Overview
Hepatogenic renal damage mainly includes: (1) glomerulonephritis caused by hepatitis B virus; (2) glomerulonephritis with IgA nephropathy predominantly produced by disorders of immunity, physiology, and metabolism in the body during cirrhosis; (3) functional acute renal failure caused by renal hypoperfusion when severe hepatic insufficiency occurs, i.e. hepatorenal syndrome.
The clinical manifestations of cirrhosis secondary to renal tubular acidosis are similar to those of non-hepatic patients. The vast majority have incomplete distal renal tubular acidosis, and a few patients have polyuria, polydipsia, nocturia, dysuria, and hypokalemic muscle weakness. Most patients have signs and symptoms of severe liver disease, as well as persistent alkalinuria, hypercalciuria, and hypocitraturia, which may be combined with urinary tract stones and secondary hyperparathyroidism. In hepatic renal tubular acidosis, in addition to the reduced ability of the kidneys to excrete H+, it is often accompanied by marked hypokalemia. In addition, hepatic encephalopathy can be induced or aggravated because of the reduced ability of the kidneys to excrete ammonia.
Etiology
Currently, it is mostly believed to be related to the following factors:
1. Immune complex deposition in the glomerulus.
2. Altered renal hemodynamics.
3. impaired sodium excretion.
4. renal tubular acidosis due to immunologic compromise.
Symptoms
The clinical manifestations of cirrhotic renal damage can be divided into two phases, i.e. compensated liver function and decompensated liver function. Some of them may stay in the compensatory stage for a long time without necessarily entering the decompensatory stage.
1. Early performance
Compensated liver function is the early stage of cirrhosis, with mild symptoms such as loss of appetite, fatigue, nausea, vomiting, abdominal distension, discomfort or vague pain in the upper abdomen, normal or loose stools, and so on. Yellowish color. Spider nevi or dilated capillaries are seen on the face, neck, upper chest, back, shoulders and upper limbs, with liver palms. The liver is mildly enlarged, smooth and hard, and may have mild pressure pain, and the spleen is mildly to moderately enlarged. Liver function tests are in the normal range or mildly abnormal.
2. Intermediate manifestations
Clinical manifestations of hepatic decompensation, such as lethargy and fatigue, irregular low-grade fever, dark and gray complexion, hyperpigmentation and anemia, may appear in the stage of hepatic decompensation. There are various gastrointestinal symptoms such as nausea, vomiting, loose stools, abdominal distension and bleeding from nose, gums gastrointestinal tract and purpura. Mild to moderate jaundice, male patients have decreased libido, testicular atrophy, hair loss breast development; female patients have amenorrhea and infertility at the same time there are manifestations of portal hypertension such as splenomegaly, accompanied by a decrease in the number of white blood cells, red blood cells and platelet counts, varicose veins of the lower esophagus and fundus of the stomach often rupture due to the emergence of vomiting blood, black stools and shock. Abdominal wall and periumbilical varices. Hemorrhoids form and cause blood in the stool when ruptured. Ascites is the most prominent manifestation of liver cirrhosis, the liver size varies, usually first large and then small hard texture, nodular, sometimes with pressure pain. About half of the patients have mildly increased serum bilirubin level. Total cholesterol, especially cholesterol, is often below normal, albumin is decreased, globulin is increased, and the albumin/globulin ratio is decreased or inverted. Protein electrophoresis γ-globulin is significantly elevated, SGPT is significantly elevated, prothrombin time is prolonged, immunoglobulin IgG, IgA, IgM are increased, with IgG being the most significant.
3.Late stage performance
When cirrhosis secondary renal damage, cirrhotic glomerulonephritis and tubular acidosis can occur, early patients often have no obvious clinical symptoms, only a small amount of proteinuria. The deterioration of renal function in patients with cirrhosis secondary to IgA nephropathy turns slowly and is a benign process. Some patients have proliferation of mesangial cells, endothelial cells and/or epithelial cells, accompanied by immune complex deposition in the mesangial area and subendothelium. These patients often have proteinuria and hematuria, and may also have edema hypertension and renal decompensation.
Examination
1. Liver ultrasonography
Ultrasonography may show cirrhotic changes, but the kidneys are mostly unchanged.
2. Serum albumin to globulin ratio (A/G)
(1) Positive serum HBV antigen and positive renal section HBV antigen are evidence to confirm the diagnosis of hepatitis B virus associated nephritis.
(2) In cirrhotic glomerulonephritis, urinary changes become evident with the aggravation of proliferative lesions proteinuria, tubularuria, and microscopic hematuria, but microscopic hematuria is less common than in primary IgA nephropathy. Most patients have positive circulating immune complexes, elevated blood immunoglobulins, and especially elevated IgA, and a few patients have decreased blood C3.
(3) Patients with hepatorenal syndrome have negative or trace amounts of urinary protein, normal urine sediment or a small number of red and white blood cells and tubular patterns; thrombocytopenia, anemia and abnormal liver function; Ccr is significantly decreased, and blood urea nitrogen and creatinine are elevated.
Diagnosis
Diagnosis can be made on the basis of the above clinical manifestations and laboratory tests.
Complications
Upper gastrointestinal bleeding, hepatic encephalopathy, bacterial infection cirrhosis, hepatorenal syndrome, cirrhotic renal damage complications.
Differential diagnosis
1. Hepatitis B-associated nephritis should be differentiated from hepatitis B virus carriers with primary glomerulonephritis and secondary glomerular diseases such as lupus nephritis.
2. Renal insufficiency in the advanced stage of liver disease should be differentiated from simple prerenal azotemia, acute tubular necrosis and acute allergic interstitial nephritis.
Treatment
1. Hepatitis B virus-associated nephritis is referred to the treatment of primary glomerular disease. Glucocorticosteroids may promote HBV replication, but the efficacy is not certain, and should be applied with caution; antiviral therapy, such as interferon and traditional Chinese medicine may have some efficacy.
2. Cirrhotic glomerulonephritis, generally does not need special treatment, mainly should protect the liver to prevent further damage to liver function; a few people with rapid deterioration of renal function or nephrotic syndrome, the principle of diagnosis and treatment is the same as IgA nephropathy.
3. In hepatorenal syndrome, the key lies in the treatment of liver disease and its complications; avoid excessive diuresis and large amount of ascites, use nephrotoxic drugs cautiously, correct electrolyte disorders; on the basis of improving liver function, appropriate dilatation and diuresis, static small-dose dopamine, prostaglandin, or phentolamine, etc., which may improve renal hemodynamics; appropriate amount of ascites or ascites filtration and concentration of reflux, which can reduce intra-abdominal pressure and help to improve renal blood circulation; appropriate amount of ascites or ascites filtration and concentration of reflux, can lower intra-abdominal pressure, which is conducive to the improvement of renal blood circulation. Favorably improve renal blood circulation; dialysis indications are the same as chronic renal insufficiency. Surgical treatment if necessary.
Prognosis
The prognosis is better if the hepatic renal damage is mild and the symptoms can be improved rapidly after treatment; if the duration of ascites and azotemia is short, and no ascitic puncture and drainage are done; if the normal blood pressure can be maintained; if the causative factors of renal failure can be found and corrected in time.
The prognosis is better for those who can find out the causes of renal failure and correct them in time. Those who have end-stage changes such as oliguria with urine output less than 300ml per day, obvious azotemia, deep coma and low blood pressure; those whose serum sodium is higher than 125mmol/L; those whose urinary sodium excretion is lower than 5mmol/L; as well as those who have hepatic encephalopathy, gastrointestinal hemorrhage and infection, and hyperkalemia and other complications have a very poor prognosis. Once hepatorenal syndrome occurs, the prognosis is poor and the mortality rate is very high. The main cause of death is hepatic complications rather than renal disease.
Prevention
There is no specific treatment for hepatic renal damage, but in most cases, more specific predisposing factors can be identified. Therefore removing the triggers is of great practical importance in preventing the development of glomerular damage. Treatment should be directed primarily at the liver disease itself. Attention should be paid to protecting the liver, avoiding harmful stimuli, and preventing further damage to liver function to prevent progressive damage to the kidneys.