Hepatorenal syndrome

　　1. Causes of Disease

　　HRS is commonly found in various types of decompensated liver cirrhosis (especially post-hepatitis cirrhosis, alcoholic cirrhosis, etc.), and can also be seen in other severe liver diseases, such as fulminant liver failure, severe viral hepatitis, primary and secondary liver cancer, gestational fatty liver, and other serious liver parenchymal diseases. Most patients have a predisposing factor, and the most common predisposing factor is massive upper gastrointestinal bleeding, large-volume paracentesis, excessive diuresis, postoperative surgery, infection, diarrhea, and stress state. However, some patients may develop HRS without an obvious predisposing factor.

　　Two, pathogenesis

　　The exact pathogenesis of HRS is not yet fully understood. It is generally believed that it is mainly due to severe liver dysfunction leading to changes in renal hemodynamics. It is manifested as renal vessel constriction and renal internal shunting, resulting in a decrease in renal blood flow (RBF) and a decrease in glomerular filtration rate (GFR), thus causing renal failure. These changes are functional changes rather than organic damage. As for the exact mechanism causing the renal hemodynamic changes in HRS, it is still unclear. Most scholars believe that it is not caused by a single factor, and the pathogenesis may be related to factors such as a decrease in effective blood volume, endotoxemia, imbalance of vasoactive substances, and certain hormones.

　　1. Disordered control of total blood volume Severe volume control disorder in HRS leads to a decrease in effective plasma volume, which reflects on the renal blood vessels and renal water and sodium retention through the neurohumoral system. If the effective blood volume decreases sharply due to upper gastrointestinal bleeding, large amounts of abdominal fluid drainage, large amounts of diuresis, and severe vomiting and diarrhea in severe liver disease, it leads to a decrease in RBF and a significant decrease in GFR, thus triggering FARF. In liver cirrhosis, the autonomic stability of volume control is abnormal, and the liver-kidney reflex in volume regulation also occurs, which causes sympathetic nerve excitation that controls the kidneys through the reflex mechanism of volume regulation, leading to an increase in renin-angiotensin secretion, renal blood vessel constriction, blood分流 from cortex to medulla, renal cortex ischemia, and thus reducing RBF and GFR. An increase in aldosterone production, increased reabsorption of water and sodium in the renal tubules, and increased secretion of antidiuretic hormone cause severe renal water and sodium retention, leading to the occurrence of HRS.

　　2. Endotoxemia Endotoxemia (endotoxemia, ETM) may be an important factor in the occurrence of HRS in severe liver disease patients. When HRS appears in patients with liver cirrhosis, the positive rate of endotoxins in blood and ascites is very high, while the detection of endotoxins is mostly negative when HRS does not appear. Endotoxins are lipid and polysaccharide components of the cell wall of Gram-negative bacteria, which can cause fever, vascular spasm disorder, blood pressure decrease, complement activation, schwartzman reaction, trigger DIC, affect immune function, and so on. In severe liver disease, due to intestinal dysfunction, a large number of Gram-negative bacteria multiply in the intestines, producing a large amount of endotoxins, and the absorption of endotoxins by the intestines increases significantly. In liver cirrhosis, due to the relatively low immune status of patients, the function of the liver reticuloendothelial system is reduced, and the endotoxins reabsorbed from the gastrointestinal tract cannot be inactivated completely. If combined with infection, this condition becomes more serious. In severe liver disease, due to the decrease in the detoxification function of liver cells, the endotoxins absorbed by the intestines can enter the systemic circulation in large quantities through the liver or collateral circulation. ETM can also worsen liver damage, and the two affect each other, causing a vicious cycle. Endotoxins have obvious renal toxic effects, which can cause strong constriction of renal blood vessels, redistribution of renal blood, reduction of renal cortex blood flow, reduction of RBF and GFR, leading to oliguria and azotemia.

　　3. Imbalance of Vasoactive Substances and Hormones: The imbalance in the production of vasoactive substances and some hormones leads to renal vasoconstriction. These substances mainly include:

　　(1) Renin-angiotensin-aldosterone system (RAAS): The RAAS has long been considered an important regulatory system for regulating renal blood flow and internal environment stability in physiological and pathological conditions. Clinical studies have shown that in patients with advanced liver cirrhosis and HRS, plasma renin and aldosterone levels increase. The mechanism is related to the decrease in effective blood volume in patients with advanced liver cirrhosis, which stimulates the increase in renin secretion, leading to the increase in angiotensin and aldosterone. It is also related to the decrease in renin substrates, which leads to the decrease in angiotensin, followed by the damage to the normal negative feedback mechanism, resulting in the continuous secretion of renin. Liver cirrhosis patients treated with β-blockers can reduce renin activity, but due to the decrease in cardiac output, it affects renal blood regulation, which can lead to a decrease in RBF. When treated with angiotensin-converting enzyme inhibitors, the blood pressure of patients with increased RAAS activity can be significantly reduced, while the blood pressure decrease of patients with low activity is not significant. Therefore, when liver cirrhosis patients use these drugs, they should pay attention to the above issues.

　　(2) Prostaglandin (PG): Metabolic disorders of prostaglandins in patients with severe liver dysfunction play an important role in the pathogenesis of HRS. PG is a metabolite of arachidonic acid, a group of substances with various physiological activities. Among them, PGE2, PGA2, and PGI2 have vascular dilating effects, while PGF2α and thromboxane (TXA2) have vasoconstrictive effects. Thromboxane B (TXB2) is the hydrolysis product of TXA2, and the content of TXB2 in the urine increases in HRS. In liver cirrhosis patients, regardless of whether there is ascites or not, the synthesis of PGE2 in the kidneys is significantly reduced, the level of PGI2 in the urine decreases, and the content of TXB2 increases. Imbalance between vasodilatory and vasoconstrictive metabolites of arachidonic acid plays an important role in the pathogenesis of HRS, which can lead to renal vascular spasm and ischemia of renal tissue.

　　(3) Kinin-releasing enzyme-kinin system (K-KS): The kinin-releasing enzyme in the kidneys is synthesized by the cells of the distal renal tubules and then released into the tubular lumen and blood circulation. In liver cirrhosis, the concentration of kinin-releasing enzyme precursor and bradykinin decreases, and in addition to the above changes in HRS, urinary kinin-releasing enzyme also decreases. These factors also play an important role in the pathogenesis of HRS.

　　(4) Pseudo-neurotransmitters: In liver cirrhosis, the level of aromatic amino acids in the patient's blood increases, which is converted into phenylethylamine and normetanephrine through non-specific decarboxylation and hydroxylation reactions. These pseudo-neurotransmitters can compete with true neurotransmitters and norepinephrine for receptor binding, blocking the normal conduction of sympathetic nerves, causing small blood vessels to dilate, peripheral vascular短路, reducing the effective blood volume of the kidneys, and leading to renal failure.

　　(5)心房利钠肽(心钠素，ANP)的作用：ANP由心房肌细胞释放入血后，在肝、肾、肺等脏器中被降解。ANP具有降低血压，增加GFR及排钠作用，但不造成持续性RBF增加。此外，ANP还能降低血浆肾素及醛固酮水平。当肝脏受到严重损害时，必然会影响到血浆ANP水平。肝硬化时ANP分泌减少与肾脏钠调节缺陷有关，其相对降低还可能与有效血容量减少致心房内压和大静脉内压降低有关。虽然失偿性肝硬化患者循环中ANP水平报道不一致，但在出现HRS时，血中ANP含量均显著降低。(6)肾小球加压素(GP)的作用：GP是一种分子量小于500D的葡糖苷糖，由肝脏分泌，它具有降低肾入球小动脉张力并使之扩张的作用，可促使GFR升高，但不会引起全身血压升高。严重肝功能衰竭时，GP活性显著降低。这可能与肝脏合成GP减少有关。随着肝功能衰竭加重，GP的产生明显减少，则GFR急剧下降，因而可引发HRS的发生。

　　Furthermore, atrial natriuretic peptide (ANP, also known as atrial natriuretic peptide) plays a role: After ANP is released into the blood by atrial muscle cells, it is degraded in organs such as the liver, kidney, and lung. ANP has the effects of lowering blood pressure, increasing GFR, and excreting sodium, but does not cause a sustained increase in RBF. In addition, ANP can also reduce the levels of plasma renin and aldosterone. When the liver is severely damaged, it will inevitably affect the level of plasma ANP. The decrease in ANP secretion during liver cirrhosis is related to renal sodium regulation defects, and its relative decrease may also be related to a decrease in effective blood volume, leading to a decrease in atrial pressure and pressure in the great veins. Although the levels of ANP in the circulation of decompensated liver cirrhosis patients are reported to be inconsistent, when HRS occurs, the ANP content in the blood is significantly reduced. (6) The role of glomerular pressor hormone (GP): GP is a glucoside sugar with a molecular weight less than 500D, secreted by the liver, which has the effect of lowering the tension of the glomerular arterioles and dilating them, which can promote an increase in GFR but will not cause an increase in systemic blood pressure. The activity of GP is significantly reduced in severe liver failure, which may be related to a decrease in the synthesis of GP by the liver. As liver failure worsens, the production of GP is significantly reduced, leading to a sharp decrease in GFR, thereby triggering the occurrence of HRS.

　　In addition, vasoactive intestinal peptide (VIP) with the effect of expanding blood vessels may be related to the occurrence of HRS. The increase of antidiuretic hormone (ADH) is also related to the occurrence of oliguria in HRS.

　　1. Liver failureIt is a clinical syndrome that occurs due to widespread and severe damage to liver cells, with severe disturbance of metabolic function in the body, abbreviated as liver failure. Liver failure occurs in many severe liver diseases, with dangerous symptoms and a poor prognosis.

　　2. Gastrointestinal bleeding:Abnormal liver function may cause abnormal coagulation function, leading to gastrointestinal bleeding, which is divided into upper gastrointestinal bleeding and lower gastrointestinal bleeding. Upper gastrointestinal bleeding refers to bleeding in the gastrointestinal tract above the Treitz ligament, including the esophagus, stomach, and duodenum. Lower gastrointestinal bleeding refers to bleeding in the gastrointestinal tract below the Treitz ligament, including the small intestine, colon, and rectum.

　　3. Infection:Patients with liver-kidney syndrome often have poor immunity and are prone to local and systemic inflammatory reactions caused by pathogens such as bacteria, viruses, fungi, and parasites entering the human body.

　　4. HyperkalemiaIn patients with impaired liver and kidney function, it is easy to develop hyperkalemia, the most common cause of which is renal failure, with main symptoms including fatigue and arrhythmia.

　　Due to the difficulty in treating hepatorenal syndrome, it is particularly important to actively treat the primary liver disease and prevent further development into hepatorenal syndrome. The most fundamental preventive measure is to improve liver damage, strengthen nutritional support therapy, prohibit alcohol consumption and the use of drugs harmful to the liver, and appropriately use liver-protecting drugs. In treatment, it is necessary to prevent systemic hemodynamic disorders from occurring for the purpose of achieving a certain goal. For example, when diuretic treatment is required, it is necessary to prevent a decrease in effective circulating blood volume; when peritoneal puncture and fluid drainage are performed, attention should be paid to volume expansion therapy; electrolyte disorders should be corrected promptly; and antibiotics should be used early if concurrent infection is found. Although it is still very difficult to prevent the occurrence of hepatorenal syndrome, in the treatment of liver cirrhosis, it is necessary to prevent any cause of decreased effective blood volume, correct abnormal renal hemodynamics, and this has a positive significance for preventing the occurrence of hepatorenal syndrome.

　　First, laboratory examination

　　The laboratory examination characteristics of hepatorenal syndrome are as follows:

　　Oliguria is often a severe manifestation, occasionally mild, with daily urine volume

　　In most patients, the urine sodium level is less than 10 mEq/L, and the urine can be completely free of sodium.

　　Patients with hyponatremia and hepatorenal syndrome cannot effectively eliminate water load, especially when water load is given without diuretic treatment, and hyponatremia will gradually worsen.

　　The filtration fraction of Na排泄 is below 1%, indicating that the renal tubular function is normal and can reabsorb Na.

　　The urine pH value is usually acidic, unless in patients with alkalosis.

　　Trace amounts of protein may be present in the urine, and the presence of proteinuria does not indicate worsening renal damage.

　　The blood creatinine concentration shows progressive increase, but rarely reaches a high level. In patients with significant muscle wasting, blood creatinine is a means of detecting poor glomerular filtration rate. Over time, the blood creatinine concentration progressively rises, and patients often die before the blood creatinine reaches 10 mg/dl.

　　The most common acid-base imbalance in liver cirrhosis with ascites is respiratory alkalosis. Sometimes, diuretics are used to control ascites, which can lead to hypochloremic alkalosis. Severe alkalosis that progresses continuously can damage the kidney's ammonia secretion mechanism, causing ammonia to return to the liver and triggering hepatic encephalopathy. In patients with hepatorenal syndrome and azotemia, the typical anion gap acidosis caused by renal failure can occur in conjunction with metabolic alkalosis and respiratory alkalosis (triple acid-base imbalance).

　　Two, Other auxiliary examinations

　　Patients with liver-kidney syndrome may not have obvious renal damage, but there are also descriptions in the literature of glomerular damage related to liver cirrhosis, which was once thought to be related to liver-kidney syndrome.

　　1. The earliest reports on renal damage related to liver cirrhosis came from autopsies. Since 1965, there have been reports on renal biopsy changes in patients with liver cirrhosis.

　　The main changes under light microscopy are glomerulosclerosis, thickening of the basement membrane, thickening of the capillary wall, and occasionally an increase in cells. Therefore, the term 'liver cirrhosis glomerulosclerosis' was proposed. The changes in the glomeruli under light microscopy are variable, including glomerular mesangial proliferation, membranous glomerulonephritis, membranoproliferative glomerulonephritis, diffuse proliferative glomerulonephritis, and crescentic glomerulonephritis, with the degree of lesions ranging from none to sclerotic changes.

　　2. Immunofluorescence examination of renal biopsy specimens found IgA deposition with and without complement deposition, with IgA mainly deposited in the glomerular mesangium, especially in patients with alcoholic liver cirrhosis, where in addition to IgA mesangial deposition, antibody deposition was also found in the glomerular capillary wall.

　　3. Studies on ultrastructure show that the renal abnormalities in patients with liver cirrhosis under electron microscopy include thickening of the basement membrane, increased glomerular matrix, electron-dense deposits in the capillary basement membrane and glomerular mesangium, and irregular black granules clearly surrounded by a clear band in the glomerular mesangium.

　　One, Diet

　　1. Foods to eat: Light and easy-to-digest foods, fresh vegetables and moderate amounts of fruit, drink water appropriately, and control the intake of high-protein foods (such as lean meats, milk, eggs, etc.). Winter melon, watermelon, and luffa can promote diuresis. Red bean soup, black bean soup, mung bean soup, and sweetened drinks can clear heat and promote diuresis. Honey, banana, pear, radish, walnut meat, black sesame, can moisten the intestines and promote defecation, and these foods can be used in combination with medicine and used regularly.

　　2. Foods to avoid: Avoid drinking alcohol and spicy foods, eat less greasy and rich in animal protein foods (such as fatty meat, shrimp, crab, etc.), and avoid eating beans and their products (such as tofu, sprouts, bean powder, etc.).

　　Two, Wuweizi Duzhong Sheep Kidney Soup

　　Ingredients: Sheep kidney 2 pieces, Duzhong 15 grams, Wuweizi 6 grams.

　　Preparation: Cut the sheep kidney open to remove the fat membrane, wash and slice. Wash Duzhong and Wuweizi separately. Put the above ingredients together in a pot, add an appropriate amount of boiling water, simmer over low heat for 1 hour, and season for eating.

　　Three, Chinese Yam and Mung Bean Porridge

　　Ingredients: Dried Chinese yam 25 grams, mung bean 15 grams, lotus seed 25 grams, lotus seed 20 grams, a little sugar.

　　Preparation: Put the above 4 ingredients in a pot, add an appropriate amount of water, simmer until cooked, then add sugar and mix well. Take 1 dose per day, and 5 doses make up a course of treatment.

　　Four, Winter Melon Pork Kidney Soup

　　Ingredients: Winter melon 250 grams, pork kidney 1 pair, Job's tears 9 grams, Astragalus 9 grams, Chinese yam 9 grams, mushrooms 5 pieces, chicken broth 10 cups.

　　Method: Wash the ingredients clean, peel and remove the core of the winter melon, cut into pieces, and remove the root of the mushroom. Cut the pork kidney in half, remove the white part, cut into slices, wash, and blanch in hot water. Pour chicken broth into the pot, heat, add ginger and scallion first, then add mung bean seed and Astragalus membranaceus, and boil for 40 minutes over medium heat. Then add pork kidney, mushroom, and Chinese yam, and cook until done. Boil for a few more minutes over low heat, and season with salt to taste.

　　First, treatment

　　HRS itself has no specific treatment, mainly对症 treatment. Considering that severe liver disease is the basis for the occurrence of HRS, and improvement of liver function is the premise for the recovery of hepatorenal syndrome, liver disease should be treated first. For HRS patients, various effective treatment measures to improve liver function should be actively selected for treatment, which is of great significance for the prevention and treatment of functional renal failure. As for renal failure, it should be treated from the following aspects.

　　1. Prevent and treat the triggers of renal failure:Mainly prevent and treat gastrointestinal bleeding, avoid excessive diuresis and large or multiple paracenteses, prevent infection, use nephrotoxic drugs such as kanamycin and gentamicin with caution, prevent and treat electrolyte disorders, hepatic encephalopathy, hypotension, and other triggers and complications.

　　2. General supportive therapy:Appropriately limit fluid intake, correct electrolyte disorders, low protein and high sugar, provide high-calorie diet, and avoid using drugs that reduce renal blood flow, such as norepinephrine.

　　3. Specific treatment

　　(1) Volume expansion therapy: Some believe that the blood volume of patients with functional renal failure is higher than normal, and the effect of volume expansion therapy is not good, and it is easy to induce esophageal variceal bleeding and pulmonary edema. It is recommended to avoid its use. However, for patients with low output and high resistance type, after volume expansion therapy, renal function can be temporarily improved and urine output can be increased, but it is not necessarily possible to prolong survival time. Therefore, for factors that cause a decrease in blood volume, such as excessive diuresis, large or multiple paracenteses, bleeding, dehydration, or patients with low output and high resistance type hemodynamics, volume expansion therapy can be used. Generally, dextran, albumin, plasma, whole blood, or filtered and concentrated ascites can be used for volume expansion.

　　(2) Vasoactive drugs for improving renal blood flow:

　　① Octapeptide vasopressin (or phenylalanine vasopressin): It is a vasoactive drug that can correct and improve hemodynamic disorders. It can reduce renal vascular resistance, increase renal cortical blood flow, and improve glomerular filtration rate. It can start with a low dose of 0.001μg/min. When the arterial pressure rises by more than 0.67kPa (5mmHg), it can increase renal blood flow and renal cortical blood flow. It is generally considered suitable for patients with functional renal failure who have hypotension.

　　② Metaraminol: It is a vasoactive drug that can increase systemic arterial pressure. Short-term application can increase urine output, but it has no effect on renal blood flow and glomerular filtration rate. Continuous intravenous infusion of metaraminol at 200-1000μg/min can increase blood pressure by 4kPa (30-40mmHg) compared to before treatment, which can increase urine output and urinary sodium excretion, improve creatinine clearance and hippurate clearance, and is suitable for patients with high output and low resistance type functional renal failure. It can correct hyperoutput, reduce arteriovenous shunting, and prevent blood flow from shunting to other parts of the body, thereby increasing renal blood flow and improving renal function.

　　③ Dopamine: Slow infusion of dopamine excites the β-receptor of the heart, and also has an excitatory effect on the dopamine receptor in the renal, mesenteric blood vessels, manifested as increased heart contraction and cardiac output, renal blood vessel dilation, increasing renal blood flow, and decreased plasma renin activity. However, it has no significant improvement in glomerular filtration rate, urine output, and urinary sodium excretion, so its efficacy cannot be definitely confirmed.

　　④ Prostaglandin A1: It is a strong vasodilator that can relieve renal vascular spasm, increase renal plasma flow and glomerular filtration rate, and increase urinary sodium excretion. However, a dose of 1μg/(kg·min) can cause a decrease in blood pressure.

　　In addition, there is phenoxybenzamine (phenoxazine), which is an α-receptor blocker that can dilate renal blood vessels, increase renal plasma flow, but has a minor effect on glomerular filtration rate. Other agents such as acetylcholine, phentolamine, opium, aminophylline, mannitol, angiotensin, and isoproterenol all have no significant efficacy and have certain side effects.

　　⑤ Prostaglandin E1: 50-200μg per dose added to 300ml of 5% glucose solution for slow infusion, 1-2 weeks, can improve renal vasoconstriction and reduced glomerular filtration rate in the syndrome of肝肾 dysfunction.

　　(3) Drugs for preventing and treating endotoxemia:

　　① Lactulose: 60% lactulose syrup, 30ml per dose, 3 times a day, taken orally, for a course of 4 weeks, has a significant inhibitory effect on the endogenous PAF production, and has a good effect on the prevention and treatment of endotoxemia in liver cirrhosis.

　　② Specific antagonists of platelet-activating factor: such as CV-3988, WEB2170, BN52063, have all begun to be used in clinical practice.

　　(4) Calcium channel blockers: Suitable for progressive liver cirrhosis, especially in cases with oliguria renal failure. The commonly used drug verapamil is 40mg per dose, 3 times a day, taken orally, which can quickly improve microcirculation and significantly reduce intrapulmonary shunting, thus improving liver and renal function.

　　(5) Adrenal cortical hormones: There are reports of significant therapeutic effects obtained by using adrenal cortical hormones to treat functional renal failure. This may be due to the improvement of liver function, which in turn leads to the improvement of renal function. However, due to the limited number of observed cases, it can be used as a trial treatment when other treatments are ineffective.

　　(6) Venous return of concentrated ascites: In recent years, through ultrafiltration devices (plate-type or hollow fiber dialyzers), the patient's own ascites is concentrated for venous return, which is effective in eliminating a large amount of ascites. Ascites return can supplement human serum albumin, increase plasma colloid osmotic pressure, increase effective circulating volume, and has certain therapeutic effects on refractory ascites. The efficacy of repeated small-volume paracentesis during liver cirrhosis is not certain. Simply paracentesis can cause the loss of a large amount of protein, worsen hypoproteinemia, often leading to hypovolemia, orthostatic hypotension, recurrence of ascites, leakage or infection, etc. In addition, it also poses a risk of诱发 hepatic encephalopathy in patients with liver cirrhosis. The therapy of ascites return can recover a large amount of protein in a short time, not only is cheaper than the cost of pharmaceutical albumin, but also can avoid many complications of paracentesis. Ascites return increases plasma osmotic pressure, plays a dilating role, and can significantly improve symptoms.

　　① Common abdominal fluid reinfusion methods:

　　A. Extracorporeal concentration method: After the abdominal fluid is drained, it passes through a high-flow filter, and the water in the abdominal fluid is removed in the form of ultrafiltrate. The concentrated abdominal fluid is then infused into the vein. This method is suitable for abdominal fluid with a low protein content, the method is simple, and does not require extracorporeal circulation.

　　B. Intra-body concentration method: The drained abdominal fluid does not need to be concentrated and is directly infused into the venous return circuit. Water is removed through hemodialysis or hemofiltration, and the abdominal fluid is equivalent to a replacement fluid. The ultrafiltration rate is adjusted according to the speed of abdominal fluid infusion to maintain volume balance. This method is suitable for abdominal fluid with a high protein content and requires extracorporeal circulation, establishment of a blood access, heparinization, dialysis machines, and certain blood purification technology.

　　C. Abdominal fluid dialysis: Connect the abdominal puncture catheter to a Y-shaped tube, and connect the 'arteriovenous' circuit with the dialyzer according to the single needle dialysis method, using abdominal fluid instead of blood for single needle dialysis. The abdominal fluid flow rate is 200ml/min, the dialysate flow rate is 500ml/min, and the duration is 2-5h per session.

　　② Abdominal fluid reinfusion precautions:

　　A. The reinfused abdominal fluid must be sterile exudate, excluding infectious, bloody, or cancerous abdominal fluid.

　　B. Strictly implement sterile operation.

　　C. When the abdominal fluid is infused into the venous return circuit, it must pass through a filter to prevent embolism.

　　D. Add an appropriate amount of heparin to the abdominal fluid container to prevent coagulation.

　　E. Pay attention to volume balance.

　　(7) Hemodialysis: Early application in selected cases can have certain efficacy in correcting excessive fluid overload, hyperkalemia, azotemia, and acidosis. Hemodialysis should pay attention to complications such as bleeding and hypotension. For patients with a hopeful improvement in liver function, dialysis treatment should also be given in a timely manner to extend life and wait for the recovery of liver function. In cases of toxic liver disease, hemoperfusion (HP) treatment for hepatic encephalopathy can improve and restore the patient's consciousness to varying degrees. The indications for HP treatment of hepatic encephalopathy are mainly fulminant hepatic failure, and early application can improve survival rates. It is believed that HP clears certain substances that cause hepatic encephalopathy, such as aromatic amino acids, bile acids, thiol, middle molecular substances, pseudoneurotransmitters, Na-K-ATPase inhibitors, etc. HP can cause thrombocytopenia and defects in coagulation factors in the blood circulation. To resolve this contradiction, platelets and frozen plasma are often infused during perfusion. The ideal frequency of HP is considered to be every 12 hours, which is more in line with the time it takes for toxic substances in hepatic encephalopathy to transfer from the brain to the blood flow. Some people have envisioned that串联使用hemodialysis and hemoperfusion devices can partially act as artificial liver, and is also a very ideal treatment for acute renal failure, thus potentially achieving better results in the treatment of HRS.

　　(8) New Artificial Liver: A new artificial liver device that combines plasma exchange and hemodialysis, significantly improves survival rates. This device is suitable for patients waiting for liver transplantation.

　　(9) Surgical Treatment:

　　① Portocaval or splenorenal venous anastomosis: There have been reports of cases treated with portocaval or splenorenal venous anastomosis for hepatorenal syndrome, with renal function recovery.

　　② Abdominal-cervical venous shunting surgery, after many years of clinical application, it is considered to have good efficacy. After shunting surgery, renal function is significantly improved, salt and water excretion is significantly increased, and the levels of aldosterone, renin activity, norepinephrine, and antidiuretic hormone in the blood also decrease significantly. Complications include fever, disseminated intravascular coagulation (DIC), shunt tube occlusion, hypokalemia, infection, and leakage of ascites. Less common complications include variceal bleeding, intestinal obstruction, pulmonary edema, air embolism, and pneumothorax. This method can be selectively applied to patients with ascites, but cannot be used as a definite treatment method for hepatorenal syndrome. In recent years, new shunts with pumps (Denver shunt and Cordis-Hakim ascites valve) have been developed to reduce the chance of blockage, but complications are still not rare.

　　③ Liver Transplantation: Successful in situ liver transplantation, the patient's consciousness clears, blood bilirubin decreases, prothrombin time returns to normal, urine output and urinary sodium excretion increase, blood urea nitrogen and creatinine decrease, creatinine clearance rate increases, liver function recovers quickly, renal function gradually recovers about 2 weeks after transplantation, and the long-term prognosis depends on the survival status of the transplanted liver.

　　II. Prognosis

　　HRS often occurs in decompensated liver cirrhosis and severe liver disease, so liver function failure often occurs first. Once HRS appears, the prognosis is extremely poor, and the mortality rate is very high. The average life expectancy after azotemia is less than 6 weeks. HRS can cause oliguria, azotemia, hyponatremia, hyperkalemia, hypotension, and deep coma, with rare survivors. Most die of liver function failure, upper gastrointestinal bleeding, or severe infection. A few die of renal failure, and a few survivors first have an improvement in liver function, followed by a gradual recovery of renal function. If the liver disease can be rapidly improved after treatment, or if the trigger of renal failure can be found and removed in time, the prognosis is better.