Hepatorenal Syndrome

Contents of
  • Prevalence of
  • What is the cause of the syndrome?
  • What changes in the body cause the syndrome?
  • What are the signs of suspected pathology?
  • Classification
  • How is the diagnosis carried out?
  • Treatment options
  • Forecast
  • Prevention problems
  • Related videos

Hepatorenal syndrome is a secondary kidney pathology that accompanies a severe lesion of the hepatic parenchyma. It is characterized by functional renal failure more often without organic damage. Rarely there is a thrombosis of small vessels, deposits of fibrin in capillaries and glomeruli of kidneys, damage of tubules.

Prevalence of

Hepatorenal syndrome in liver cirrhosis occurs in 8-10% of cases. Signs indicate a progressive course of liver disease. They are considered negative confirmation of a poor prognosis for the patient's life. Depending on the type of kidney damage, the lethal outcome occurs within a period of two weeks to six months.

In the presence of signs of portal hypertension in a patient with cirrhosis of the liver in the first year in 20% of patients develops hepatorenal syndrome, if the pathology lasts 5 years - in 40% of cases. More often than not, it affects people between the ages of 40 and 80.Differences are not established depending on gender.

What is the cause of the syndrome?

The specific cause of hepatorenal syndrome( GDS) is unknown. Isolated factors that occur in liver disease are distinguished: spastic reduction of the capillaries of the kidneys disrupts the blood flow and causes a lack of oxygen in the tissues( hypoxia), a direct effect on the renal tissue of toxic substances and uncleared blood slags, a changed metabolism of arachidonic acid, leading to a violation of the ratio of thromboxane andprostaglandins.

In childhood, the main cause of the syndrome( in half of cases) is viral hepatitis with hepatic insufficiency. In addition, the pathology can complicate:

  • the effects of biliary tract artiasis in the form of chronic hepatitis;
  • Wilson-Konovalov's disease;
  • is an autoimmune type of hepatitis;
  • malignant liver tumor;
  • long-term treatment with paracetamol.

In adults, in addition to cirrhosis of the liver, GDS can develop in bacterial peritonitis( according to statistics in 25% of cases), after the removal of a significant volume of ascites fluid( laparocentesis) without compensatory administration of albumin( in 15% of cases), bleeding from dilated varicose veins of the stomach andesophagus( 10%).

What changes in the body cause the syndrome?

The basis of disorders in hepatorenal syndrome is associated with a drop in renal blood flow due to narrowing of the arteries of the kidneys and a significant expansion of other vessels of the abdominal cavity. The mechanism of pathological abnormalities of kidney function( pathogenesis) is associated with sodium retention, reduced release of water molecules, slowing down filtration in the glomeruli, a drop in the capacity of the kidneys.

The role of hormones and electrolytes, spastic vasoconstriction is well studied in the pathogenesis of hypertension

. With compensated cirrhosis, hypertension develops in the portal vein system and arterial vessels expand. This effect is accompanied by a delay in sodium. It is important that at the initial stage there is no significant effect in sodium preserving systems, the content in the blood of noradrenaline, renin and aldosterone remains within the normal range.

When the degree of sodium delay becomes extremely high, the mechanism involves an increase in the production of renin, an increase in the concentration in the blood plasma of aldosterone and norepinephrine. Patients with ascites( a fluid accumulation in the abdominal cavity) receive a diet with a reduced salt content, but the kidneys are not able to excrete even a small amount of sodium in the urine.

The function of the renin-angiotensin-aldosterone system is affected by abnormalities in the work of the heart and vascular tone: the expansion of arterial capillaries( vasodilation), the fall in the return to the heart of venous blood, and the reduction of cardiac output. These physiological mechanisms activate the sympathetic nervous system and all the hormonal factors that support the work of the myocardium.

The main enzyme that converts weakly active angiotensin I into active forms is the angiotensin converting enzyme( ACE).He is constantly present in the blood, supports hemodynamics. Enzymes-assistants( endoperoxide, chymase, cathepsin G) are less involved in the pathogenesis of disorders. They act at the tissue level.

Under the influence of activated angiotensin there is a significant spasm of the renal arteriolus, the pressure inside the glomerulus decreases, the filtration in the nephron decreases. As a result, the reabsorption of sodium in the nephron closest to the glomerulus decreases. The accumulation of sodium occurs in distant tubules.

Normally, this leads to inhibition of renin release to restore the rate of filtration. With hepatorenal syndrome, the mechanism does not work. The functioning of the system depends on the reaction of aldosterone( the hormone of the adrenal glands).It regulates the volume of extracellular fluid, the concentration of potassium in the blood. On sodium affects indirectly.

The synthesis of prostaglandins depends on the metabolism of arachidonic acid.

The renal transmission capacity is largely related to the level of prostaglandins. These are vasodilators that can counteract the narrowing effect. In patients with GDS, the synthesis of prostaglandin E2, kallikrein, 6-keto-prostaglandin is reduced. An increase in the synthesis of vasoconstrictors: endothelin-1, adenosine, leukotriene E4, C4 and D4, thromboxane A2.

The mechanism of vasodilation of the vessels of the abdominal cavity with severe liver damage is caused by an increase in the release of glucagon. Its content is increased with cirrhosis, contributes to a decrease in the sensitivity of arterioles of mesenteric vessels to angiotensin, catecholamines. This leads to loss of tonus and enlargement.

Hepatorenal syndrome is caused by imbalance between substances of the vasodilator and vasoconstrictor type.

What are the signs of pathology?

The syndrome develops in patients with severe liver disease, therefore the main symptoms are signs of active process and decompensation:

Hepatomegaly syndrome
  • jaundice of mucous membranes and skin;
  • painful itching and rashes on the skin;
  • bright pink palms;
  • change in the shape of the terminal phalanges of the fingers and nails( "drum sticks" and "watch glass");
  • vascular "stars" on the face, chest, back;
  • xantelasms on the eyelids;
  • significantly enlarged abdomen due to sweating of fluid into the abdominal cavity with expansion of superficial veins;
  • edema on the legs and hands, facial pastness;
  • brain damage( encephalopathy) with sleeplessness at night and drowsiness during the day, disturbance of the psyche, mood;
  • bleeding from the gastrointestinal tract, manifested by a black fluid stool or vomiting with blood;
  • possible umbilical hernia;
  • in men there is an increase in the mammary glands( gynecomastia);
  • little excreted urine - for a day not more than 500 ml.

Ascites causes the enlargement of the subcutaneous veins on the abdomen
Palpation is determined by a significantly enlarged liver and spleen.


Two types of GDS are distinguished according to the clinical course. I type - develops in patients with acute liver failure in poisoning, alcoholic cirrhosis, in 25% of patients with spontaneous peritonitis of bacterial origin, every tenth with gastrointestinal bleeding, after laparocenesis, if necessary surgical intervention.

The acute infectious disease transferred on a background of a cirrhosis has value. Sometimes there are cases when the cause can not be established. For the formation of renal failure sufficient period of 2 weeks. Distinctive criteria:

  • serum creatinine levels higher than 221 μmol / l;increased residual nitrogen;
  • the glomerular filtration rate in the kidneys is reduced by 50% from normal to below 20 ml / min.;
  • electrolyte changes are possible, especially sodium reduction( hyponatremia).

The prognosis is unfavorable. It is established that, in the absence of treatment, a lethal outcome occurs within two weeks or a month. Type II - usually accompanies liver pathology with less severe manifestations. Renal failure is formed slowly, but progressively. In this case, the serum creatinine does not reach the same level as in type I.

A feature of the course is marked ascites and swelling with little or no response to the administration of diuretics( refractory ascites).Without treatment, the patient's survival period is not more than 6 months.

How is the diagnosis carried out?

The diagnostic algorithm consists of sequential execution of two stages. Initially, it is necessary to detect a decrease in glomerular filtration of the kidneys. To do this, use the study of blood biochemistry: the content of nitrogenous substances of urea, residual nitrogen, creatinine( signs of azotemia), a decrease in sodium and protein.

The urine is also absent or sharply reduced sodium. The measurement of daily diuresis shows oliguria before full anuria( shortening or stopping of urine output).The second stage consists in differential diagnosis of hepatic renal syndrome with other diseases and causes of renal failure.

It should be taken into account that in patients with liver pathology the synthesis of urea and creatinine decreases, therefore in tests even at the initial stage of renal failure these indicators may indicate a norm.

Differential diagnosis

To diagnose, the following should be excluded:

  • effects of shock and pathological fluid loss( bleeding, vomiting, diarrhea);
  • manifestation of bacterial infection;
  • nephrotoxicity of drugs used in therapy;
  • response in the form of improved renal function and reduced creatinine to stop the use of diuretics, carrying out an aqueous stress test;
  • all causes, accompanied by the release of protein and erythrocytes in the urine( with hepatorenal syndrome this does not happen);
  • possible mechanical obstructions for urinary excretion in diseases of the parenchyma of the kidneys, ureters, bladder.

Kidney ultrasound reveals both vascular disorders and inflammatory processes, shadows of concrements

Renal failure can cause medications. It is called "iatrogenic", it is much better treated. Such an effect comes under the influence of uncontrolled intake of diuretics, lactulose, non-steroidal anti-inflammatory drugs, Cyclosporine, antibiotics aminoglycosides and demeclocycline.

The drugs act on the kidneys by significantly reducing the production of prostaglandins, reducing the glomerular filtration rate. With alcoholism in a patient with cirrhosis of the liver, immunoglobulins of type A are deposited in the kidneys, b2-microglobilis is detected in urine.

For the verification of renal blood flow, the duplex Doppler ultrasound method is used. With its help, the resistance of the arterial bed is evaluated. If the cirrhosis without ascites and excretion of nitrogenous slags in the blood increases, then we should think about the high risk of the formation of hepatorenal syndrome. The growth of vascular resistance in the presence of GDS is regarded as an unfavorable sign.

Critical Criteria in Diagnostics

Diagnostic criteria combine the main and indirect characteristics that should be considered. The main( main) signs: the presence of a chronic liver pathology complicated by ascites in the patient, a low glomerular filtration rate-a total creatinine level of 1.5 mg / kg or more, a clearance of less than 4 ml / min per day, a daily urine protein500 mg, the absence of a positive reaction to restore the volume of circulating plasma.

Additional( indirect) signs: daily diuresis is less than 1 liter, urine has a sodium concentration of up to 10 mmol / l, an excess of osmolality of urine over the blood plasma, in the serum sodium content is less than 13 mmol / l. With the progression of pathology, the level of creatinine and urea in the blood increases. The concentration of sodium does not exceed 120 mmol / l.

Urine analysis shows no significant changes, except low sodium levels. In the kidneys, it is possible to develop acute tubular necrosis. Ascites can not be treated with diuretics. At a comatose state of the patient falls arterial pressure and diuresis. Duration of the terminal stage from several days to a month or more.

Terlipressin acetate is a vasopressin antagonist

Treatment options for

Studies show that the survival of patients with hepatic renal syndrome is affected mainly by progressive hepatic failure. Therapy, aimed at improving kidney function is practically unsuccessful, does not have a significant effect on the course of the disease.

In the diet of patients, the amount of salt is sharply limited. On a background of hepatic encephalopathy, the patient is transferred to a reduced protein content. The diet and diet are calculated, as for patients with cirrhosis and edema.

In conservative treatment, different schemes are used:

  • intravenous drip for 8-12 hours Terlipressin with Albumin, the duration of the course is determined by the doctor;
  • administration of tablets Midodrin three times a day with a gradual increase in dosage, Octreotide in combination with intravenous infusion of albumin;
  • is drip intravenously with norepinephrine and Albumin in a course of 5 days.
These schemes use substances that dilate the vessels of the kidneys, but they should be simultaneously used with protein preparations.

In addition, for individual indications prescribe: Acetylcysteine ​​- an antioxidant drug, used by a course of 5 days with an overdose of Paracetamol, Dopamine - acts through stimulation of the receptor apparatus of smooth muscles of blood vessels.

It is used only intravenously, it improves blood circulation in the kidneys.

. Liver transplantation - not all patients are relieved. In 35% of cases it is necessary to carry out renal hemodialysis( for comparison - in patients without hepatorenal syndrome after transplantation hemodialysis is needed only in 5% of cases).After surgery, the mandatory use of cyclosporins.

In the second month after transplantation, the kidney function improves, but does not return to normal. This moderate indicator is observed in patients without GDS.There is a gradual disappearance of all hormonal disorders, the amount of sodium in urine and blood is restored, water is released.

Forecast of

Survival of patients receiving Terlipressin with Albumin is 87% during the month. When treated with a single drug without a protein substitute - 13%.During the operation of liver transplantation, it is possible to achieve 50% of the 10-year survival rate of patients with hepatorenal syndrome. Therefore, in the treatment of the most important is the preparation of the patient for transplantation, prolongation of life until the moment of radical replacement of the liver.

Statistics of liver transplantation results show that 70-80% of patients without GDS and 60% with hepatorenal syndrome achieve a three-year survival rate. Patients with hepatorenal impairments last longer after an operation of transplantation in the intensive care unit. They are more prone to complications.

Prevention problems

When treating patients with cirrhosis of the liver to prevent hepatorenal syndrome, experts recommend using a combination of Cefotaxim and albumin transfusion. Especially they are shown in case of threat of type I GDS.

Patients with alcoholic cirrhosis are encouraged to include in courses of treatment Pentoxifylline, to control the risk of bacterial inflammation. Carrying a laparocentesis in patients with ascites, it is necessary to pour 6-8 grams of albumin intravenously on each released liter. Therapy of cirrhosis of the liver requires caution in the use of diuretics, taking into account contraindications to nephrotoxic drugs.

Obtaining results from liver transplantation in hepatorenal syndrome sets the task of treating and prolonging the life of patients awaiting surgery. Every year, research provides new information to understand the causes of the syndrome, to find methods of therapy.

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