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Gastrolearning XII lezione L'insufficienza renale nel cirrotico - Prof. P. angeli (Università di Padova)
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Acute renal failure in patients with cirrhosis
“Gastrolearning”Padova 8 Aprile 2013
P. AngeliUnit of Hepatic Emergencies and Liver Transplantation
Dept. of MedicineUniversity of Padova, Italy
pangeli@unipd.it
• Diagnosis of AKI/HRS
• Pharmacological treatment of HRS
Hepatorenal syndrome (HRS)
Topics
Hepatorenal syndrome (HRS)
Diagnosis of AKI/HRS
Phenotypes of renal dysfunction in patients with cirrhosis
AKI in cirrhosis
G. Garcia-Tsao et al. Hepatology 2008 ; 48 : 2064—2077 (modified).
Definition of ARF/AKI = a rapid reduction in kidney function currently defined as a percentage increase in serum creatinine of more or equal to 50 % (1.5-fold from baseline) to a final value equal or higher than 1.5 mg/dl.
Hospitalized patients with cirrhosis
ARF/AKI (19%)
CKD (1%)
Definition and staging of Acute Kidney Injury (AKI) according to AKIN criteria
R.L. Mehta et al. Crit. Care 2007 ; 11 : R31.
Definition of AKI = an abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl ( 26.4 μmol/l), or a percentage increase in serum creatinine of more or equal to 50 % (1.5-fold from baseline).
Stage Serum creatinine criteria
1°Increase in serum creatinine equal or less than 200 % ( 2-fold ) from baseline
2°Increase in serum creatinine to more than 200% to 300% (> 2- to 3-fold) from baseline
3°
Increase in serum creatinine to more than 300 % (> 3-fold) from baseline or serum creatinine of more or equal to 4.0 mg/dl ( 354 μmol/l) with an acute increase of at least 0.5 mg/dl (44 μmol/l) or need for renal replacement therapy
AKI in cirrhosis
Definition
AKI in cirrhosis
Further and larger prospective studies are needed to assess the ability of new criteria versus the conventional criteria of renal dysfunction in the prediction of survival in patients with cirrhosis.
P. Angeli et al. Liver Int. 2012 (Epub ahead of print)
Criteria Sensibility95 % CI
Specificity95% CI
PPV95% CI
NPV95% CI
LR+95% CI
LR-95% CI
Conventional criterion 0.5152(0.33 - 0.69)
0.9450(0.90 - 0.97)
0.6071(0.40 - 0.78)
0.9220(0.87 - 0.95)
9.3664(4.8 - 18.17)
0.5131(0.36 - 0.73)
AKIN criteria 0.6667(0.48 - 0.82)
0.8100(0.74 - 0.86)
0.3667(0.24 - 0.50)
0.9364(0.88 - 0.96)
3.5088(2.41 - 5.10)
0.4115( 0.25 - 0.66)
Accuracy of conventional criterion vs AKIN criteria in the precition of in-hospital mortality in a series of 233 patients with cirrhosis and ascites
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
Patient survival with the acute kidney injury (AKI) andnon-AKI groups
AKI in cirrhosis
CD. Tsien et al. Gut 2013 ; 62 : 131-137
0
20
40
60
80
100
No AKIN AKI stage 1 AKI stage 2 AKI stage 3
P<0.001
P<0.0001
P<0.0001
P=N.S.P<0.025
P<0.01
Initial acute Kidney Injury Network (AKIN) stage (panel A) and in-hospital mortality
S. Piano et al. (J. Hepatol. 2013 ; in press)
Serum creatinine < 1.5 mg/dl
Renal failure in cirrhosis
Initial Stage 1 (72.1%) Initial Stage 2 (14.8%) Initial Stage 3 (13.1%)
Dynamics of AKI stage after initially fullfilling AKIN criteria (1)
Peak Stage 1 (52.5%)
72.7 %65.6 %
Peak Stage 2 (16.4%)
11.4 %
Peak Stage 3 (31.2%)
15.9 % 44.4 %
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
Criteria Sensibility95 % CI
Specificity95% CI
PPV95% CI
NPV95% CI
LR+95% CI
LR-95% CI
Conventional criterion 0.5152(0.33 - 0.69)
0.9450(0.90 - 0.97)
0.6071(0.40 - 0.78)
0.9220(0.87 - 0.95)
9.3664(4.8 - 18.17)
0.5131(0.36 - 0.73)
AKIN criteria 0.6667(0.48 - 0.82)
0.8100(0.74 - 0.86)
0.3667(0.24 - 0.50)
0.9364(0.88 - 0.96)
3.5088(2.41 - 5.10)
0.4115( 0.25 - 0.66)
AKIN withProgression
0.5455(0.36 - 0.71)
0.9450(0.90 - 0.97)
0.6207(0.42 - 0.79)
0.9265(0.88 - 0.95)
9.9174(5.15 - 19.06)
0.4810(0.33 - 0.70)
Accuracy of conventional criterion vs AKIN criteria in the precition of in-hospital mortality in a series of 233 patients with cirrhosis and ascites
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
Non-progressors(n° = 37)
Progressors(n° = 16)
P
Age (years) – mean (SD) 67.4 (10.6) 70.4 (7) 0.3707
Gender M/F – n° (%) 20 (54%) / 17 (46%) 8 (50%) / 8 (50%) 1.00
Child Pugh score – median (min-max) 10 (5-14) 10.5 (5-14) 0.9286
MELD score – median (min-max) 19 (9-38) 21 (11-37) 0.5540
Albumin (g/dl) – median (min-max) 2.7 (1.9-4.3) 2.7 (1.8-4.5) 0.8824
Bilirubin (µmol/L) – median (min-max) 63.3 (7.9-477.8) 85.3(8.9-631) 0.5571
Protrombin time (%) – mean (SD) 45.3 (13.9) 48.4 (16.0) 0.3563
Baseline sCr (mg/dl) – median (min-max) 1.1 (0.48-3.0) 1.2 (0.7-2.9) 0.3090
Baseline sCr ≥ 1.5 mg/dl – n (%) 14 (37.8) 5 (31.3) 0.7363
19 (51.4) 15 (93.7)
Bacterial infections – n (%) 24 (64.9) 11 (68.8) 1.000
Leukocyte counts el/µl – median (min-max) 6,500 (1,240-18,480)6,170 (2,750-
13,570)0.9764
Characteristics of patients with and without progression of initial stage of Acute Kidney Injury (AKI) according to the Acute Kidney Injury Network criteria
(AKIN)
S. Piano et al. (J. Hepatol. 2013 ; in press)
0.0041sCr ≥ 1.5 mg/dl at diagnosis of AKI –n (%)
Renal failure in cirrhosis
%
0
20
40
60
80
100
sCr < 1.5 mg/dl sCr > 1.5 mg/dl-
Probability of AKIN stage progression according to the cut off of 1.5 of serum creatinine (sCr)
S. Piano et al. (J. Hepatol. 2013 ; in press)
p < 0.01
Renal failure in cirrhosis
Initial Stage 1 (72.1%) Initial Stage 2 (14.8%) Initial Stage 3 (13.1%)
Dynamics of AKI stage after initially fullfilling AKIN criteria (2)
Peak Stage 1 (52.5%)
72.7 % 65.6 %
Peak Stage 2 (16.4%)
11.4 %
Peak Stage 3 (31.2%)
15.9 % 44.4 %
S. Piano et al. (J. Hepatol. 2013 ; in press)
Resolution
62.5 % 36.8 %40 %
Renal failure in cirrhosis
%
0
20
40
60
80
100
sCr < 1.5 mg/dl sCr > 1.5 mg/dl-
Probability of AKIN 1 stage regression accordind to the cut off of 1.5 of serum creatinine (sCr)
S. Piano et al. (J. Hepatol. 2013 ; in press)
p < 0.01
Renal failure in cirrhosis
Proposal of an algorithm for AKI management
Withdrawal of diuretics (if not yet applied) and volume expansion with albumin
(1g/kg) for 2 days
Initial AKI# stage 1 and sCr ≥ 1.5 mg/dl° or initial AKI# stage > 1
Initial AKI# stage 1 and sCr < 1.5 mg/dl°
° = sCr at the first fulfilling of AKIN crieria
#= AKI at the first fulfilling of AKIN crieria
* Treatment of SBP includes albumin infusion
Close monitoringRemove risk factors (withdrawal of nephrotoxic drugs, vasodilators and NSADs, taper/withdraw
diuretics treat infections*when diagnosed)
Progression ?
NO
Close follow up
YES
Response ?
YES NO
Does AKI Meet criteria of HRS ?
Specific treatment for other AKI phenotypes
NO
Terlipressin and albumin
YES
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
• The acceptance of the main point that derived from the application of AKIN criteria that is to focus attention on and to manage promptly even small increases in sCr.
• A clear dinstinction between AKI and hepatorenal syndrome (which is only one of the possible phenotypes of AKI)
• A more rationale application of the therapeutic resources (avoiding of potentially dangerous consequences of an overtreatment of AKI as a consequence of an uncritical application of the AKIN criteria)
• The definitive removal of any cut off of serum creatinine from the criteria for diagnosis of HRS
Clinical consequences of our proposal of an algorithm for AKI management
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
Proposal of an algorithm for AKI management
Withdrawal of diuretics (if not yet applied) and volume expansion with albumin
(1g/kg) for 2 days
Initial AKI# stage 1 and sCr ≥ 1.5 mg/dl° or initial AKI# stage > 1
Initial AKI# stage 1 and sCr < 1.5 mg/dl°
° = sCr at the first fulfilling of AKIN crieria
#= AKI at the first fulfilling of AKIN crieria
* Treatment of SBP includes albumin infusion
Close monitoringRemove risk factors (withdrawal of nephrotoxic drugs, vasodilators and NSADs, taper/withdraw
diuretics treat infections*when diagnosed)
Progression ?
NO
Close follow up
YES
Response ?
YES NO
Does AKI Meet criteria of HRS ?
Specific treatment for other AKI phenotypes
NO
Terlipressin and albumin
YES
S. Piano et al. (J. Hepatol. 2013 ; in press)
Renal failure in cirrhosis
Hepatorenal syndrome (HRS)
Treatment of HRS
Pharmacologic therapy for HRS
• Albumin (20-40 g/day intravenously)
• Terlipressin (0.5-2 mg/4-6hr intravenously)
J. Uriz et al. J. Hepatol. 2000 ; 33 : 43-48.
Hepatorenal syndrome (HRS)
Hepatorenal syndrome (HRS)
0
20
40
60
80
100
Noradrenalin Terlipressin
P. Sharma et al. Am. J. Gastroenterol. 2008 ; 103:1689–1697.
Percent of responders after at day 15
P = N.S.
50 % 40 %
Hepatorenal syndrome (HRS)
Cumulative probability of survival during therapy of patients treated with noradrenaline and terlipressin
V. Singh et al. J. Hepatol. 2012 ; 56 : 1293–1298
Hepatorenal syndrome (HRS)
0
500
1000
1500
2000
2500
3000
Noradrenalin Terlipressin
P. Sharma et al. Am. J. Gastroenterol. 2008 ; 103:1689–1697.
Cost of treatment in USD excluding that of albumin
P < 0.05
6 mg/day for 15 days
1.5 mg/h for 15 days
Patients with response to treatment
Hepatorenal syndrome (HRS)
0
20
40
60
80
100
Group A (Terlipressin) Group B (Midodrine + Octreotide)
All responders Full responders
% P < 0.0175.0
25.0
P < 0.01
54.2
8.3
M. Cavallin et. al. (manuscript in preparation)
Pharmacologic therapy for HRS
• Albumin (20-40 g/day intravenously)
• Terlipressin (0.5-2 mg/4-6hr intravenously)
J. Uriz et al. J. Hepatol. 2000 ; 33 : 43-48.
Hepatorenal syndrome (HRS)
The facts
• Vasoconstrictors and albumin are effective in less of 50 % of patients with type 1 HRS.
• Vasoconstrictor and albumin improve survival slightly.
• Vasoconsctrictors and albumin can not be used in all patients with type 1 HRS.
• In up to 25 % of patients the treatment should be discontinued for adverse effects.
• High cost of treatment.
Hepatorenal syndrome (HRS)
P. Angeli et al. Liver Int. 2012 (Epub ahead of print)
Limitations of terlipressin plus albumin
• Inherent
• Extrinsic
Hepatorenal syndrome (HRS)
HRS is a functional renal failure caused by intrarenal vasoconstriction which occurs in patients with end stage liver disease as well as in patients with acute liver failure or alcoholic hepatitis.HRS is characterized by impaired renal function, marked alterations in cardiovascular function, and overactivity in the endogenous vasoactive systems.
Hepatorenal syndrome (HRS)
Definition of HRS
F. Salerno et al. Gut 2007 ; 56 : 1310-1318.
CKD AKI
Serum creatinine > 1.5 mg/dl for 3 months
/type 2 HRS* /type 1 HRS*
* Proteinuria < 0.5 g/l and no hematuria
Hepatorenal syndrome (HRS)
JM. Trawale et al. Liver Int. 2010 ; 30 : 725-732.
Serum creatinine levels >1.5 mg/dl
Proteinuria > 0.5 g/day Haematuria
18
20
9
5
4
2
7
JM. Trawale et al. Liver Int. 2010 ; 30 : 725-732.
Hepatorenal syndrome (HRS)
Renal vascular injury
Acute tubulointerstitialinjury
Chronic tubulointerstitial
injury
10 (18)
13 (18)12 (18)
JM. Trawale et al. Liver Int. 2010 ; 30 : 725-732.
Hepatorenal syndrome (HRS)
0
100
200
300
400
no HRS HRS
NGAL urinary levels in patients with cirrhosis and ascites according to the diagnosis of type 1 HRS
M. Cavallin at al. AASLD 2011
P < 0.025
(ng/ml)
Hepatorenal syndrome (HRS)
Instrinsic AKI
*
*
*
*
** *
*
*
*
*
*
**
*
*
*****
** *
E. Singer et al. Kidney Int. 2011 ; 80 : 405-414
0
100
200
300
400
500
Full responders Partial or non responders
p < 0.0025
M. Cavallin. et. al. AASLD 2011
NGAL urinary levels in patients with type 1 HRS according to the response to terlipressin and albumin
(ng/ml)
Hepatorenal syndrome (HRS)
The ratio of urinary excretion of -glutamyltranspeptidase to glomerular filtration rate in patients with type 1 HRS
treated with vasonsctrictors and albumin
0
100
200
300
400
500* = P < 0.05 ; ** = P < 0.025
*
**
*
B D5 D10 B D5 D10
Nonresponders Responders
D20
P. Angeli et al. Hepatology 1999 ; 29 : 1690-1697.
Normal range
Hepatorenal syndrome (HRS)
Peripheral arterial vasodilation “hypothesis”
Portal hypertension/liver failure
Reduction of effective circulating volume
Severe renal arterial vasoconstriction
Maximal activation of endogenous vasocontrictor systems
RW. Schrier, et al. Hepatology 1988 ; 8 : 1151-1157 (revised)
Increased release of NO, CO and other vasodilators
Splanchnic arterial vasodilationTerlipressin
Albumin
Hepatorenal syndrome (HRS)
Hepatorenal syndrome (HRS)
HRS after SBP resolution
No HRS after SBP resolution
P
MAP (mm Hg) 738 838 < 0.025
SVR (dyn sec/cm ) 1268320 968226 N.S.
Plasma NE (pg/ml) 1290.5415.3 317.195.3 <.025
CO (l/min) 4.60.7 6.82.0 < 0.01
RAP (mm Hg) 4.62.7 4.11.7 N.S.
PCWP (mm Hg) 7.4 2.6 7.02.3 N.S.
HR (bpm) 879 7916 N.S.
5
Systemic heamodynamics before and after the onset of HRS after the resolution of SBP
L. Ruiz-del-Arbol et. al. Hepatology 2003 ; 38 : 1210-1218
Baseline At the diagnosis of
HRS P
MAP (mm Hg) 809757
< 0.001
HVPG (mm Hg) 19.53.020.04.0
< 0.005
SVR (dyn sec/cm ) 1158285 1096327 N.S.
CO (l/min) 6.01.2 5.41.3 < 0.001
RAP (mm Hg) 6.92.65.72.2
< 0.05
PCWP (mm Hg) 9.2 2.67.52.6
< 0.001
Systemic heamodynamics before and after the onset of type 1 HRS in patients with cirrhosis and ascites without a precipitating factor
L. Ruiz-del-Arbol et. al. Hepatology 2005 ; 62 : 439-447.
5
Hepatorenal syndrome (HRS)
Peripheral arterial vasodilation “hypothesis” (revised)
Portal hypertension/liver failure
Reduction of effective circulating volume
Severe renal arterial vasoconstriction
Maximal activation of endogenous vasocontrictor systems
RW. Schrier et al. Hepatology 1988 ; 8 : 1151-1157 (revised)
Increased release of NO, CO and other vasodilators
Splanchnic arterial vasodilation Reduced cardiac output
?
Hepatorenal syndrome (HRS)
Hepatorenal syndrome (HRS)
Y. Narahara et al. J. Gastroenterol. Hepatol. 2009 ; 24 : 1791-1797
Parameter BaselineAfter
terlipressinP
Heart rate (bpm) 83 ± 16 72 ± 16 < 0.005
Mean arterial pressure (mm Hg) 89 ± 11 105 ± 14 < 0.005
Systemic vascular resistance (dynes/s · cm5) 1295 ±293 1653 ± 465 < 0.005
Cardiac output (l/min) 5.2 ± 1.0 4.9 ± 1.1 < 0.05
Pulmunary capillary wedged pressure
(mm Hg)9.6 ± 3.1 12.3 ± 2.6 < 0.005
Systemic hemodynamics at baseline and 30 min. after terlipressin in patients with cirrhosis and ascites
Hepatorenal syndrome (HRS)
ParameterContrl
subjects (n° = 46)
Patients with cirrhosis and
without ascites (n° = 36)
Patients with cirrhosis and
responsive ascites
(n° = 31)
Patients with cirrhosis and
refractory ascites
(n° = 46)
Heart rate (beat/min) 67±10 70±10 68±11 78±13*#
Mean arterial pressure (mm Hg)
97±7 99±10 96±11 87±9*##
Systemic vasciular
resistance (din s/cm5m2) 3371±648 2925±641*** 2860±776*** 2439±573***#
Stroke volume (ml/beat) 64±10 75±12** 77±11** 73±17**
Cardiac output (L/min) 4.27±0.80 5.28±1.11*** 5.29±1.42*** 5.60±1.50***
Systemic hemaodynamics according to the stage of cirrhosis
* = p < 0.01 ; ** = p < 0.001 ; *** = p < 0.001 versus control subjects ; # = p < 0.05 ; ## = < 0.001 versus other groups of patients with cirrhosis
M. Cesari et al. (manuscript submitted)
Cardiac output in cirrhotic patients according to the Child-Pugh-Turcotte class
3000
6000
9000
12000
15000
Class A Class B Class C
Basal After i.v. albumin (40 g)
K. Brinch et al. J. Hepatol. 2003 ; 39 : 24-31
* = P < 0.025
* *
(ml/min)
* ** * = P < 0.01
Hepatorenal syndrome (HRS)
0
5
10
15
20
P < 0.005
Overall transvascular transport of albumin in cirrhosis
J. H. Henriksen et al. J. Hepatol. 2001 ; 34 : 53-60.
Controls Cirrhotics with ascites
Cirrhotics with refractory ascites
P < 0.01
(% IVM • h )-1
Hepatorenal syndrome (HRS)
Effects of albumin on cardiac contractility in cirrhotic rats
-10.0 -9.5 -9.0 -8.5 -8.0
0
5
10
15
20
25
L
VD
P (
mm
Hg)
Control
Cirrhotic
Log . Isoproterenol
Cirrhotic + albumin
* = P < 0.01
**
Cirrhotic + starch
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
?
Hepatorenal syndrome (HRS)
NAD(P)H•
p67
p47
gp91
rac
•O2-
O2 H+
NAD(P)+
p22phox
NADH/NADPH Oxidase
The NADPH/NADH oxidase
Hepatorenal syndrome (HRS)
0
0,5
1
1,5
2
control rats treated with V control rats treated with A
rats with cirrhosis treated with V rats with cirrhosis treated with A
Mem
bra
ne
/ cyt
osol
rat
io
(fol
d o
f in
crea
se)
*p <0.05 vs controls ; # = p <0.05 vs rats with cirrhosis treated with V
*
#
p47-phox Rac-1
*
#
Effects of albumin on the NADH/NADPH oxidase in the cardiac tissue according to treatment with saline (V) or albumin (A)
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
?TNF-
Hepatorenal syndrome (HRS)
0
0,2
0,4
0,6
0,8
1
1,2
1,4
1,6
1,8
Control rats treatedwith V
Control rats treatedwith A
Rats with cirrhosistreated with V
Rats with cirrhosistreated with A
Fol
d of
incr
ease
*
#
* p<0.05 vs control rats # p<0.05 vs rats with cirrhosis treated with V
Levels of NF-kB traslocation in the cardiac tissue according to treatment with saline (V) or with albumin (A)
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
Pro
tein
exp
ress
ion
(fol
d of
incr
ease
) *
#
* p<0.05 vs controls
Effects of albumin on TNF- protein expression in the cardiac tissue according to treatment with saline (S) or albumin (A)
# p<0.05 vs rats with cirrhosis treated with A
0
0,5
1
1,5
2
2,5
Control rats treatedwith S
Control rats treatedwith A
Rats with cirrhosistreated with S
Rats with cirrhosistreated with A
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
Pro
tein
exp
ress
ion
(fol
d of
incr
ease
) *
#
* p<0.05 vs controls
Effects of albumin on iNos protein expression in the cardiac tissue according to treatment with saline (S) or albumin (A)
# p<0.05 vs rats with cirrhosis treated with A
0
0,5
1
1,5
2
2,5
Control rats treatedwith S
Control rats treatedwith A
Rats with cirrhosistreated with S
Rats with cirrhosistreated with A
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
TNF-
Hepatorenal syndrome (HRS)
?
Hepatorenal syndrome (HRS)
* = p < 0.01 vs controll
Effects of albumin on β-adgrenergic signaling in cardiac tissue according to treatement with saline (V) or albumin (A)
0
0,5
1
1,5
2
2,5
β1 β2 Adcy3 Gαi2
control rats treated with V control rats treated with A
rats with cirrhosis treated with V rats with cirrhosis treated with A
**
*
*
# #
* p<0.05 vs controls ; # p<0.05 vs ascites with saline
Gen
e ex
pres
sion
(F
old
of
incr
ease
)
**
Hepatorenal syndrome (HRS)
A. Bortoluzzi et al. Hepatology 2013 ; 57 : 266-276
Hepatorenal syndrome (HRS)
Limitations of terlipressin plus albumin
• Inherent
• Extrinsic
Hepatorenal syndrome (HRS)
Response to tretament (%) according to the baseline serum creatinine value
0
10
20
30
40
50
60
3.0 mg/dl < 3 - 5 mg/dl > 5.0 mg/dl
TD. Boyer et al. J. Hepatol. 2011 ; 55 ; 315-321.
%
MANAGEMENT OF RENAL DYSFUNCTION IN PATIENTS WITH CIRRHOSIS
Summary • The application of conventional criterion is more accurate than a formal
application of AKIN criteria in the prediction of in-hospital mortality in patients with cirrhosis and ascites.
• Nevertheless, the addition of either the progression of AKIN stage or the cut-off of serum creatinine ≥1.5 mg/dl, to the AKIN improves their prognostic accuracy in these patients .
• The potential effects of implementation of the conventional criterion with the most innnovative aspects of AKIN criteria, should be tested by interventional clinical trials in the next future.
• Terlipressin and albumin are effective in patients with type 1 HRS.• Noradrenalin and albumin but not midodrine, octreotide and albumin can
represent an alternative in the treatment of type 1 HRS. • Some of the limits of the treatment with terlipressin and albumin may be
related to the fact that HRS may not be completely functional in nature and/or to the fact that the global effect of the treatment on cardiac output may be negative in some patients.
Hepatorenal syndrome (HRS)
P. Angeli et al. Liver Int. 2013 ; 33 : 16-23
Recommended