Cirrhotic renal damage

　　There are many causes of liver cirrhosis, mainly viral hepatitis, chronic alcoholism, malnutrition, intestinal infection, drug or industrial toxicant intoxication, and chronic heart failure. Liver cirrhosis causes diffuse glomerulosclerosis lesions in the kidneys, leading to abnormal anatomy and function of the kidneys. The pathogenesis of hepatic glomerulosclerosis is not yet clear. Currently, it is believed to be related to the following factors:

　　1. Related to immune complexes

　　There is significant IgA deposition in renal glomerular deposits, and the antigen may come from bacteria, viruses, or food components in the digestive tract. Due to the dysfunction of Kupffer cells in liver cells in liver cirrhosis, the damaged liver cannot clear exogenous antigens from the intestines. Moreover, due to the formation of collateral circulation, these antigenic substances enter the blood circulation directly without being processed by the liver, thereby triggering the production of antibodies.

　　2. Changes in renal hemodynamics

　　In decompensated liver cirrhosis, the glomerular filtration rate and renal plasma flow vary widely, ranging from hypernormal values to severe renal failure. The mechanism of occurrence of these abnormal values is unclear.

　　3. Impaired sodium excretion

　　Many studies have shown that patients with decompensated portal cirrhosis often have significant sodium retention, and the urine excreted almost contains no sodium. Sodium overload forms ascites and edema, and there is an inverted situation where sodium excretion increases at night. The excretion of sodium chloride in urine depends on glomerular filtration and tubular reabsorption. It has been proven from experiments on liver cirrhosis patients and animals that all renal unit segments increase the reabsorption of sodium chloride.

　　Renal damage due to liver cirrhosis originates from liver cirrhosis, so its complications can be referred to as those of liver cirrhosis. Among the more common complications are upper gastrointestinal bleeding, hepatic encephalopathy, bacterial infection, and hepatorenal syndrome.

　　1. Upper gastrointestinal bleeding

　　Upper gastrointestinal bleeding is a major complication of liver cirrhosis, with 50% presenting with massive bleeding, and the rebleeding rate after 72 hours is as high as 40%. In liver cirrhosis, fibrosis and proliferation of connective tissue in the liver tissue damage the blood vessels within the liver, causing them to twist and occlude. A large number of blood vessels within the liver decrease, leading to portal vein blood flow obstruction. The blood from the portal vein flows through collateral circulation to the esophageal and gastric fundus venous plexus, causing venous congestion, dilation, and thinning of the venous vascular wall. The thinning vascular wall can rupture due to rough food, chemical stimulation, and increased intra-abdominal pressure, among other factors, leading to bleeding. Clinical symptoms include hematemesis (dark red or bright red) and melena.

　　2, Hepatic encephalopathy

　　The products of protein metabolism in the body are substances containing nitrogen elements. When these nitrogen-containing substances remain in the blood at a level exceeding a certain level, they can cause central nervous system dysfunction characterized by nervous and mental abnormalities and coma, mainly induced by harmful substances entering the brain from the intestines.

　　3, Bacterial infection

　　Liver cirrhosis patients due to decreased resistance, obvious reduction in immune function, are prone to be invaded by intestinal bacteria and toxins, and develop various infections, such as bronchitis, pneumonia, urinary tract infection, tuberculous peritonitis, primary peritonitis, etc.

　　4, Hepatorenal syndrome

　　When decompensated liver cirrhosis presents with a large amount of ascites, due to insufficient effective blood volume and other factors, functional renal failure can occur, known as hepatorenal syndrome. It is manifested by oliguria (urine output less than 400ml/d), azotemia, hyponatremia, and reduced urine sodium excretion. However, the routine urine test often shows no obvious abnormalities, and the renal histological examination is normal or mild. It is a late complication of liver cirrhosis renal dysfunction and is very dangerous.

　　5, Kidney stones

　　The serious complications of renal tubular acidosis are renal calcification and kidney stones. Due to the reduced secretion and excretion of H, persistent alkaline urine, hypercalciuria, and low citraturia, calcium salts are prone to settle in the kidneys and urinary tract. Moreover, due to negative calcium balance and secondary hyperparathyroidism, the decrease in blood calcium and phosphorus levels can cause osteomalacia and spontaneous fractures. The reduction of H-Na exchange and the increase of K-Na exchange lead to potassium loss in urine, which can cause hypokalemia. In addition, due to the reduced ability of the kidneys to excrete ammonia, it can induce or worsen hepatic encephalopathy.

　　Liver cirrhosis secondary renal damage can lead to liver cirrhosis glomerulonephritis and renal tubular acidosis. Early patients often have no obvious clinical symptoms, only with a small amount of proteinuria. The renal function deterioration in patients with liver cirrhosis secondary IgA nephropathy turns slow, presenting a benign process. Some patients have mesangial cell, endothelial cell, and/or epithelial cell proliferation, accompanied by mesangial area and subendothelial immune complex deposition. These patients often have proteinuria and hematuria, and may also appear edema, hypertension, and renal function decline.

　　The clinical manifestations of liver cirrhosis secondary renal tubular acidosis are similar to those of non-hepatic patients, the majority being incomplete distal renal tubular acidosis, with a few patients presenting polyuria, polydipsia, nocturia, poor urine concentration, and symptoms such as hypokalemia and muscle weakness. Patients often have severe symptoms and signs of liver disease, as well as persistent alkaline urine, hypercalciuria, and low citraturia, which may be accompanied by urinary tract stones and secondary hyperparathyroidism. In addition to the reduced ability of the kidneys to excrete hydrogen, liver cirrhosis secondary renal tubular acidosis often accompanied by significant hypokalemia. Moreover, due to the reduced ability of the kidneys to excrete ammonia, it can induce or worsen hepatic encephalopathy.

　　There is no specific treatment for liver cirrhosis and renal damage, but most of them can find relatively clear precipitating factors. Therefore, removing the precipitating factors is of great practical significance for preventing the occurrence of glomerular damage. Since the disease is derived from liver cirrhosis, it should mainly be treated for the liver itself. Attention should be paid to protect the liver, avoid harmful stimuli, and prevent further damage to liver function to prevent progressive kidney damage.

　　When patients with liver cirrhosis and renal damage present with hematuria, proteinuria, and cast urine, it should be considered that liver cirrhosis is accompanied by glomerular damage.

　　1. Urine tests

　　Proteinuria, hematuria, and cast urine can be seen, which is often gross hematuria. It is generally believed that renal failure rather than glomerular lesions is the cause. Liver tubular acidosis can manifest as persistent alkaline urine, hypercalcemia, and low citrate urine, which may be associated with urinary tract stones.

　　2. Serum tests

　　Serum tests show an increase in various immunoglobulins, with IgA being the most prominent, with increased IgA concentration, cryoglobulinemia, and reduced serum C3 concentration. In addition to the reduced ability of the kidney to excrete H in liver tubular acidosis, there is often marked hypokalemia.

　　3. Pathology

　　The pathological changes of liver cirrhosis are the obvious shrinkage of the liver, increased hardness, reduced weight, and a diffuse fine nodular surface of the liver. The histological changes are the disappearance of normal liver lobular structure, replaced by pseudolobules, and the liver cells in the pseudolobules can show varying degrees of变性, necrosis, and regeneration. The portal areas are significantly widened due to the proliferation of connective tissue. There are varying degrees of inflammatory cell infiltration, and many are in the form of small bile duct-like structures (pseudo-bile ducts). Electron microscopy shows that these pseudo-bile ducts are actually composed of newly formed liver cells and may be a manifestation of liver cell regeneration and renal calcification causing kidney stones.

　　4. Renal biopsy

　　Under the electron microscope, there are granular deposits in the glomerular mesangial matrix, with glomerulosclerosis, circular sparse areas in the basement membrane and some deposits, and deposits of immunoglobulins, especially IgA and C3. Although these conditions are not specific, if all four are present, it is a special change of hepatic glomerulosclerosis. The changes of 'hepatic glomerulosclerosis' can be different at different stages. In the early stage, there is only glomerulosclerosis without deposits, and in the late stage, the above typical lesions appear.

　　5. Other examinations

　　Routine liver, gallbladder, spleen, and kidney ultrasound and X-ray examinations can reveal typical manifestations of liver and spleen enlargement or atrophy and fibrosis, as well as changes in kidney shape and urinary tract stones.

　　Patients with liver cirrhosis and renal damage have strict dietary requirements, and their dietary adjustment methods can be referred to in the diet of patients with liver cirrhosis.

　　Firstly, taboos

　　1. Absolutely refrain from drinking alcohol to prevent exacerbating liver damage;

　　2. Avoid spicy and刺激性 foods;

　　3. Appropriately limit the intake of animal fats and oils, such as lard;

　　4. Avoid eating coarse and hard foods, fried and roasted foods, and poultry and fish with bones, as this may trigger the rupture of varices in the gastric fundus.

　　Secondly, it is advisable to consume

　　1. It is advisable to consume high-protein, high-carbohydrate, high-vitamin, low-fat, and easily digestible foods such as lean meat, fish, eggs, vegetables, etc.;

　　2. In the case of advanced liver cirrhosis with hepatic coma, a low-protein diet should be followed. For those with severe edema or ascites, a low-salt or salt-free diet should be adopted.

　　3. If constipation is accompanied, more sesame oil, honey, sesame, and bananas can be eaten to keep the bowels smooth, reduce the accumulation of ammonia, and prevent hepatic coma.

　　Three, Food Therapy Recipes

　　Breakfast: Congee (50g of rice), steamed bun (75g of flour), meat floss (15g of pork floss).

　　Snack: Sweet milk (250g of fresh milk, 10g of sugar), 150g of apple.

　　Lunch: Rice (150g of rice), fried hairtail (200g of hairtail), stir-fried napa cabbage (150g of napa cabbage).

　　Snack: Congee (30g of lotus root starch, 10g of sugar).

　　Dinner: Rice (150g of rice), fried chicken pieces (100g of chicken pieces), stir-fried tofu with tomatoes (50g of tofu, 100g of tomatoes).

　　Daily oil consumption of 25 grams, the above diet contains 2422 calories (10120 kilojoules).

　　Renal damage due to liver cirrhosis has no special treatment, but since the disease is derived from viral hepatitis and liver cirrhosis, treatment can be chosen for the liver disease itself. For the treatment of nephritis, it can be referred to the treatment of primary glomerulonephritis, but hormone and cytotoxic drugs should be avoided when liver function is impaired.

　　(1) In the case of incomplete renal tubular acidosis in liver disease, if there is no hypokalemia and metabolic acidosis, treatment may not be required. However, these patients are prone to induce hypokalemia during the use of diuretics or intravenous infusion of glucose, and attention should be paid during treatment.

　　(2) Targeted etiological liver protection therapy: Provide patients with appropriate amounts of protein and carbohydrates to ensure energy supply, give a variety of vitamins, especially B-group vitamins, and pay attention to the supplementation of trace elements.

　　(3) Adrenal cortical hormones: Prednisolone is the first choice, and low-dose immunosuppressants such as azathioprine or cyclophosphamide can be used in combination.

　　(4) Correction of acidosis and potassium supplementation: Use sodium citrate mixture (sodium citrate 140g, sodium citrate 98g, add water to 1000ml), take 20-30ml orally, 3 times a day. If hypokalemia is obvious, add 98g of potassium citrate to the above sodium citrate mixture, or take 10% potassium citrate solution 10-20ml, 3 times a day.