Hepatogenic renal damage mainly includes

1. glomerulonephritis caused by hepatitis B virus;
2. glomerulonephritis, primarily IgA nephropathy, resulting from immune, physiological, and metabolic disturbances in cirrhosis;
3. functional acute kidney failure caused by renal hypoperfusion in severe hepatic insufficiency, known as hepatorenal syndrome.

bubble_chart Clinical Manifestations

1. Hepatitis B Virus-Associated Nephritis: More common in children and males, as well as patients with hepatitis B or hepatitis B virus carriers. The clinical manifestations include asymptomatic proteinuria or nephrotic syndrome, with a few patients presenting with gross hematuria.
2. Cirrhotic Glomerulonephritis: Patients with a history of cirrhosis may exhibit abnormal urine tests (such as microscopic hematuria), hypertension, and renal insufficiency, among other symptoms. A small number of patients may show no clinical manifestations. The deterioration of renal function is relatively slow.
3. Hepatorenal Syndrome: Commonly seen in the decompensated stage of liver dysfunction. Most patients have certain predisposing factors, such as excessive diuresis, large-volume ascites drainage, gastrointestinal bleeding, or the use of certain nephrotoxic drugs. Oliguria typically occurs during or after severe liver damage, with progressive deterioration of renal function over days, weeks, or months, often accompanied by nausea, vomiting, mental apathy, and drowsiness. In severe cases, hepatic encephalopathy and unconsciousness may occur. Infections, bleeding, hypotension, and liver failure are the main causes of death in these patients.

Liver sexually transmitted disease appearance, jaundice, spider angiomas, liver palms, splenomegaly, ascites, or edema of the eyelids and lower limbs.

1. Serum HBV antigen positivity and renal biopsy HBV antigen positivity are evidence for the diagnosis of hepatitis B virus-associated nephritis.
2. In cirrhotic glomerulonephritis, urinary changes become more pronounced with the progression of proliferative sexually transmitted disease, including proteinuria, casturia, and microscopic hematuria, but gross hematuria is less common than in primary IgA nephropathy. Most patients have positive circulating immune complexes, elevated serum immunoglobulins, with particularly prominent IgA elevation, and a few patients show decreased blood C3 levels.
3. Patients with hepatorenal syndrome have negative or trace urinary protein, normal urinary sediment or a small number of red and white blood cells and casts; thrombocytopenia, anemia, and abnormal liver function; markedly decreased Ccr, and elevated hematuria nitrogen and creatinine.
4. Ultrasound examination may show changes of cirrhosis, but the kidneys are mostly unchanged.

bubble_chart Treatment Measures

1. Hepatitis B virus-associated nephritis: Refer to the treatment of primary glomerular diseases, but glucocorticoids may promote HBV replication, and the efficacy is uncertain, so they should be used with caution; antiviral therapy, such as interferon and Chinese medicinals, may have some therapeutic effect.
2. Cirrhotic glomerulonephritis generally does not require special treatment, and the main focus should be on protecting the liver and preventing further liver damage; for the few cases with rapidly deteriorating renal function or presenting with nephrotic syndrome, the diagnostic and treatment principles are the same as for IgA nephropathy.
3. In hepatorenal syndrome, the key lies in the treatment of liver disease and its complications; avoid excessive diuresis and large-volume ascites drainage, use nephrotoxic drugs with caution, and correct electrolyte imbalances; on the basis of improving liver function, appropriate volume expansion and diuresis, intravenous infusion of low-dose dopamine (e.g., 20mg dopamine in 250ml low molecular weight dextran, infused at 15–20D/min), prostaglandins, or phentolamine may improve renal hemodynamics; moderate ascites drainage or ascites filtration and concentration reinfusion can reduce intra-abdominal pressure and help improve renal blood circulation; indications for dialysis are the same as for chronic renal insufficiency. Surgical treatment may be necessary.

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bubble_chart Differentiation

1. Hepatitis B-associated nephritis needs to be differentiated from primary glomerulonephritis in hepatitis B virus carriers and secondary glomerular diseases such as lupus nephritis.
2. In advanced liver disease, renal insufficiency should be distinguished from simple prerenal azotemia, acute tubular necrosis, and acute allergic interstitial nephritis.