HEPATO RENAL SYNDROME

Definition:

1. A functional form of renal failure without renal histologic changes.

2. It is characterised by intense vasoconstriction,impaired renal perfusion and low GFR in the
setting of systemic and splanchnic vasodilatation.

Renal dysfunction in cirrhosis:

1. Common causes of Prerenal AKI:

Diuretics,lactulose,hypovolemia
2. Common causes of Renal AKI:
Glomerulonephritis,acute interstitial nephritis,acute tubular necrosis.

Pathogenesis of HRS:

1. Low blood pressure,a very low GFR(<40 ML/MIN) and increase in plasma levels of
renin,norepinephrine and antidiuretics charecterise HRS.
2. SPLANCHNIC VASODILATATION:increase in sheer stress in the splanchnic vasculature is a
result of portal hypertension leading to over production of nitric xide and other vasodilators
like NO,CO,glucagon,prostacyclin,endogenous opiates.
3. Bacterial translocation,mesenteric angiogenesis & hyporesponsiveness of the splanchnic
vasculature to vasoconstrictors.
4. Sodium retention,impaired free water excretion and decreased renal perfusion and
glomerular GFR are the main abnormalities and are progressive.
5. First abnormality:reduced ability to excrete sodium secondary to mineralocarticoid effects.
6. Second:patients are unable to exceret the sodium ingested in their diet & ascites develops.
7. Plasma rennin ,aldosterone and norepinephrine is elevated.
8. Circulatory dysfunction is greater at this stage with increased activity of the sympatheteic
nervous and rennin angiotensin system.
9. Renal perfusion & GFR are dependent on increased renal production of prostaglandins.
10. Lipid mediators are vasodilators that antagonise the vasoconstricting actions of angiotensin
II, Norepinephrine.
Diagnosis:

MAJOR DIAGNOSTIC CRITERIA FOR HRS

1.Cirrhosis With Ascites
2.Creatinine >1.5 Mg%
3.No Improvement In Creatinine After Atleast 2 Days Withdrawl Of Diuretics And Volume Expansion
With Albumin.
4.Absence Of Shock.
5.No Recent Treatment With Nephrotoxic Agents.
6.Absence Of Parenchymal Renal Disease-Proteinuria,Microhematuria,Abnormal Renal Ultrsound
Clinical types:

HRS-1:severe and rapidly progressive renal failure,doubling of creatinine to 2.5 mg% in <2 weeks
1. Infection,hemorrhage,paracentasis,surgery or acute hepatitis.
2. Has association with SBP,
3. Patients have intense SIRS & high cytokine levels in plasma & ascitic fluid.
HRS-2:moderate & steady decrease in renal function,with >1.5 mg% that fails to accept HRS-1.
Dominant clinical feature severe ascites with poor or no response to diuretics.
Goals of Treatment:

1. Improvement in liver function.

2. Treatment of decompensated hepatitis.
3. Supporting renal function.

Treatment:Volume expansion and vasoconstrictors:

1. Albumin-1g/kg for 2 days upto a maximum of 100 g/day & then followed by 20-40 g/day.
2. Vasopression-endogenous hormone acting on 3 receptors
 3. V1-vascular smooth muscle –vasoconstriction-TARGET OF INTEREST.
4. V2-osmoregulation in the kidney.
5. V3-corticotropin secretion.
6. Contraindications for vasopressin-ischemic heart disease,peripheral vascular disease &
cerebrovascular disease.

Terlipressin:

1. Terlipressin-survival benefit.
2. DOSE:1-2 mg every 4-6 hours
3. Maximal dosage of 12 mg/day with a minimum duration of 3-5 days
4. Monitoring by creatinine levels.

TIPSS:

1. Decreasing portal pressures by portosystemic anastomosis to improve the circulatory

compromise of cirrhosis is targeted as a treatment for HRS.

Hemodialysis:

1. For renal support for treating an acute or reversible decompensation.

2. As a bridge to liver transplantation

Liver transplanatation:

1. Treatment of choice.
2. GFR improves 1-2 months postoperatively.
3. Hemodynamic and nurohormonal abnormalities resolve in 6 months.