Anti-HCVAg positivity is one of the symptoms that confirm the diagnosis of noncryoglobulinemic MPGN (membranoproliferative glomerulonephritis) as well as membranous nephropathy. Hepatitis C virus (HCV) is a single-stranded RNA virus that was first identified in 1989 and is now estimated to affect approximately 100 × 106 people worldwide, mainly through blood product transmission and intravenous drug use. The relationship between HCV infection and glomerular diseases has gradually increased in the last decade, and it is now believed that HCV-related kidney damage mainly includes cryoglobulinemic MPGN, noncryoglobulinemic MPGN, and membranous glomerulopathy (MPGN). membranous nephropathy (MN). Clinical manifestations of hepatitis C The incubation period of the disease is 2 to 26 weeks, with an average of 7 or 4 weeks. The incubation period of hepatitis C caused by blood products is short, usually 7 to 33 days, with an average of 19 days. The clinical manifestations are generally milder than those of hepatitis B, mostly subclinical without jaundice type, commonly with single ALT elevation, persistent long term or repeated fluctuations, patients with low mean ALT and serum bilirubin and short duration of jaundice. However, there are also more severe cases, which are clinically difficult to distinguish from hepatitis B. Hepatitis C virus infection is more likely to be chronic than hepatitis B virus infection. It is observed that 40% to 50% develop into chronic hepatitis, 25% develop into cirrhosis, and the rest are self-limiting. Those with acute hepatitis C who develop chronicity tend to be jaundice-free, with long-term fluctuations in ALT and persistent high titers of positive serum anti-HCV. Therefore, clinical attention should be paid to the changes of ALT and anti-HCV. The majority of HCV-induced severe hepatitis is caused by chronic hepatitis B combined with HCV infection. The symptoms of HCV cryoglobulinemic nephritis are systemic vasculitis, and patients with HCV cryoglobulinemic MPGN may have a variety of nonspecific clinical manifestations, such as purpura, arthralgia, peripheral neuropathy, and hypocomplementemia. Renal manifestations include hematuria, proteinuria (mostly within the nephrotic syndrome), marked hypertension and varying degrees of renal insufficiency, with nephrotic syndrome as the initial manifestation in about 25% of patients. Mildly elevated transaminases are often present, with some patients having normal transaminases, and there may be no history of acute hepatitis. Serologic testing for hepatitis C has only recently been refined, but hepatitis C is associated with cryoglobulinemic glomerulonephritis. In addition to autoimmune active hepatitis, cryoglobulins and circulating immune complexes can be seen in a variety of acute and chronic liver diseases, and hepatitis C antigenemia is common in addition to the common purpura, weakness, arthralgia, hepatitis, nephritis, and vasculitis that can be seen in mixed cryoglobulinaemia. In mixed cryoglobulinemia, patients with renal impairment have positive serum hepatitis C virus RNA (HCV-RNA), positive anti-HCVAg, and positive cold precipitates. Cold precipitates included HCV-RNA viral core antigen and IgG anti-HCV antibodies; however, HCV-RNA was not localized to immunodeposit in the glomeruli. A 39-year-old woman with positive antibodies to hepatitis C and a history of substance abuse presented with weakness, purpura, arthralgia, facial and bilateral lower extremity edema; this patient had renal proteinuria, loss of renal function, and mixed cryoglobulinemia. Thus, the clinical presentation of the disease is not specific. There are no uniform diagnostic criteria for nephritis associated with hepatitis C. The diagnosis of the disease, in addition to being consistent with the diagnosis of hepatitis C, should be confirmed clinically with the following four items: 1. The presence of proteinuria or hematuria. 2, Positive serum hepatitis C virus RNA (HCV-RNA) and positive anti-HCVAg. 3, There is definitely the presence of cold globulin and immune complexes, i.e. positive cold precipitates, in which there are HCV-RNA viral core antigen and IgG anti-HCV antibodies. 4. Kidney biopsy showed severe mononuclear cell infiltration and large number of glomerular immune complex deposits, because HCV-RNA immune deposits were not necessarily localized in the glomerulus, so the kidney biopsy could also be negative. Renal biopsy confirms glomerulonephritis and can exclude other secondary glomerular diseases. Given that China is a highly endemic area for liver disease and HBV and HCV often overlap in infection. The possibility of simultaneous infection with both viruses exists because HCV and HBV have similar transmission routes, but it is more common to have HCV infection in addition to persistent HBV infection. to avoid missed diagnosis, tests for both HBV and HCV antigens should be routinely done in patients with glomerulonephritis. 1. Urine examination Hematuria and proteinuria, tubular urine may appear, and urine protein is mainly albumin. And mostly proteinuria in the range of nephrotic syndrome. Patients with acute jaundice may have positive urinary bilirubin and urobilinogen before the appearance of jaundice. 2, blood test Total white blood cell count is normal or slightly low, the classification count neutrophils can be reduced, lymphocytes are relatively increased. In case of renal insufficiency, urea nitrogen, creatinine and hypocomplementemia may be seen. (1) Serum bilirubin: The patient’s serum bilirubin rises day by day during the jaundice period, mostly reaching a peak within 1 to 2 weeks. (2) Serum enzyme assay: Serum alanine aminotransferase (ALT) begins to rise before the onset of jaundice and reaches a peak in the extreme phase of the disease, with very high enzyme activity in acute hepatitis, and slowly declines with serum bilirubin during the recovery period. In chronic hepatitis, ALT can fluctuate repeatedly. In heavy hepatitis, ALT decreases when bilirubin rises sharply, which is called “enzyme jaundice separation”, which is a sign of serious illness. Glutathione aminotransferase (AST) is present in about 4/5 of the mitochondria (ASTm) and 1/5 in the cytosol (ASTs), and when mitochondria are damaged, serum AST increases significantly, reflecting the severity of hepatocellular lesions. In cases of acute viral hepatitis ALT values are higher than AST values, the ALT/AST ratio approaches 1 in cases of persistent active chronic viral hepatitis lesions, and the increase in AST is often more significant than ALT in cirrhosis. ALT and AST can be increased in the active phase of viral hepatitis, but also in other liver diseases (such as liver cancer, toxic, drug or alcoholic liver damage), biliary tract disorders, pancreatitis, cardiomyopathy, heart failure and other diseases, so attention should be paid to differentiation. Serum lactate dehydrogenase (LDH), cholinesterase (ChE) and r-glutamyl transpeptidase (rGT) can be changed in acute and chronic liver damage, but the sensitivity and magnitude of the changes are much less than those of transaminases. Serum alkaline phosphatase (ALP) can be significantly increased in cases of intra- and extra-hepatic bile duct obstruction and hepatic occupying lesions. rGT can be increased in cases of cholestasis and hepatocellular damage, and can be used to identify whether increased ALP is associated with hepatobiliary disease. Alcohol abuse can also cause an increase in rGT. In chronic hepatitis, after excluding biliary disease, an increase in rGT indicates that the lesion is still active. In liver failure, hepatocyte microsomes are severely damaged, rGT synthesis is reduced, and blood rGT also decreases. (3) Protein metabolism function test: Hypoprotein (A1b)emia is an important indicator of liver disease, and low A1bemia and hyperglobulinemia are characteristic serological indicators for the diagnosis of cirrhosis. Pre-serum A1b is more sensitive to change when liver parenchyma is damaged because its half-life is only 1, 9 days, so the decrease is consistent with the degree of hepatocyte damage, and the mechanism of change is similar to Alb. ①AFP (alpha-fetoprotein): There can be short-term low and moderate elevations in acute viral hepatitis, chronic hepatitis and cirrhosis (active). Increased AFP marks active regeneration of hepatocytes, and in patients with extensive hepatocellular necrosis, increased AFP may have a better prognosis. Patients presenting with extremely high serum AFP levels are most likely to have hepatocellular hepatocellular carcinoma. ②Blood ammonia measurement: In severe hepatitis liver failure, ammonia cannot be synthesized into urea for excretion; blood ammonia can be increased in patients with good portal collateral circulation in cirrhosis. Ammonia toxicity is one of the main causes of hepatic coma, but blood ammonia levels may not be consistent with the occurrence and severity of encephalopathy. (4) Prothrombin time (Pt) and activity (PTA): In liver disease, the related coagulation factor synthesis is reduced, which can cause Pt prolongation, and the degree of Pt prolongation marks the degree of hepatocyte necrosis and liver failure, and its related coagulation factor half-life is very short, such as VII (4-6h), X (48-60h), II (72-96h), so it can reflect liver failure more quickly. Prolonged Pt can also be seen in cases of congenital coagulation factor defects, diffuse intravascular coagulation and vitamin K deficiency, which should be distinguished. (5) Tests related to lipid metabolism: Total serum cholesterol (TC) is significantly reduced in severe hepatitis, and it is thought that TC.