They have not been included in
therapeutic clinical trials.
32. . Given the absence of diagnostic
markers for HRS, the evaluation
of a cirrhotic patient with
multiple causes of renal failure is
complex
It is unclear whether a
chronically reduced baseline
GFR, from chronic intrinsic renal
disease, predisposes cirrhotic
patients to develop HRS
33. TYPE 4
More than half of patients
with ALF develop HRS
Superimposed on already
poor prognosis
MECHANISM ??
35. PREVENTION (TRIALS)
Prospective RCTs, Triggers
Norfloxacin for primary
prophylaxis for SBP reduced the 1-
year probability of HRS to
28%, compared with 41% in
controls not administered
antibiotic prophylaxis
Study strongly suggested that
HRS can be prevented in patients
with advanced cirrhosis and ascites
with a low protein content (< 1.5
36.
37. Albumin (1 g/kg
intravenously) at diagnosis
and at day 3 in patients
with SBP significantly
reduced the incidence of
type 1 HRS and the 3-
month mortality
38. Pentoxifylline, 400 mg three
times a day, to patients with
severe acute alcoholic
hepatitis was associated with
a marked reduction in HRS
incidence and in-hospital
mortality
39. Not yet been confirmed by
subsequent large studies.
In context of poor prognosis
of HRS, however, broad
acceptance of these
prophylactic measures
41. Trial on 376 patients –
using terlipressin alone/with
albumin
using octreotide plus albumin
using noradrenalin plus
albumin
42. RESULT: Terlipressin +
albumin - short-term
mortality reduction in type 1
HRS, but no such reduction in
patients with the type 2
Octreotide & noradrenaline
therapies indicated neither
harmful nor beneficial
effects
47. Role of TIPSS
Experimental
If no response to
vasoconstrictor/volume
expansion
Child-Pugh class A or B
Meet criteria for TIPSS
48. Peritoneo-venous shunting
plasma volume expansion &
improvement of circulatory
function
Role in type 2 HRS who often
have refractory ascites
No proven role in type 1
50. BEST AVAILABLE (?)
TREATMENT
can potentially permanently
reverse HRS + other
complications of CLD
Patients with HRS undergoing
transplantation, however, have
a MORE perioperative
morbidity & mortality
51. More practical in type 2
Absence of precipitating
events
Longer clinical course
Relatively less severe renal
failure
