Hepatorenal syndrome

Question 1

What is hepatorenal syndrome?

Answer 1

Represents the end-stage of a sequence of reductions in renal perfusion induced by increasingly severe hepatic injury.

The hepatorenal syndrome is a diagnosis of exclusion and is associated with a poor prognosis.

Question 2

Pathogenesis of hepatorenal syndrome

• ALF or CLD (cirrhosis) leads to ___________ 🡪 triggers ___________ (though to be due to the increases NO released by endothelium in response to bacteria transposed from Splanchnic to Systemic Circulation)
• Leads to ____________ 🡪 activation of _____________ release to retain water
• RAAS induces _____________ 🡪 reduced GFR and renal perfusion 🡪 _____
• Aldosterone causes decreased Na (and H2O) release 🡪 Induces a Fluid Overloaded state 🡪 _________

This is how Fluid Overload (Ascites) can coexist with reduced renal perfusion and AKI

Answer 2

portal hypertension;

splanchnic vasodilatation;

systemic hypotension;

RAAS + Vasopressin;

afferent arteriole vasoconstriction;

AKI;

Ascites

Question 3

How is HRS identified?

Answer 3

A progressive rise in serum creatinine

No or minimal proteinuria (less than 500 mg per day) 🡪 aka non-nephrotic

A very low rate of sodium excretion (ie, urine sodium concentration less than 10 meq/L)

Oliguria

Question 4

What is the definition of type 1 HRS?

Answer 4

at least a twofold increase in serum creatinine (reflecting a 50 percent reduction in creatinine clearance) to a level greater than 2.5 mg/dL (221 micromol/L) during a period of less than two weeks.

Question 5

What is the major clinical feature in patients with type 2 HRS?

Answer 5

The major clinical feature in patients with type 2 HRS = ascites that is resistant to diuretics (aka refractory fluid overload)

Question 6

What is the diagnostic criteria for hepatorenal syndrome? (diagnostic of exclusion)

Answer 6

Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension

Acute kidney injury, defined as an increase in serum creatinine of 0.3 mg/dL (26.5 micromol/L) or more within 48 hours, or an increase from baseline of 50 percent or more within seven days

The absence of any other apparent cause for the acute kidney injury, including shock, current or recent treatment with nephrotoxic drugs, and the absence of ultrasonographic evidence of obstruction or parenchymal renal disease

Question 7

What is the management of hepatorenal syndrome?

Answer 7

Strict I/O (input/output)

Stop diuretics despite portal HTN (will worsen dehydration)

Admit ICU: give medical Mx:

• IV albumin
• IV Terlipressin for 2 weeks (Splanchnic VasoC 🡪 ↑ MAP 🡪 ↑ renal perfusion)
• If Terlipressin is unavailable, midodrine + octreotide can be used. Midodrine is a systemic VasoC while octreotide inhibits endogenous vasodilator release (inducing splanchnic VasoC)
• Fluids

If unresponsive to medical Mx – consider dialysis or TIPS