The document discusses hepatorenal syndrome (HRS), a type of kidney failure seen in patients with cirrhosis and ascites. It provides details on three patient case studies, including their histories, examinations, investigations and management considerations. Key points covered include definitions of acute kidney injury (AKI) and HRS, pathophysiology of renal dysfunction in cirrhosis, evaluation of patients, biomarkers for distinguishing HRS from other causes of AKI, and general management approaches including use of albumin infusion.

1. HEPATORENAL SYNDROME
DR Umashankar U S

2. Case Capsule
• 53 year Male patient
• Symptomatic since 3 months
• C/O Distention of abdomen since 3 months insidious
onset, gradually progressive, generalized in nature, not
associated with pain
• Associated with lower limb swelling, bilateral, until
ankle region, not associated with pain, increases with
prolonged standing and disappears on waking up from
bed
• h/o loose stools present for three days, six – seven
episodes, large volume, watery stools
• No h/o of any drug intake

3. • Patient is a known diabetic for 6 years on
insulin
• Patient is known hypertensive on tab
amlodepine 5mg twice daily
• Hypothyroid on thyroxine 50mcg/day
• Consumes mixed diet
• Sleep –normal
• No substance abuse

4. Examination
• Conscious, oriented Afebrile
• Pulse – 94/min, regular
• BP – 102/40mmHg
• RR – 20/min
• BMI – 24.4
• JVP – normal
• Pallor – present
• Bilateral pitting pedal edema present
• Koilonychia present

5. Abdomen –
• Abdomen appears uniformly distended, flanks full
• Hernial orifices are free
• No dilated veins/ scars
• All quadrants move equally with respiration
• Umbilicus – inverted, shifted downwards
• Shifting dullness present
• No bruit / hepatic or splenic rub
• Bowel sounds – heard
• Per rectum – normal anal tone, no mass palpable/ no
malena

6. Investigation
• Hb- 7.0g%
• TLC- 4500
• DC- N55/L40/E5
• ESR- 35mm/hr
• Platelet – 70,000/microL
• Peripheral smear – normocytic normochromic
anemia
• RBS-186mg/dl, Hba1c 11.2
• A/F: High SAAG, low protein ascites with normal
cell count

7. 2/5/20 5/12/20 1/3/20
Urea 32 21 64
Creat 0.5 0.7 1.2
LFT- TB: 0.6, AST/ALT: 80/92 ALP: 105
Alb : 2.4, Glob: 3.0
PT:22s, INR: 1.32
HBsAg, Anti HCV, HIV- negative
Urine routine : no proteinuria or RBC
CXR, ECG: WNL
USG Abd: CLD with moderate ascites
2D Echo: normal study

8. Is it prerenal AKI?
Is it HRS?
Is it ATN?
Is it Diabetic nephropathy?
When should we start terlipressin ?
Is albumin alone sufficient?
What next ?

9. Case capsule 2
• 32year female married incidentally detected
to be HCV positive while evaluating for rashes
over the lower limbs
• No prior h/o jaundice or abdominal distension
or hematemesis or altered sensorium
• Non alcoholic
• No prior comorbidities
• h/o tattoing+

10. • o/e: purpuric rashes over the lower limbs
present
• No other significant findings
• Inv: hb-12, tc-600, plt-98000,esr-68
• Lft- a/g reversal present
• Urea: 74, Creat: 1.9
• Urine routine: protein ++; 24 hr protein: 1.8g
• Inr- 1.4
• Usg abdomen: Cld with mild splenomegaly, no
ascites

11. Case capsule 3
• k/c/o ethanol related cld with ascites since
three years on maximum dose of diuretics
• now presented with increasing abdominal
distension with h/o repeated need of
therapeutic paracentesis since 3 months
• Pain abdomen since 5 days
• Decreased urine output since 2 days
• Altered sleep pattern since one day

12. • o/e: palllor +, pedal edema+, icterus+
• Bp: 98/50mmhg, pr: 98
• No flaps
• P/A: Distended, dialated veins +, flanks full,
shifting dullness absent, fluid thrill +
• Inv :
• Hb-8, tc-11200, plt- 45800
• Lft- ot/pt 56/34, alb/ glob 2.0/3.1
• Inr 1.3
• Na-123, K 3.5
• HIV, HbSAg, Anti HCV- Neg

13. Urine R/M: bland cast present, protein 1+, no rbc
Usg abdomen : CLD with massive ascites with splenomegaly, kidneys
normal
A/F Analysis: tc 500 with predominant neutrophils, alb=0.3, total
protein- 0.8
2D echo: Grade 2 diastolic dysfunction
WHAT NEXT??
12/1/20 31/4/20 8/7/20 2/11/21 2/3/21
Urea 21 54 42 68 84
Creat 0.8 1.2 0.9 2.1 3.8

14. Renal dysfunction
• AKI - 19% of cirrhotic patients
• The combination of liver disease and kidney dysfunction :
1. Simultaneously (e.g., polycystic diseases and viral
hepatities)
2. Chronic forms of kidney disease secondary to
compensated liver disease (e.g., IgA nephropathy);
3. AKI resulting from common complications of liver disease,
especially infections
4. Functional renal failure resulting from decompensated
liver disease - HRS

15. Spectrum of AKI in Cirrhosis
Reappraising the spectrum of AKI and HRS in cirrhosis Juan Carlos etal ;Nature review

18. Pathophysiology
• Three important components contribute to the
initiation and perpetuation of altered renal perfusion.
(1) arterial vasodilatation in the splanchnic and systemic
circulation,
(2) renal vasoconstriction
(3) cardiac dysfunction.
• Form the basis for current therapies and preventive
strategies.

21. Effects of cardiac dysfunction
• Systolic incompetence
• Cirrhotic Cardiomyopathy
• Low cardiac output, low MAP, and low renal
blood flow are correlated with development
of renal failure in cirrhosis

22. Effects of inflammation and infection
Bernardi M, Angeli P, Claria J, et al. Gut 2020;69:1127–1138

23. Effects On Renal Vasculature
• HRS -intense renal
vasoconstriction in absence
of structural abnormality of
the blood vessels
• Renal auto regulation is
operational above a mean
arterial pressure( MAP) of
65 mmHg
• CLD despite a decent renal
perfusion pressure, the
blood flow is severely
compromised

24. Renal microcirculation imbalance
• Synergic interplay of inflammation and microvascular
dysfunction -PAMPs and DAMPs exert on proximal epithelial
tubular cells.
• These cause a mitochondria-mediated metabolic down
regulation and reprioritisation of cell functions to favour
survival processes above all else.
• The sacrificed functions - absorption on the lumen side of
sodium and chloride.
• The consequent increases of NaCl delivery to the macula
densa triggers further intrarenal activation of the RAAS - thus
lowers GFR.
• Severe cholestasis may further impair renal function by
worsening inflammation and/or macrocirculatory dysfunction.

25. Causes of AKI in cirrhosis

26. Reappraising the spectrum of AKI and HRS in cirrhosis Juan Carlos etal ;Nature review

27. Evolution of Defn of HRS

28. Definition Of HRS
• Diagnosis of cirrhosis and ascites
• Diagnosis of AKI
increase in serum creatinine of ≥0.3 mg/dl
and/or
≥50% from baseline and/or
Urinary output ≤ 0.5 ml/kg B.W. ≥6 h
• No response after 2 consecutive days of diuretic
withdrawal and plasma volume expansion with albumin
1g/kg of body weight
• Absence of shock
• No current or recent use of nephrotoxic drugs
• No macroscopic signs of structural kidney injury
International Ascites Club 2017Consensus Diagnosis, prevention and treatment of HRS in
cirrhosis. Gut

29. Definitions
Baseline sCr
• A value of sCr obtained in the previous three
months, when available, can be used as
baseline sCr.
• More than one value within the previous
three months - the value closest to the
admission time to the hospital .
• Without a previous sCr value –admission sCr
EASL Practice Guidelines for management of decompensated cirrhosis. JHepatol (2018).

30. AKI
• Functional criteria-
Increase in sCr ≥50%
within seven days
from the baseline
or
increase in sCr ≥0.3
mg/dl within two days
• Structutal criteria- nil
EASL Practice Guidelines for management of decompensated cirrhosis. JHepatol (2018).

31. AKD &CKD

32. Classification of HRS
OLD
CLASSFN
NEW
CLASSFN
CRITERIA
HRS-1 HRS-AKI
a) Absolute increase in sCr ≥0.3 mg/dl within 48 h
and/or
b) Urinary output ≤ 0.5 ml/kg B.W. ≥6 h
or
c) Percent increase in sCr ≥50% using the last
available value of outpatient sCr within 3 months
as the baseline value
HRS-2
HRS-
NAKI
HRS-
AKD
a) eGFR <60 ml/min per 1.73 m2 for <3 months in
the absence of other (structural) causes
b) Percent increase in sCr <50% using the last
available value of outpatient sCr within 3 months
as the baseline value
HRS-
CKD
a) eGFR <60 ml/min per 1.73 m2 for ≥3 months in
the absence of other (structural) causes

33. What is new in the definition and
classification?
• Most recent ICA consensus the definition of AKI in
cirrhosis modified to align with KDIGO sCr criteria
• Classified based on severity; into three stages
• Stage 1 - increase in sCr ≥0.3 mg/dl or an increase in
sCr ≥1.5-fold to 2-fold from baseline
• Stage 2- increase in sCr >2-fold to 3-fold from baseline
• Stage 3 - increase of sCr >3-fold from baseline OR
sCr ≥4.0 mg/dl with an acute increase ≥0.3 mg/dl OR
initiation of renal replacement therapy

34. • The original definition of HRS-1 required that
the diagnosis be established at an advanced
stage of AKI (at least stage 2) that limits the
efficacy of vasoconstrictor therapy.
• The consensus definition of AKI defines
baseline sCr - avoid a diagnostic delay of at
least 2 days.
• The imputation method recommended by
KDIGO to calculate baseline sCr

35. Assessment of renal dysfunction
• Kidney function is defined on the basis of GFR.
• M/c biomarker of GFR is serum creatinine.
• GFR can be estimated either by applying
estimating equations to single serum
creatinine values

36. Problems with Creatinine
• Low serum creatinine levels
1. Reduced production of creatinine from
creatine in liver,
2. Greater volume of distribution due to
increases in extracellular fluid and ascites
3. Significant muscle wasting
4. Creatinine measured by colorimetric
methods -artificially lowered in jaundiced
patients

38. Non Creatinine Biomarker
• Cystatin C - The best-validated non creatinine
biomarker
• Encoded by the CST3 gene,
• Produced in a stable rate by all nucleated cells and
released into the blood stream .
• Freely filtered by the renal glomeruli and subsequently
metabolized in the proximal tubules.
• Based on its reported independence from the effects
of age, gender and body composition it has been
suggested that increased cystatin C levels may be a
more sensitive indicator of renal dysfunction than
conventional creatinine based measures

39. Evaluation of cirrhosis patient with
kidney dysfunction
• Liver function tests: INR, bilirubin, protein, albumin
• Liver enzymes: AST, ALT, ALP
• Renal function: daily serum creatinine and electrolytes
• Complete blood count: hemoglobin and white cell
count
• Full sepsis workup
• Blood cultures × 2
• Urine culture
• Ascitic fluid cell count and culture
• Chest X-ray
• Spot urine protein–creatinine ratio

40. Absence of abnormal renal imaging.
• Renal ultrasonography is the modality of
choice
• Exclude bladder neck obstruction (bladder
scan is less reliable in the presence of ascites
• Changes in parenchymal echogenicity are
indicative of an intrinsic kidney disease, either
glomerular, tubular or tubulointerstitial.

41. Urinary sodium
• Minor criterion in the original 1996 ICA definition of
HRS-1
• The most likely reason for its continued popularity is –
1. low FENa that is, <1% and low urinary sodium (that
is, <20 mEq/l), are almost universally present in HRS-1
2. FENa >2% or a urinary sodium >40 mEq/l are s/o
intrinsic tubular injury and are highly inconsistent
with HRS-1
• FeNa 0.1-1% - HRS-1 and ATN overlap
• FeNa < 0.1%- better diagnostic utility

42. Urinalysis and urine microscopy
• For exclusion of HRS-1 - >50 RBC/HPF) or proteinuria (>500 mg/day)
• Dysmorphic RBCs, acanthocytes-glomerular disease even when
found in low quantities (1–5/HPF)
• Leukocyturia- infections, can be a trigger for HRS
• Culturing the urine yield no growth of any bacteria and/or if WBC
casts are present- AIN should be considered a potential cause of
AKI.
• Muddy-brown granular casts - toxic or ischaemic ATN,
• Cholaemic nephropathy – bilirubin stained tubular epithelial cell
casts
• Careful inspection of the urinary sediment by an experienced
physician can aid interpretation of the aetiology of kidney disease in
cirrhosis.

44. • Interleukin-18 (IL-18),
• Kidney injury molecule-1 (KIM-1),
• Liver type fatty acid-binding protein (L-FABP)
• Urinary albumin
• Neutrophil gelatinase-associated lipocalin (NGAL).
• Comparing the three distinct diagnoses, all biomarkers
were significantly elevated in ATN-AKI relative to
prerenal AKI
• NGAL, IL-18, and albumin were statistically significant
Biomarkers of renal damage

45. NGAL
• Most investigated biomarker
• Consistent in patients diagnosed with HRS, raising the
possibility of NGAL as an objective test to distinguish
primarily functional AKI from structural AKI in patients
with cirrhosis
• Guide decisions regarding vasoconstrictor therapy.
• Cut-off with the best predictive accuracy for ATN
diagnosis - 220 mcg/g of creatinine
• 86% ATN-AKI had values of urinary NGAL above this
threshold, whereas the majority of patients with HRS-
AKI or prerenal AKI (88% and 93%, respectively) had
values below

46. MANAGEMENT

47. General measures
• The exclusion of reversible or treatable
conditions.
• A diligent search for precipitating factors
(infection, gastrointestinal bleeding) & prompt
treatment
• Nephrotoxic drugs should be removed.
• Hypovolemia and anemia from gastrointestinal
bleeding - volume replacement in the form of
blood or blood products.

48. Nonselective βblockers should be stopped (at least temporarily)

49. ALBUMIN
• Globular, water- soluble 67 kDa protein
• Negatively charged at neutral pH
• Translated from a single gene as
preproalbumin, imported into the
endoplasmic reticulum for cleavage of
its N- terminal prepropeptide by a serine
protease, transported to the Golgi and
continuously secreted into the
bloodstream.
• Its persistence in the circulation derives
from its constant uptake and recycling
by hepatocytes, a process regulated in a
pH- dependent manner by the neonatal
crystallisable fragment receptor (FcRn)
• Its absence lead to hypoalbuminaemia

50. Albumin
• plasma expander
• pleotropic scavenger
• antioxidant
• immunomodulatory
molecule
• solubilisation and
transport of molecules

51. • Albumin also prevents renal dysfunction and death in
patients with SBP.
• Improves effective blood volume by attenuating
peripheral arterial vasodilation and endothelial
dysfunction (plasma von Willebrand factor reduction)
• Albumin administration also improves effective blood
volume, thus leading to vasoconstrictor systems
deactivation, and increases arterial pressure in patients
with HRS treated with terlipressin, effects not observed
with terlipressin alone.

52. • Enhances cardiac work and improves cardiac
inotropism related to the reversal of the negative
effects of TNF-α and oxidative stress on cardiac
contractility
• Shown to be effective in reducing post
paracentesis circulatory dysfunction and in
preventing AKI and death from spontaneous
bacterial peritonitis

53. • Increase in systemic vascular resistance and
CO due to albumin are mainly related to the
non-oncotic properties of the molecule
• Albumin has been used intravenously at the
mean dose of 20–40 g/day.(EASL,2018)

54. Long term albumin in cirrhosis

55. • HRS by definition is a diagnosis of exclusion
and patients with HRS will not respond to
volume replacement with albumin alone
• The ICA recommends the use of 20–40 g of
albumin per day in combination with
vasoconstrictors, after an initial dose of 1 g/kg
of body weight up to 100 g/day on the initial 2
days

56. Vasoconstrictor therapy
• The rationale is to reduce the extent of
systemic vasodilatation.
• Rise in the systemic arterial blood pressure-
improve the renal perfusion pressure.

57. Assessment of response
• No response- No regression of AKI
• Partial response- Regression of AKI stage with a
reduction of sCr to ≥0.3 mg/dl above the baseline
value
• Full response-Return of sCr to a value within 0.3
mg/dl of the baseline value
EASL Practice Guidelines for management of decompensated cirrhosis. JHepatol (2018).

58. Duration of treatment
• Treatment should be maintained until a
complete response
Or
• For a maximum of 14 days either in case of
partial response or in case of non-response

59. Terlipressin
• Selective vasopressin 1 receptor agonist
vasoconstrictor used in treatment of type 1
HRS.

60. Terlipressin
• Vasoconstrictor for both the systemic and
splanchnic circulations
• Terlipressin plus albumin should be
considered as the first-line therapeutic option
for the treatment of HRSAKI
• Dose : IV boluses at the initial dose of 1 mg
every 4–6 h OR continuous i.v. infusion at
initial dose of 2 mg/day
Rodriguez E, et al.Terlipressin and albumin for type-1 hepatorenal syndrome associated with
sepsis. J Hepatol 2014.

61. • Titration: Non response (decrease in SCr<25% from the
peak value), after 48-72 hours, the dose of terlipressin
should be increased in a stepwise manner to a
maximum of 12 mg/day
• Place: Can be given in wards
• Caution: patients with cardiac diseases, peripheral
vascular disease
• ECG- recommended in all patients before starting
treatment
• Predictors of response: bilirubin level of <10mg/dL
and a rise in MAP of >5 mmHg on day 3 of treatment
Rodriguez E, et al.Terlipressin and albumin for type-1 hepatorenal syndrome associated with
sepsis. J Hepatol 2014.

62. Adverse effects
• 9% and 22% in the two studies
• abdominal cramps
• increased bowel movements
• Arrhythmia
• Ischemia to the bowels
• MI
• Peripheral gangrene
Rodriguez E, et al.Terlipressin and albumin for type-1 hepatorenal syndrome associated with
sepsis. J Hepatol 2014.

63. • 23 of 97 (23.7%) patients receiving terlipressin achieved HRS
reversal vs 15 of 99 (15.2%) receiving placebo had attained
primary end point of change in SCr
A post hoc analysis showed a clear correlation between survival
and relatively small changes in SCr level

64. Phase 3 study. Verified reversal of HRS was reported in 63 patients (32%) in the
terlipressin group and 17 patients (17%) in the placebo group (P = 0.006). HRS
reversal among patients with systemic inflammatory response syndrome is 31
(37%) vs 3 (6%), respectively (P<0.001)
CONCLUSIONS : In this trial involving adults with cirrhosis and HRS-
1, terlipressin was more effective than placebo in improving renal function but
was associated with serious adverse events, including respiratory failure.

65. Norepinephrine
• Catecholamine neurotransmitter, inotrope
• Causes peripheral and splanchnic vasoconstriction
• Dose: 0.5–3 mg/hour (0.1-0.7 μg/kg/min)as an IV
infusion.
• Increase by 0.05 μg/kg/min every 4 hr
• Titration: ≥10mmHg increase in MAP
or
≥200mL increase in 4 hour urine output
until HRS reversal or for15days
• Place – ICU with close monitoring of vitals
• Advantage: cheaper and easily available

66. Adverse events
• Hypertension
• Arrythmias
• Confusion
• Anxiety
• Headache
• Sweating
• Tremors
• Urinary retention
• Peripheral gangrene

67. EVIDENCE
• Pilot study of 12 patients with cirrhosis,
refractory ascites, and type 1 HRS, the use of
intravenous norepinephrine in combination with
albumin and intravenous furosemide resulted in
the reversal of HRS in 10 of the 12 patients after
a median of 7 days
• Follow-up study: comparing the efficacy of
norepinephrine vs. terlipressin. Norepinephrine
resulted in a 70% complete response rate
compared to that of ≥80% with terlipressin

68. MIDODRINE+OCTREOTIDE+ALBUMIN
• α1 agonist
• Prodrug  metabolized to desglymidodrine in liver.
• Increases MAP
• Peak concentrations after 1hr of ingestion
• Half life is about 4-6 hr.
• Primarily excreted in urine as desglymidodrine by
active renal excretion

69. • Acts on smooth muscles of venules and
arterioles.
• Given along with octreotide+albumin
• Dose: The starting dose is 2.5 mg three times
daily, and the dose should be titrated upwards
in 2.5-mg increments every 24 hours until a
maximum of 15 mg three times daily.
• Titration: every 24 h to achieve an increase in
systolic blood pressure of approximately 10–
15 mmHg.

70. Adverse events
• Supine and sitting
hypertension,
• Paresthesia
• Pruritus (mainly of the
scalp),
• Piloerection, chills
• Urge incontinence
Contraindications
• Severe organic heart
disease,
• Urinary retention,
• Pheochromocytoma
• Thyrotoxicosis

71. Octreotide
• long-acting analogue of somatostatin
• antagonizes the action of various splanchnic
vasodilators
• Reduce the extent of splanchnic vasodilatation
• Midodrine or octreotide alone have not been proven
to be useful for patients with HRS
• Dose: subcutaneously at a dose of 100 μg three times
daily or intravenously at 25μg/hour after an initial
bolus of 25 μg.
• A/E – gall bladder hypokinesia, gall stones,
hypothyroidism, dysglycemia, bradycardia.

73. TIPS
• May improve renal function in patients with type 1 HRS
• Applicability is very limited in type 1 HRS
• TIPS has been studied in patients with type 2 HRS and
in the management of refractory ascites, frequently
associated with type 2 HRS.
• In these patients, TIPS has been shown to improve
renal function
• Advantages
• Serum creatinine levels declines, sodium excretion
increases, and neurohumoral responses improves after
TIPS, although survival may not be affected

74. • The major benefit was seen in patients
with type 2 HRS.
Limitations
• An increase in the rate of hepatic encephalopathy
• A worsening of liver function (marked by a rise in
serum bilirubin)
• A bleeding complication due to the procedure
• A risk of renal injury associated with intravenous
contrast, which is often necessary, even if carbon
dioxide is used as the main contrast agent.

75. Renal replacement therapy.
1. should be considered in non-responders to
vasoconstrictors.
2. Patients with end-stage kidney disease.
• The indications for RRT are same as in the
general population including:
• severe and/or refractory electrolyte and acid-
base imbalance
• severe or refractory volume overload
• Symptomatic azotaemia

76. Liver support systems
Artificial liver support systems, either the molecular
adsorbents recirculating system (MARS) or Fractionated
plasma separation and adsorption (Prometheus)
showed promising beneficial effects in patients with
type 1 HRS.
• Experimental only

77. Liver Transplantation
• It is the only therapeutic modality that has the
potential to reverse both liver dysfunction and HRS.
• Rates of postoperative complications and in-hospital
mortality are higher in patients transplanted with HRS
than in those transplanted without HRS.
• Renal function improves after transplantation and is
associated with a reduction in plasma levels of
vasoactive factors.
• Recovery is frequently incomplete

78. • 3-year survival rate of patients transplanted with HRS is
approximately 60% compared with 70% to 80% for
patients transplanted without HRS.
• Continuing to consider the baseline MELD and/or
MELD-Na score rather than those during or after the
end of the treatment
• Independent Predictors of survival post op are
• The duration
• Degree
• Type (HRS or acute tubular necrosis) of renal
dysfunction
• Patients who require hemodialysis carry a high
mortality risk

79. Association between renal function at the time of deceased donor
liver transplant and survival after transplant

80. Simultaneous liver-kidney transplantation(SLK)
It can be indicated in patients with cirrhosis and CKD in
the following conditions:
a) estimated GFR (using MDRD6 equation) ≤40 ml/min
or measured GFR using iothalamate clearance ≤30
ml/min,
b) Proteinuria ≥2 g a day,
c) kidney biopsy showing >30% global
glomerulosclerosis or >30% interstitial fibrosis, or
d) inherited metabolic disease.

81. SLK is also indicated in patients with cirrhosis and
sustained AKI irrespective of its type, including HRS-AKI
when refractory to drug therapy, in the following
conditions:
a) AKI on RRT for ≥4 weeks or
b) estimated GFR ≤ 35 ml/min or measured GFR ≤25
ml/min ≥4weeks.
Beyond this in the presence of risk factors for
underlying
undiagnosed CKD (diabetes, hypertension, abnormal
renal imaging and proteinuria >2 g/day)
Nadim MK, et al. Simultaneous liver-kidney transplantation summit: current state
and future directions. Am J Transplant 2012

83. Prevention of Hepatorenal Syndrome
(HRS)
• Measures to prevent variceal bleeding (e.g., beta
blockers, band ligation)
• Pentoxifylline for severe alcoholic hepatitis
• Avoid intravascular volume depletion (diuretics,
lactulose, GI bleeding, large-volume paracentesis
without adequate volume repletion)
• Judicious management of nephrotoxins (ACEIs, ARBs,
NSAIDs, antibiotics)

84. • Prompt diagnosis and treatment of infections (SBP,
sepsis)
• SBP prophylaxis

85. Conclusion
• The hepatorenal syndrome is one of many potential
causes of AKI in patients with acute or chronic liver
disease.
• Arterial vasodilatation in the splanchnic circulation.
• Newer classification of HRS is HRS-AKI(formerly HRS
Type 1),HRS NAKI(formerly HRS Type 2).
• Vasoconstrictors and albumin are recommended in all
patients of AKI-HRS.
• Terlipressin plus albumin should be considered as the
first-line therapeutic option for the treatment of HRS-
AKI.

86. • Terlipressin can be used by i.v. boluses at the initial
dose of 1 mg every 4–6 h.
• Albumin solution (20%) should be used at the dose
20–40 g/day.
• LT is the best therapeutic option for patients with
HRS regardless of the response to drug therapy.