Definition: Hepatitis B virus associated glomerulo -nephritis (HBV-GN) is defined as an immune complex glomerular disease caused by chronic HBV infection, with proteinuria as the main manifestation, may be accompanied by microscopic hematuria, and some patients may develop renal insufficiency and uremia . It is a common secondary glomerular disease in children in China and is the main cause of membranous nephropathy in children. With the development and integrity of immune function, some patients may spontaneously remit. It can also develop in adults, but rarely remits spontaneously, and the prognosis is worse than that of children.
In 1971, Combes et al. first found HBsAg (hepatitis B surface antigen) components deposited on the glomerular basement membrane in a kidney puncture specimen from a 53-year-old patient with membranous nephropathy, and then successively found hepatitis B virus antigen in the kidney tissue of patients with membranous hyperplastic nephritis and IgA nephropathy, and the relationship between HBV and renal disease also gained attention. 1989 HBV-GN Symposium held in Beijing in 1989 named it hepatitis B virus-associated glomerulonephritis, referred to as hepatitis B-associated nephritis. In order to further standardize the diagnosis and treatment of HBV-GN, the Nephrology Group of the Pediatrics Branch of the Chinese Medical Association held a symposium in Zhuhai in November 2000 and formulated a draft diagnosis and treatment plan for HBV-GN. In 2008, the Nephrology Group of the Pediatrics Branch of the Chinese Medical Association revised the guidelines on the basis of the original diagnosis and treatment routine, with reference to the latest research results at home and abroad, and in accordance with the principles of evidence-based medicine. Guidelines.
Not all renal damage that occurs in patients with hepatitis B can be called HBV-GN. According to the definition: only immune complex glomerular disease caused by chronic HBV infection can be diagnosed as HBV-GN. In other words, HBV should be the causative agent, and the nephropathy should improve or even completely remit after effective clearance of viral antigens. In fact, clinically, nephropathy combined with hepatitis B infection (such as microscopic lesion nephropathy, diabetic nephropathy combined with hepatitis B) is far more common than HBV-GN, such patients have no hepatitis B virus antigen in the kidney tissue, and simple antiviral treatment cannot improve the nephropathy, so it is not HBV-GN, and the treatment can be treated separately. The Institute of Nephrology, Nanjing General Hospital, Nanjing Military Region, reported that HBV-GN accounted for 2.5‰ of 13519 kidney biopsies, while hepatitis B infection accounted for 70-100‰ of kidney disease inpatients, so the vast majority were not HBV-GN. HBV-related kidney damage also includes nodular polyarteritis and renal tubular injury such as tubular acidosis, which is not The majority of patients with HBV infection are not HBV-GN.
Epidemiology
1. incidence: the occurrence of HBV-GN is closely related to HBV infection, and the incidence of HBV-GN is also roughly parallel to the high rate of HBV infection. Children’s immune function is not yet well developed, and the incidence of HBV-GN is significantly higher than that of adults. In 1982, the Nephrology Group of the Pediatrics Branch of the Chinese Medical Association collected kidney biopsies from 20 hospitals nationwide, and HBVGN accounted for 8.7% of children with kidney biopsies. Nanjing General Hospital of Nanjing Military Region reported HBV-GN accounted for 2.5‰. The incidence rate of males is 1.5-2 times that of females.
2. Distribution of pathological types: The pathological changes of HBV-GN are characterized by membranous nephropathy (MN), membranoproliferative glomerulonephritis is the next most common pathological change, and other pathological types are rare. Among 745 cases of HBV-GN in children counted by Zhou et al, there were 507 cases of membranous nephropathy (70.6%), 49 cases of membranoproliferative nephritis (6.8%), 25 cases of IgA nephropathy (3.5%), and 66 cases of non-IgA tethered membranoproliferative nephritis (9.2%). Thus, membranous nephropathy is the main pathological type of HBV-GN, and membranoproliferative nephritis is also present in some cases and is also considered as one of the characteristic pathological changes of HBV-GN. From the above data, IgA nephropathy, especially membranoproliferative nephritis, is not less common than membranoproliferative nephritis, but it is not considered as a characteristic pathological change of HBV-GN, because there is a large disagreement about it at home and abroad, and many scholars believe that IgA nephropathy or membranoproliferative nephritis is a non-specific manifestation of nephritis recovery,; and unlike HBV-related membranoproliferative nephropathy (HBVMN) where the nephropathy can be complete remission, there is no information that antiviral therapy alone can lead to complete remission in patients with this type of IgA nephropathy.
Atypical membranous nephropathy: The pathological features of MN of HBV-GN are different from those of primary MN, which is “atypical membranous nephropathy”, often accompanied by some degree of thylakoid hyperplasia, endothelial cell hyperplasia and increased infiltrating cells in the glomerulus. In addition to C3 and IgG deposition, IgM, IsA, CA and Clq deposition are often present, which may appear as granular deposits distributed along capillary loops and also in the thylakoid region. It is sometimes difficult to distinguish from lupus nephritis by light microscopy alone, but the diagnosis of HBVMN is supported by the presence of viral particles on electron microscopy.
3. HBV antigen deposition: The 2008 guidelines changed the diagnostic criteria for HBV-GN from HBV antigen deposition in renal tissue to glomerular deposition. Glomerular HBV antigen detection rate varies depending on the antibody and detection method used (immunofluorescence, PAP, ABC) and the type of pathology. The overall HBsAg positivity rate was 354/379 (93.4%) and the HBeAg positivity rate was 164/313 (52.4%) in HBV-GN in 12 hospitals in China. Due to the problem of detection reagents, few HBeAg deposition tests were performed in China. Cui Min et al. of Nanjing General Hospital, Nanjing Military Region reported that the HBeAg positivity rate was 20/25 (80%) and HBcAg positivity rate was 22/25 (88%) in HBV-related membranous nephropathy. Combined with HBV-GN reports from Hong Kong, Taiwan and abroad, the rates of ltBeAg positivity were 55/61 (90.2%) and HBcAg positivity were 64/68 (94%). It is difficult to determine which HBV antigen is most appropriate for testing, and it is recommended that all 3 antigens be examined to corroborate each other and reduce missed diagnoses.
HBV-DNA has different degrees of distribution in the glomerular thylakoid cells, endothelial cells, epithelial cells, renal tubules, renal interstitium and blood vessels in HBV-GN patients, but the detection rate of renal tissues is also significantly lower than that of HBV antigen detection, roughly around 50% of the old J. The clinical utility value is limited, and it is not suitable for the diagnosis of HBV- GN criteria, the 2008 guidelines exclude it.
Pathogenesis.
Circulating immune complex-mediated inflammatory response
The three major antigens of HBV (HBsAg, HBcAg, HBeAg) are deposited in the glomerular capillary wall or thylakoid region. Chen Jia et al. reported that the positivity rate of HBV markers in renal tissues was 73.
Among them, the positive rate of HBsAg was 63.3% and the positive rate of HBcAg was 40%,
The detection rate of both HBsAg and HBcAg was 30%. It is generally believed that the relative molecular mass of substances that can cross the glomerular basement membrane and localize under the epithelium should be small [generally ( 3-5) × 105 , < 1
×The relative molecular mass of HBeAg is small, and its relative molecular mass is still < 106 after binding to its antibody HBeAb, and its isoelectric point is raised to 6.4-8.4.
HBsAg and HBcAg have larger relative molecular masses (> 106) and carry a negative charge, and can cross the glomerular basement membrane to reach the subepithelium.
The circulating immune complexes do not easily cross the GBM and deposit in the subepithelium, but they can be deposited in the thylakoid region and subendothelium, and pathological studies have also confirmed their deposition in these sites. The deposition of immune complexes in renal tissue activates complement and a series of cytokines leading to immune renal damage, which is the main pathogenesis of HBV-GN.
Imbalance of cellular immune function in the body
Studies have shown that patients with HBVMN have an imbalance of T-cell subsets, with a decrease in CD4+ T cells and an increase in CD8+ T cells, a decrease in CD4+/CD8+, and a decrease in CD4+/CD8
+ The decrease in CD4+ T cells results in insufficient production of specific antibodies to clear free HBV and its antigenic components, resulting in the persistence of HBV in the body.
The decrease in CD4+ T cells resulted in insufficient production of specific antibodies to clear free HBV and its antigenic components, causing HBV to persist in the body and continuously infect cells. They also found that HBVMN patients had low levels of HBeAg-HBeAb complexes in the circulation, while HBV carriers without kidney damage did not.
This suggests that HBVMN patients may have some kind of cellular immune deficiency and are unable to clear the virus effectively. Meanwhile, the cytotoxic T-cell activity of HBVMN patients was lower than that of HBV carriers, and IL2
and IFNγ levels were also significantly lower than those of the latter, but the secretion of IL10 by Th2 was higher than that of the latter, suggesting a decrease in the clearance of HBV, indicating that HBVMN patients may not be able to generate sufficient cellular immune responses to HBV.
This suggests that HBVMN patients may not be able to generate sufficient cellular immune response to HBV and are prone to HBVGN when HBV infection occurs.
Clinical manifestations
1. Clinical features: pediatric patients are mostly in the age of 2-12 years old, the average age is 6 years old, boys are significantly more than girls, can be up to 90%. Most of the clinical manifestations are nephrotic syndrome (73%), with some manifestations of non-nephrotic range proteinuria and microscopic hematuria. Sarcopenic hematuria, hypertension and renal insufficiency are less common. Most had no symptoms of liver disease, and nearly half of the children had elevated alanine aminotransferase (ALT). Cheng Zhen et al. of Nanjing Military General Hospital observed 51 adult patients with HBVMN, 82.5% of whom were male. The mean age was 35 years. HBV-DNA was positive at the onset of disease and 66.2% of patients had ALT less than 100 U/L with a follow-up of 12-252 (44.4±37.0) months. Of the 10 patients without antiviral therapy, 5 entered chronic renal failure and 1 developed uremia, suggesting a poor renal prognosis.
C3 was decreased in about half of the patients with a mild degree of decline, and some patients could show a decrease in complement C4, which may be related to insufficient hepatic synthesis of complement in active hepatitis. HBV replicates in hepatocytes and may alter its own antigenic components, which are released into the blood with the destruction of hepatocytes, leading to autoimmunity. a variety of antibodies can be detected in the body after HBV infection, including anti-DNA antibodies, cytoskeletal component antibodies, and Anti-hepatocyte membrane lipoprotein antibodies, all confirming the presence of autoimmunity. Accordingly, some HBV-GN patients may have positive serum autoimmune indicators such as antinuclear antibodies (ANA), SSA, SSB, cardiolipin antibodies and cryoglobulins, which are sometimes easily misdiagnosed as lupus nephritis.
2. Hepatitis B marker examination: about 3/4 of children with serological examination are positive for HBsAg, HBeAg and core antibody (HBcAb) (commonly known as the major triplet), the rest are positive for HBsAg, HBeAb and HBcAb (commonly known as the minor triplet), some are positive for HBsAg or HBsAg with HBeAg, but almost all are positive for HBV-DNA. There are isolated reports of cases where all 3 antigens of the serum were negative while HBV antigen deposits could still be found in the kidney.
Diagnostic criteria
Definitive diagnosis still relies on renal biopsy, and according to the 2008 guidelines for the diagnosis and treatment of HBV-GN, the diagnosis is based on the following.
1. Positive serum hepatitis B virus markers: most are positive for HBsAg, HBeAg and HBcAb at the same time (commonly known as major triplets), a few are positive for HBsAg, HBeAb and HBcAb at the same time (commonly known as minor triplets), and individual serum HBsAg negative but positive for HBV-DNA.
2. Nephropathy or nephritis with the exception of other glomerular diseases: most of them show nephrotic syndrome, a few show proteinuria and hematuria.
3. 1 or more HBV antigen deposition in the glomerulus: most have HBsAg, HBcAg or HBeAg deposition in the glomerulus.
4. renal pathological changes: most of them are membranous nephritis, a few are membranoproliferative nephritis and thylakoid nephritis.
The criteria for confirming the diagnosis are: ① having both the above-mentioned bases l, 2 and 3; ② having both the above-mentioned bases l and 2 and having membranous nephropathy in bases 4; ③ individual patients having both the above-mentioned bases 2 and 3, and having negative serum hepatitis B virus markers can also confirm the diagnosis.
Differential diagnosis
Patients with hepatitis B infection may show a decrease in complement C3 and C4, and a variety of antibodies such as antinuclear antibodies (ANA), SSA, SSB, cardiolipin antibodies, and cryoglobulins may also be detected, and immunofluorescence tests may show the phenomenon of “full brightness”, which is sometimes easily misdiagnosed as lupus nephritis. In patients with HBVMN, Sm and ds-DNA antibodies are rare, and renal tissues may stain positive for hepatitis B antigen, while crescent and collateral necrosis are relatively rare.
As mentioned in the previous epidemiological data, hepatitis B patients present with renal damage mostly in combination with two diseases, HBV-GN is, after all, a minority of cases. So if the kidney biopsy of a hepatitis B patient is membranous nephropathy, how to identify whether it is HBV-GN or combined with idiopathic membranous nephropathy? First look at whether the patient’s blood is positive for HBV-DNA, if it is negative for HBV-DNA in the absence of antiviral, then HBV-GN is highly unlikely. Next look at the e antigen, HBV-GN
In addition, it is important to look at whether the hepatitis B antigen, especially the e antigen and c antigen, is typically deposited in the kidney tissue. Finally, the newly discovered phospholipase A2 receptor antibody is specific for patients with idiopathic membranous nephropathy, which can be detected in 70% of patients with idiopathic membranous nephropathy, while HBV-GN patients lack this antibody, which can be used for differentiation.
Those with pathological manifestations of membranoproliferative nephritis need to be differentiated from plasma cell disease, cold globulinemia kidney damage, and hepatitis C-related kidney damage.
Evolution and progress of HBV-GN treatment regimen in China
The 1988 guidelines for the treatment of HBV-GN advocated treatment according to primary membranous nephropathy and membranoproliferative nephritis, i.e., treatment of HBV-GN with glucocorticoids, but the efficacy has been controversial. A few patients did achieve complete remission of nephropathy with glucocorticoids, but most patients had ineffective treatment, which instead led to HBV replication and fulminant hepatitis, and sudden withdrawal of glucocorticoids could also aggravate liver injury. However, it remains unclear which patients will benefit from hormone therapy. Therefore, current studies do not support the use of corticosteroids for HBV-associated nephropathy. Meanwhile, clinical studies have found that both the natural clearance of HBV and the effective response after antiviral therapy can lead to a subsequent improvement of HBV-GN, indicating that the key to treatment is the clearance of HBV; therefore, in the 2000 version of the treatment protocol, we began to recommend antiviral therapy with drugs such as interferon (IFN) and adenosine, and proposed that “immunosuppressants should not be applied”, and since then a large amount of evidence has shown that antiviral therapy is effective for HBV-GN, even for patients with HBV-GN who do not have liver function impairment, and/or whose liver biopsy is also normal. Therefore, in the new guidelines in 2008, it was clearly proposed that the application of IFN and nucleoside antiviral therapy is the main treatment for HBV-GN and the basis for other treatments, while a more flexible approach is taken to glucocorticoid therapy, pointing out that it can be used with discretion and caution when necessary (especially in membranoproliferative nephritis) and without contraindications such as active hepatitis, and is contraindicated in isolation.
Antiviral therapy for HBV-GN
The main anti-HBV drugs are IFN and nucleoside analogues. IFN includes polyethylene glycol IFN and generic IFN; the main nucleoside analogues are lamivudine, adefovir, telbivudine, entecavir and tenofovir. 2008 guidelines recommend IFN and lamivudine. The specific choice of drug should be determined by the patient’s condition and wishes. However, entecavir currently appears to be the preferred treatment option due to its efficacy, low viral resistance rate and low side effects.
IFN
IFN binds to cell membrane receptors, alters the activity of relevant intracellular enzymes, stimulates the production of antiviral proteins, thereby inhibiting the transmission of viral mRNA messages and further inhibiting viral multiplication, and activates macrophages and monocytes, increases T suppressor cell and NK cell activity, and enhances immune recognition to clear infected cells. Wang Zhaohui et al. treated 9 patients with HBV-associated nephritis with IFN-α, and those with effective treatment had reduced proteinuria and decreased viral replication in vivo. In another randomized controlled study of IFN-α treatment for children with HBV-GN in China, proteinuria disappeared and was accompanied by negative serum HBeAg in the treatment group within 3 months, while 50% of the control group still had heavy proteinuria; however, after stopping IFN-α treatment, there could be However, positive conversion of HBVDNA and recurrence of proteinuria could occur after stopping IFN-α treatment.
The effect of IFN treatment was related to the dose and treatment time, but also to gender, HBVDNA level and ALT level. Women, HBVDNA <2×1011copies/L and high ALT levels often achieve better results. For HBV-GN, the efficacy of adults receiving interferon appears to be much lower than that of children. There is a report of 4 cases of adult HBV-MPGN using 3MU subcutaneous injection 3 times a week for 6 months, and all proteinuria remained persistent. The IFN dose also varies from person to person as seen in studies from around the world. Also with IFN-α2b, Lai et al. used 3 MU intramuscularly 3 times a week for 3 months and 1/5 were in complete remission.
Sithebe et al. increased the dose to 10MU/m2 intramuscularly 3 times a week for a total of months, 10/24 complete remission; Taiwanese scholar Lin Ching-Yuan et al. observed the efficacy of high-dose IFN-α 5MU (weight <20kg) or 8MU (weight ≥20kg) for a long course (12 months) of HBV-GN treatment, all 20 cases in the treatment group were in complete remission and 16 cases had negative serum e antigen. The 2008 guidelines for HBV-GN in children, based on the observations of Lin Qingyuan and Sithebe et al. and with reference to the views of the Infectious Diseases Society, recommended an IFN dose of 3-6 MU/m2 per dose (≤10 MU/m2) for the treatment of HBV-GN, administered intramuscularly three times a week for 4-6 months in HBeAg-positive individuals and 12 months in negative individuals, with a course of treatment of at least 3 months and a long course (12 months ) is more effective. This dose is significantly higher than the recommended dose (1-3MU/m2) in the 2000 version of the HBV-GN treatment protocol. IFN-α therapy is not effective in resting HBsAg carriers (HBsAg positive with normal serum ALT and undetectable or lower than normal serum HBVDNA) and should not be used in patients with decompensated liver disease and autoimmune diseases (hyperthyroidism, SLE, etc.) and transplants.
Regular IFN requires long-term injection and poor compliance, while polyethylene glycolized IFN changes the pharmacokinetics of regular IFN and significantly improves the biological activity of IFN. It has been used in children with HCV-associated nephritis only in the past 2 years, but it has not been used for HBV-GN, and it is promising to be a new treatment option in the future.
Lamivudine
Lamivudine is a nucleoside antiviral agent that acts on the DNA polymutase of hepatitis B virus, thereby inhibiting DNA synthesis and viral replication, and has a good antiviral effect. For children with HBV-GN who do not want to be treated by injection, new guidelines recommend oral treatment with lamivudine. This drug is the only antiviral nucleoside analog approved by the FDA for use in children, and is convenient to take orally with good compliance. Hong Kong scholar Tang et al. observed 10 cases of HBVMN treated with lamivudine, all with elevated glutamate transaminase and positive HBV-DNA, and another 12 patients with HBVMN without lamivudine treatment as controls. The results showed that patients in the lamivudine-treated group had significantly reduced urinary protein, increased serum albumin, normal glutamate transaminase levels, and HBVDNA turned negative within 1 year of treatment, and 4 patients In the untreated group, one patient was in complete remission at 6 months of follow-up and three patients were in complete remission at 12 months of follow-up. No cirrhosis or tumors occurred during the follow-up period. Khedmat et al. conducted a meta-analysis of 10 studies (containing 119 patients) and showed that all patients on lamivudine had remission of proteinuria, with 72.7% complete remission and no relapse within 1 year after remission, concluding that lamivudine is effective in stopping the progression of HBV-GN. Cheng Zhen et al. of Nanjing Military General Hospital observed 51 patients with HBVMN with ALT less than 100 U/L, 41 of whom were treated with nucleoside analogues (NA) (19 with entecavir and 22 with lamivudine) as the NA group and 10 were not treated with NA as the control group. All patients were on ARB or ACEI. follow-up 12-252 (44.4±37.0) months. Complete remission of nephropathy was defined as urine protein turning negative and creatinine normal; partial remission was defined as urine protein reduced by more than 50% and less than 3.5 g/d and normal renal function. The pre-treatment urine protein quantification, creatinine and serum ALT levels in the NA/control group were 3.45±2.18
vs 4.45±3.30g/d, 0.85±0.56 vs 0.82±0.28umol/l, 51.7±26.3 vs
34.7±21.0U/L (P>0.05). At the final follow-up, there were 22 cases (53.7%) in the NA group/control group, respectively vs
1 (10%) patient in complete remission (P<0.01), 14 (34.1%) vs. 4 (40%) in partial remission, 5 (12.2%) vs.
Two cases in the NA group progressed to chronic renal failure without one case on dialysis, while five cases in the control group had chronic renal failure, one of which entered maintenance dialysis, and there were no deaths. At 1 year of treatment, the complete remission rate of urinary protein in the NA/control group was 31.7
At 1 year of treatment, the complete remission rate of urine protein was 31.7 vs 20%, HBeAg conversion rate 50 vs 0%, HBV-DNA conversion rate 62.5% vs 0%, and at 2 years, the complete remission rate of urine protein was 57.1 vs
The rates of complete urinary protein remission at 2 years were 57.1 vs 20%, HBeAg reversion rate 63.6 vs 0%, and HBV-DNA reversion rate 64.7 vs 0% (all P<0.01).
Table survival curve analysis showed that the odds of normal renal function at 5 years follow-up were 88% in the NA group and 49% in the control group, a significant difference (P<0.001). 5 patients in the NA group were virologically non-responsive (HBV-DNA titers did not decrease after 6 months of treatment), 6 were tested for YMDD variants, and 3 had variants, 2 of which were added to adefovir and 1 was changed to entecavir. None of them developed fulminant hepatitis, and no serious adverse reactions caused by NA were observed. The above results suggest that patients with HBVMN with serum ALT below the upper limit of 2 times normal receiving NA can significantly improve the remission rate of nephropathy and improve renal prognosis, while increasing the chance of HBeAg and HBV-DNA conversion with fewer adverse effects. However, due to the high proportion of lamivudine resistance mutations, attention should be paid to this issue during long-term treatment.
Entecavir
Entecavir is an orally administered antiviral drug, an epoxyhydroxydeoxyguanosine, approved by the FDA in 2005 for the treatment of chronic HBV infection. It is more effective than lamivudine and has a low incidence of drug resistance, with a 3-year incidence of resistance of about 1% and few adverse effects. It can be used for the treatment of lamivudine-resistant HBV infection, but the dose should be doubled. The generally recommended dose for nucleoside primary patients is 0.5 mg/d, and the 1 mg/d dose of entecavir for HBV-GN in lamivudine-resistant patients is less reported. Ikee et al. reported a case of a 57-year-old female patient with a 3-year history of hypertension and a renal biopsy diagnosis of HBVMN who developed HBeAg serological conversion and HBVDNA conversion within 4 months of oral entecavir, followed by proteinuria complete remission. Oral entecavir was continued for 1 year after viral conversion, but 3 months after stopping the drug HBV-DNA was again detected in the serum, and blood HBeAg and urine protein remained negative. Entecavir can still be used in patients with renal failure, but the drug dosage should be reduced according to GFR.
Adefovir
Adefovir inhibits viral replication by inhibiting HBVDNA polymerase and preventing DNA strand lengthening, and has an inhibitory effect on both wild-type HBV and lamivudine-resistant mutant HBV. No treatment of HBV-GN with adefovir has been reported. However, its use for HBV-GN is generally not advocated because it can cause renal tubulointerstitial lesions and proteinuria.
Tebivudine
Tebivudine inhibits HBV replication more vigorously than lamivudine, but there is cross-resistance between the two, with an incidence of genotypic resistance of 2.7%-4.4% after 1 year, at an adult dose of 600 mg/d. There are no reports of its use in HBV-GN. In renal failure the drug dosage should be reduced according to GFR, and it should be noted that this drug can cause neuromuscular lesions.
Other treatment.
General treatment: avoid fatigue, infection, give a low-salt, high-quality protein diet, control protein intake and give renal preservation therapy in severe renal insufficiency. Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor antagonists (ARB) may improve proteinuria and protect renal function, and are recommended to be added in the absence of hypotension.
It is important to emphasize that the improvement of nephropathy after HBV-GN antiviral therapy takes a long time, from 3-6 months for the fast ones to 1 year for the slow ones, so you must be prepared to adhere to the treatment for a long time, never stop or change the medication at will, and never listen to charlatans or small advertisements to take the so-called recipes.
Prognosis
Some scholars have followed up 52 cases of HBV-MN in children, and the complete remission rates were 64% and 92% at 1 and 7 years, respectively, and only one case had mild renal impairment, indicating that HBV-MN in children has a good prognosis and can mostly remit on its own.
The prognosis of HBV-MGN in children is good, and most of them can remit on their own, while HBV-GN in adults tends to have a prolonged course and a poor prognosis, and without effective treatment, 1/3 of patients can slowly progress to renal failure.
References.
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