Chronic hepatitis B and asymptomatic carriage of HBV is associated with HBV-GN . Patients with HBV-GN have a high morbidity rate. In general, the clinical manifestations are not specific, and the hepatic and renal functions are normal for several years. The initial symptoms detected in medical examinations are usually proteinuria and hematuria. By this time, the renal damage is severe and irreversible. Important laboratory examinations include the evaluation of serum HBV markers, changes in renal hemodynamics and a pathological examination including a renal biopsy. These examinations are important for early diagnosis and treatment.
Some studies have investigated the relationship between HBV infection and IgA nephropathy. Lai et al. found that the morbidity due to IgA nephropathy was high in an area of high HBV prevalence. The frequency of HBsAg-positivity in IgAN serum was higher than that in healthy control serum. HBsAg, HBcAg and the corresponding immune complexes were deposited in the glomeruli. Furthermore, the deposit site was the same as that of IgA. This finding is notable because HBV and its immune complexes deposited in the glomeruli play a major role in the pathogenesis of IgAN . The above mentioned studies give a hint at the close relationship between HBV infection and renal damage. HBV can involve the kidney as well as the liver, and renal function must thus be monitored in HBV-infected patients . Thus, when the damage of HBV is evaluated, doctors need to focus on the change in hepatic function and to monitor the renal function index. The renal damage is related to virus replication and, more importantly, is linked to the immune response . Chronic HBV infection can induce renal damage, and antigen-antibody immune complexes against HBs, HBc, or HBe together with complement components have been demonstrated to induce renal damage .
In the present study, the detection of HBsAg and HBcAg along with the expression of Ig types and the presence of complement components in the glomerular deposits suggests that an immune complex mechanism leads to glomerular injury. The antigen-antibody complex in renal tissues is mainly derived from blood circulation, and the circulating immune complex is detained passively in the glomeruli. The immune complex damages the kidney by activating the complement system and cytokines, which is one of the major mechanisms of the pathogenesis of HBV-GN. Jiang W  suggested that these autoimmunity factors may play a role in the morbidity of HBV-GN. HBcAg in renal tissue as a target antigen can initiate cytotoxic T-cell-linked immunologic injury in renal tubular epithelial cells. The pathogenesis of HBV-GN is closely related to the immune state in human, and the damage of cells after HBV infection is provoked by the immune response in the host. If a patient’s immune system is inadequate, the virus cannot be eliminated. In this state, the illness can be delayed for several years, contributing to the pathogenesis of HBV-GN.
The present study revealed that the degree of glomeruli damage was different in patients with different serum HBV infection markers. The serum HBV infection markers were predominantly HBsAg, HBeAg and anti-HBc and HBsAg, anti-HBe and anti-HBc, which were related to the severity of urine protein leakage.
The pathological type of HBV-GN as determined by renal biopsy was most frequently MsPGN, followed by MPGN. The pathological subtypes of patients with elevated BUN and Scr levels were MsPGN and MPGN. This result was different from that of previous studies that have shown that the most common histological type was MN [5–9]. The reported prevalence of HBV-GN closely parallels the geographic patterns of HBV prevalence, with marked differences in the epidemiology of HBV infection among continents and regions. Lu et al. reported that HBV S gene mutations were closely associated with HBV-GN. However, HBV serotype or genotype characteristics differ between areas; the serotype ayw and genotype A of HBV are predominant in HBV-GN in South Africa, while the endemic HBV strains are serotype adw and genotype B in south China, and serotype adr and genotype C in Korea . However, the effects of these differences on the pathological subtype composition and syndrome of HBV-GN remains unclear. There have been no further worldwide reports of HBV-GN since the report by Levy and Chen  in the 1980s, until now. The current data based on over one hundred million people in Northeast China will provide a useful basis for further investigations into HBV-GN.
HBsAg and HBcAg were deposited in the glomeruli of 50% of the patients with the MsPGN subtype of HBV-GN, and HBsAg and HBcAg were deposited in the glomeruli in the MPGN patients of 36.6% and 43.9%, respectively. With respect to the renal function staging of the 329 cases, most patients with HBV-GN were in stage I (68.3%), and this condition was ignored by patients or doctors. Once the GFR has changed substantially, the kidneys have been irreversibly damaged. Thus, the detection of HBsAg and HBcAg in glomeruli of patients with HBV infection can predict the severity of the disease.
In general, the prognosis mainly depends on the pathological subtype. In this study, the prognosis of HBV-GN ranged from spontaneous remission to renal failure. The MPGN and MsPGN subtypes of HBV-GN represented over half (52.7%) of the 38 cases in GFR stages III-V. Patients with the minimal glomerulonephritis subtype of HBV-GN experience slow disease progression with a benign prognosis; those patients with the MsPGN subtype have a poor prognosis, and those with the MPGN subtype have the worst prognosis. Patients with MsPGN and MPGN can advance to chronic renal function failure.
Most patients with HBV-GN were male. Patients aged from 30 to 39 years old had the highest incidence of HBV-GN. Their initial symptom was edema, in agreement with another study . The deposits of HBsAg, HBcAg, and simple HBcAg increased with the increase in the levels of deposits of IgA, IgG, IgM and C3 in the glomeruli. At present, the process from the onset and aggravation of HBV-GN to renal function failure is closely related to the quantity of HBsAg, HbcAg, immune globulin deposits and the pathological subtype.