Page 128 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Hepatorenal Syndrome
Renal ischemia and ultimately oliguric renal Incomplete hepatic inactivation of media-
failure, a disease combination called hepatore- tors that have a direct vasoconstrictor effect
nal syndrome, occurs relatively frequently in on the kidney (e.g., leukotrienes) also contrib-
patients with cirrhosis of the liver. Several fac- utes to renal vasoconstriction.
tors contribute to the development of this syn- Renal ischemia normally stimulates the re-
drome, but it has not as yet been agreed which lease of vasodilating prostaglandins that pre-
of the factors are most significant or whether vent further reduction in renal perfusion
there are others which are important, too. (→ p. 296). If there is insufficient formation of
Kidney, Salt and Water Balance tially. The hydrostatic pressure in the capillar- opment of renal failure accelerated. A de-
In liver cirrhosis, congestion in the portal
prostaglandins (e.g., due to administration of
prostaglandin synthesis inhibitors), this pro-
venous system due to narrowing of the vascu-
tective mechanism is abolished and the devel-
lar bed within the liver (→ p.170) occurs ini-
creased ability to synthesize prostaglandins
ies rises and excessive amounts of fluid are fil-
(lack of precursors?) has in fact been found in
tered into the abdominal cavity (ascites,
patients with the hepatorenal syndrome.
→ p.170). Because of the high protein perme-
ability of the liver sinusoid, plasma proteins
Renal vasoconstriction can possibly also be
elicited by hepatic encephalopathy (→ p.174).
are also lost into the extracellular space. In ad-
leads to a change in amino acid concentration
the liver parenchyma. The resulting hypopro-
+
teinemia results in the increased filtration of
and a rise in NH 4 concentration in blood and
plasma water and thus in the development of
brain. This causes swelling of the glial cells
5 dition, fewer plasma proteins are produced in The reduced metabolic activity of the liver
peripheral edemas. The formation of ascites and a profound disturbance of transmitter me-
and peripheral edemas occurs at the expense tabolism in the brain that, via activation of the
of the circulating plasma volume. The result is sympathetic nervous system, causes renal vas-
hypovolemia. cular constriction.
In the further course of the disease periph- Due to the impaired synthesizing activity of
eral vasodilation occurs. Vasodilating media- the liver, less kininogen is formed, and there-
tors (e.g., substance P) produced in the gut fore too few vasodilating kinins (e.g., bradyki-
and endotoxins released by bacteria are nor- nin), facilitating renal vasoconstriction.
mally detoxified in the liver. In liver cirrhosis Lastly, an abnormal fat metabolism may
the loss of liver parenchyma and the increased contribute to kidney damage in liver failure.
amount of blood passing from the portal circu- Among other consequences, the liver forms
lation directly into the systemic circulation, less lecithin-cholesterol acyltransferase
short-circuiting the liver (→ p.170), brings (LCAT), an enzyme that esterifies cholesterol
those substances into the systemic circulation with fatty acids (→ p. 246) and plays an impor-
unhindered. The mediators have a direct vaso- tant part in breaking down or transforming li-
dilator effect, while the endotoxins exert a va- poproteins. In familial LCAT deficiency (due to
sodilator effect by stimulating the expression an enzyme defect) renal failure regularly oc-
of nitric oxide synthase (iNOS). This may lead curs, probably through lipid deposition in the
to a fall in blood pressure, causing massive kidney.
sympathetic stimulation. This, together with
the hypovolemia, results in diminished renal
perfusion and thus a fall in GFR. The reduced
renal blood flow promotes the release of renin
and thus the formation of angiotensin II, ADH,
and aldosterone (→ p. 266). ADH and aldoste-
rone increase the tubular reabsorption of wa-
ter and sodium chloride (loss of potassium;
118 → p.124), and the kidney excretes small vol-
umes of highly concentrated urine (oliguria).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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