HBV-related nephritis
Introduction
Introduction to hepatitis B virus associated nephritis Hepatitis B virus-associated glomerulonephritis (HBV-GN) is abbreviated as hepatitis B nephritis. It refers to glomerulonephritis caused by immune reaction in the form of immune complex damage caused by HBV infection in human glomeruli or HBV without direct invasion of renal tissue. The clinical manifestations are proteinuria, hematuria or nephrotic syndrome, and the typical pathological change is membranous nephropathy. The incidence of HBV infection with glomerulonephritis is about 6.8%~20.0%, which is more common in children. basic knowledge The proportion of illness: 10% Susceptible people: more common in children Mode of transmission: mother-to-child transmission, blood transmission Complications: renal insufficiency, hypertension, chronic hepatitis
Cause
Causes of hepatitis B virus associated nephritis
The cause of kidney damage in hepatitis B patients or HBV carriers may be that HBV directly infects the kidney or causes autoimmune disease; in addition, hepatitis B virus antigen and antibody can form immune complexes, and antigen-antibody complexes can cause disease. HBV is a spherical particle (dane particle) with a diameter of 42-45 nm. It is a DNA virus composed of a double-layered shell and a core. It contains double-stranded DNA and DNA polymerase. One of the negative strands is a long chain, about 3.2 kb, and the other is The positive strand is a short strand, about 2.8 kb, and there are four reading frames on the long-chain DNA, encoding HBsAg, HBcAg, HBeAg, DNA polymerase and X protein, in hepatitis B virus-associated nephritis, deposited in glomerular capillaries. The walls are mainly HBsAg and HbeAg. Ozawa and Hattor have respectively eluted from the renal tissues of HBV-GN patients and found anti-HBsAg antibodies and anti-HBeAg antibodies; immunoelectron microscopy showed that the above HBV antigens and immunoglobulins were deposited in glomeruli At the same locus, these results support that HBV-GN is an immune complex nephritis caused by the HBV antigen component.
HBV antigen and antibody complex disease (38%):
Immunopathology confirmed that renal damage caused by HBV-associated nephritis is related to immune damage caused by HBV immune complex deposited in glomeruli. Recent studies have confirmed that chronic active hepatitis and persistent hepatitis can form immune complexes, not only in small kidneys. There is HBsAg in the ball. HBsAg-containing immune complexes are also found in the joints and capillary walls of some patients with polyarthritis and vasculitis. Some people have confirmed HBsAg in the glomeruli of patients with glomerulonephritis, and in the blood. High concentrations of HBsAg were also detected, indicating that this glomerulonephritis has a specific immune pathogenesis. Multiple antigens of HBV (HBsAg, HBcAg, HBeAg) were detected from the renal tissue of patients with glomerulonephritis, most Scholars believe that immune complexes caused by HBV antigens are indeed important in the pathogenesis of certain pathological types of glomerular diseases, such as HBsAg is the main cause of membranous nephritis (MN) and other glomerular diseases in China. The detection of antigen, HBsAg involved in the pathogenesis of MN, speculated that there are two possibilities:
(1) The deposition of HBsAg is derived from the blood circulation, and the HBsAg deposited in the renal tissue is not a complete virus outer shell, but a fragment of HBsAg.
(2) HBsAg is derived from the local expression of viral proteins in renal tissues and binds to corresponding antibodies derived from the blood circulation to form an in situ immune complex.
HBV infection causes autoimmune disease (23%):
HBV multiplies in hepatocytes, may change its own antigenic components, and is released into the blood with the destruction of liver cells; HBV can directly invade lymphocytes and monocytes, thereby causing immune dysfunction, and various autoantibodies appear in vivo after HBV infection. Such as anti-DNA, anti-hepatic cytolipid antibody, these have confirmed the existence of autoimmunity, autoimmune disease can lead to nephritis.
HBV directly infects kidney tissue (20%):
Recent studies by HBV have found that HBV DNA is detected in kidney tissue, suggesting that HBV directly infects kidney tissue and causes disease. Domestic Zhou Shidong et al found that HBVAg is often expressed in the glomerulus, and the renal tubule is often positively expressed, especially HBcAg, and found that the nephritis lesions in the HBcAg-positive group were significantly heavier than the negative group, suggesting that the presence of HBVAg may cause T-cell attack to cause tissue damage.
Prevention
Hepatitis B virus associated nephritis prevention
The key to the prevention of this disease is to actively prevent and treat hepatitis B, especially vertical infection of mother and baby. In recent years, research on hepatitis B vaccine has made great progress, and it has been listed as a widely used program of immunization, which has created favorable conditions for hepatitis B prevention and treatment. In order to prevent vertical infection of mothers and children, long-term follow-up observation of hepatitis B vaccine recipients, 47 (89%) of 53 patients were positive for HBs antibody after 5 years old, and no HBs antigen positive patients were found. In the future, with the control of hepatitis B, the incidence of this disease is bound to decline.
Complication
Hepatitis B virus associated nephritis complications Complications, renal insufficiency, hypertension, chronic hepatitis
There are renal insufficiency, high blood pressure, chronic hepatitis, and individual liver failure can occur.
Symptom
Hepatitis B virus-associated symptoms of nephritis Common symptoms Big Sanyang Lips and yellow hepatitis B surface antibody (... hypoproteinemia kidney damage ascites renal failure protein urine hematuria
The onset age is mostly children and adolescents, males are mostly, and clinical manifestations are diverse.
1, kidney symptoms
All patients had microscopic hematuria or proteinuria, and the onset was hidden, which was found during urine examination. Some patients may have onset of nephritic syndrome or nephrotic syndrome, manifested as nephrotic syndrome, accompanied by varying degrees of edema, may have a large amount of ascites, manifested as mesangial capillary nephritis, 40% have elevated blood pressure, 20% Renal insufficiency. Patients with membranous nephropathy, no elevated blood pressure and renal insufficiency.
2, liver symptoms
Most patients with no history of hepatitis and clinical manifestations of hepatitis, some patients may have liver enlargement or abnormal liver function.
Examine
Hepatitis B virus associated nephritis
1. Urine: Hematuria and proteinuria, tubular urine, and urine protein are mainly albumin.
2. Blood biochemistry: There are often albumin decline, cholesterol increase, alanine aminotransferase and aspartate aminotransferase can be elevated or normal, plasma protein electrophoresis 2 and beta globulin are elevated, and gamma globulin is often normal.
3. Hepatitis B serological markers and HBV-DNA: Most patients are hepatitis B big three positive (HBsAg, HBeAg and HBcAb positive), a small number of patients are small Sanyang (HBsAg, HbeAb and HBcAb positive), only HBsAg positive patients, blood HBV-DNA is generally positive.
4. Immunological examination: There may be hypo-complementemia and cryoglobulinemia. About 50% of patients have decreased blood levels of complement, and blood IgG and IgA increase, suggesting that the lesion is active and the circulating immune complex is positive. HBsAg, HBcAb, HBeAg, HBeAb, DNA polymerase (DNA-P) and HBV-DNA were detected in the blood. Among them, HBeAg, DNA polymerase (DNA-P) and HBV-DNA are currently considered to be the most sensitive for diagnosing HBV infection. Index, however, HBsAg positive can support the diagnosis of hepatitis B-related nephropathy, and may also suggest that hepatitis B and glomerulonephritis coexist. Therefore, patients with glomerulonephritis should be routinely examined for HBsAg to avoid missing diagnosis. And delay treatment.
5. Renal biopsy: It is the final means to determine HBV-GN and is a prerequisite for the diagnosis of HBV-GN.
(1) Pathology: HBV infection has organ ubiquitinity. In addition to mainly involving the liver, renal damage can be caused by the kidney. The renal pathological type of HBV-associated nephritis is diverse, the most common is membranous glomerulonephritis. Followed by membrane proliferative glomerulonephritis, mesangial proliferative glomerulonephritis, focal segmental mesangial hyperplasia or focal segmental sclerosing glomerulonephritis and IgA nephropathy, histopathology, pathology Types of HBV-associated nephritis are similar to the corresponding types of primary glomerulonephritis.
(2) Renal tissue biopsy: diagnosis of HBV-associated nephritis must be done for renal biopsy, because serum HBV antigen is positive, not enough to be used as a basis for the diagnosis of HBV-associated nephritis, if nephritis patients detect HBV antigen positive in renal tissue sections After the exclusion of lupus nephritis, idiopathic membranous nephropathy and other nephropathy, the diagnosis of HBV-associated nephritis can be made. Immunofluorescence is found in the glomerular capillary vasospasm and mesangial area, and HBsAg, IgM, IgG can be seen. The deposition of C3, some authors reported that HBeAg and HBcAg in glomerular deposition, electron microscopic examination of HBV-associated nephritis can sometimes find virus-like particles, and visible tubular network inclusions, suggesting that the disease is associated with viral infection.
6. Others should be routinely done B-ultrasound, electrocardiogram and other checks.
7. Many reports have included glomerular hepatitis B virus antigen staining into the diagnostic criteria for hepatitis B-associated nephritis. All pathological types of hepatitis B-related nephritis renal biopsy specimens were positive for HBsAg staining.
Diagnosis
Diagnosis and diagnosis of hepatitis B virus associated nephritis
diagnosis
At present, there is no unified diagnostic standard for HBV-associated nephritis. The diagnosis of hepatitis B virus-associated nephritis, in addition to the diagnosis of hepatitis B, should have the following four clinically diagnosed:
1. With proteinuria or hematuria, there must be an immune complex nephritis.
2. Hepatitis B virus antigen (HBAg), such as serum HBsAg positive.
3. Confirmation of deposition of hepatitis B virus or its antigen in kidney tissue (if HBV-DNA or HBeAg can be found to indicate replication of hepatitis B virus in kidney tissue).
4. Renal biopsy confirmed glomerulonephritis, and can exclude secondary glomerular diseases such as lupus nephritis.
The fourth point is the most basic condition, lacking it. In view of China's high prevalence area of hepatitis B, and glomerulonephritis is also a common disease in China, in order to avoid missed diagnosis, in patients with glomerulonephritis, HBV antigen test should be routinely performed. In addition, the incidence of HBV carriers in China is high, and patients with serum HBsAg-positive glomerulonephritis are not necessarily HBV-associated nephritis. It is likely that serum HBV antigen-positive patients have glomerulonephritis or primary kidney caused by other causes. Small ball nephritis should be noted for recognition. Because there are few primary membranous nephropathy in children in China, the serum HBV marker is positive in children, and renal biopsy is membranous nephropathy can be diagnosed as HBV-GN. Because China is a highly infected area of HBV The routine detection of HBV markers in renal biopsy is of great significance for the early diagnosis and reasonable treatment of hepatitis B-associated nephropathy.
In addition, the diagnosis of this disease can refer to the opinion of the special symposium on hepatitis B (abbreviated as hepatitis B virus) related nephritis held in Beijing in October 1989.
Diagnostic conditions:
1 serum hepatitis B virus marker positive.
2 suffering from glomerulonephritis and exclusion of secondary glomerular diseases such as lupus nephritis.
3 Hepatitis B virus (HBV) antigen or HBV-DNA was found in the kidney tissue section.
4 renal tissue pathological changes to membranous nephritis.
Description: It can be diagnosed according to the first, second, and third, regardless of the pathological changes of the renal tissue; it meets the first and second conditions in the diagnosis and the pathological diagnosis of renal tissue is membranous nephritis, although it is not in the renal tissue section. HBV antigen or HBV-DNA can be found as a diagnosis; China is a high-risk area with HBV infection, such as glomerular disease patients with HBV antigenemia, which is not enough as a basis for HBV-GN-associated nephritis, should pay attention to differential diagnosis .
Differential diagnosis
Hepatitis B-associated nephritis needs to be differentiated from nephritis caused by other causes, such as systemic lupus erythematosus nephritis, idiopathic membranous nephropathy, glomerulonephritis after streptococcal infection.
1. Lupus nephritis: diagnosis of HBV-associated nephritis must first rule out lupus nephritis, more lupus nephritis patients with renal biopsy can be seen in HBsAg deposits, similar to the pathology of HBV-associated nephritis, but lupus nephritis The clinical basis of hepatitis B, the deposit of HBsAg is the basis of non-specific retention or lupus nephritis, its significance is still unclear, and the clinical and pathological manifestations of lupus nephritis are complex, often manifested as extensive damage of multiple systems. Can be combined with its clinical manifestations, as well as detection of lupus cells, anti-nuclear antibodies, Smith antibodies and renal biopsy to identify.
2. Idiopathic membranous nephropathy: Idiopathic membranous nephropathy occurs mostly in children and is similar in children with HBV-associated glomerulonephritis, but in addition to clinical manifestations, the renal pathology is not completely consistent, idiopathic membrane The membranous lesions of nephropathy are rarely associated with mesangial deposits, and no sediments are found under the endothelium; while HBV-MN has multiple membranous lesions with mesangial area immune complex deposition, some with subendothelial deposition. And the mesangial cells have nodular proliferation, and the presence or absence of immune complex deposition under the electron microscope can be used as an identification method for the two.
