Severe preeclampsia: and onset of
hepatorenal syndrome: How?? Activation
of the renin–angiotensin system, which results in
the vasoconstriction of vessels systemically and also in
the kidney specifically. The kidney
failure in hepatorenal syndrome is believed to primarily to arise
from abnormalities in blood vessel tone in the kidneys. The
predominant theory (termed the underfill theory)
is that blood vessels in the kidney circulation are constricted because of the
dilation of blood vessels in the splanchnic circulation (which
supplies the intestines), which is mediated by factors released by liver
disease. Nitric oxide prostaglandins,
and
other vasoactive substance have been hypothesized as powerful mediators of
splanchnic vasodilation in cirrhosis. .The consequence of this
phenomenon is a decrease in the "effective" volume of blood sensed by
the juxta glomerular apparatus, leading to the
secretion of renin and
the activation of the renin–angiotensin system, which results in
the vasoconstriction of vessels systemically and in the kidney specifically. However,
the effect of this is insufficient to counteract the mediators of vasodilation
in the splanchnic circulation, leading to persistent "under filling"
of the kidney circulation and worsening kidney vasoconstriction, leading to
kidney failure. .Studies to quantify this theory have shown that
there is an overall decreased systemic vascular resistance in
hepatorenal syndrome, but that the measured femoral and
kidney fractions of cardiac output are respectively increased
and reduced, suggesting that planchnic vasodilation is
implicated in the kidney failure. Many
vasoactive chemicals have been hypothesized as being involved in mediating the
systemic hemodynamic changes, including atrial natriuretic factor, prostacyclin, thromboxane A2,[17] and endotoxin
In addition to this, it has been observed that the administration
of medications to counteract splanchnic vasodilation (such as ornipressin terlipressin, and octreotid leads
to improvement in glomerular filtration rate (which is
a quantitative measure of kidney function) in patients with hepatorenal
syndrome, providing further evidence that splanchnic vasodilation is a key
feature of its pathogenesis.
The underfill theory involves
activation of the renin–angiotensin–aldosterone system, which leads to an
increase in absorption of sodium from the kidney tubule (termed renal
sodium avidity) mediated by aldosterone,
which acts on mineralocorticoid receptors in
the distal convoluted tubule. This is
believed to be a key step in the pathogenesis of ascites in
cirrhotics as well. It has been hypothesized that the progression from ascites
to hepatorenal syndrome is a spectrum where splanchnic vasodilation defines
both resistance to diuretic medications in ascites (which is commonly seen
in type 2 HRS) and the onset of kidney vasoconstriction (as described above)
leading to hepatorenal syndrome
Hepatorenal syndrome is a particular
and common type of kidney failure that affects individuals
with liver cirrhosis or, less commonly, with fulminant liver failure. The syndrome
involves constriction of the blood vessels of the kidneys and
dilation of blood vessels in the splanchnic circulation, which supplies the
intestines. The classification of hepatorenal syndrome identifies two
categories of kidney failure, termed type 1 and type
2 HRS, which both occur in individuals with either cirrhosis or fulminant liver failure. In both
categories, the deterioration in kidney function is quantified either by an
elevation in creatinine level in the blood, or by decreased clearance of creatinine in the urine.
Hepatorenal syndrome (often abbreviated HRS)
is a life-threatening medical condition that consists of rapid deterioration in kidney function in
individuals with cirrhosis or fulminant liver failure.
HRS is usually fatal unless a liver transplant is performed,
although various treatments, such as dialysis,
can prevent advancement of the condition.
HRS can affect individuals with
cirrhosis, severe alcoholic hepatitis, or liver failure, and
usually occurs when liver function deteriorates rapidly because of a sudden
insult such as an infection, bleeding in the gastrointestinal
tract, or overuse of diuretic medications.
HRS is a relatively common complication of cirrhosis, occurring in 18% of
people within one year of their diagnosis, and in 39% within five years of
their diagnosis. Deteriorating liver function is
believed to cause changes in the circulation that supplies the intestines,
altering blood flow and blood vessel tone in
the kidneys.
The kidney failure of HRS is a consequence of these changes in blood flow,
rather than direct damage to the kidney. The diagnosis of hepatorenal syndrome
is based on laboratory tests of individuals susceptible to the condition. Two
forms of hepatorenal syndrome have been defined: Type 1 HRS entails a rapidly
progressive decline in kidney function, while type 2 HRS is associated
with ascites
that does not improve with standard diuretic medications.
The risk of death in hepatorenal
syndrome is very high; the mortality of individuals with type 1 HRS is over 50%
over the short term, as determined by historical case series.
The only long-term treatment option for the condition is liver transplantation.
While awaiting transplantation, people with HRS often receive other treatments
that improve the abnormalities in blood vessel tone, including supportive care
with medications, or the insertion of a transjugular intrahepatic
portosystemic shunt (TIPS), which is a small shunt placed to reduce
blood pressure in the portal vein. Some patients may require hemodialysis to
support kidney function, or a newer technique called liver
dialysis which uses a dialysis circuit with albumin-bound
membranes to bind and remove toxins normally cleared by the liver, providing a
means of extracorporeal liver support until
transplantation can be performed.
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