评估目前几种用于肾脏病治疗的免疫抑制治疗方案的乙型肝炎病毒(HBV)激活危险性，为合并HBV感染的肾炎患者制订更加合理的免疫抑制治疗方案提供依据。

回顾性分析2006年1月至2013年12月于广东医科大学附属医院肾活检确诊为肾小球肾炎的患者275例，分为HBsAg阳性组(102例)与HBsAg阴性组(173例)；HBsAg阳性组按不同的免疫抑制方案分为单用糖皮质激素(激素，Pred)组，激素＋环磷酰胺(Pred＋CTX)组，激素＋硫唑嘌呤和(或)雷公藤多甙(Pred＋AZA / TwHF)组，对比接受不同免疫抑制治疗方案患者的肝损伤发生率；HBsAg阳性组按是否抗病毒治疗分为抗病毒组及未抗病毒组，对比接受抗病毒治疗与未接受抗病毒治疗患者肝损伤的发生率。应用二元logistic回归分析肝炎活化的风险因素。

HBsAg阳性组与HBsAg阴性组免疫抑制治疗期间，肝损伤发生率分别为32.4%(33/102)及7.6%(13/172)，差异有统计学意义(χ²＝28.421，P<0.001)；HBsAg阳性组78.4%的肝损伤事件发生于接受免疫抑制治疗6个月内；Pred＋CTX组肝损伤的发生率66.7%(6/9)高于Pred组[37.8%(23/61)]以及Pred＋AZA/TwHF组[25.0%(8/32)]，但差异无统计学意义(χ²＝5.41，P＝0.067)；免疫抑制治疗方案为HBV活化的危险因素(OR＝7.501，P＝0.027)。抗病毒组治疗前谷氨酸转氨酶(ALT)水平较未抗病毒组高(t＝3.133, P＝0.03)，HBV-DNA载量>10⁵(copies/ml)患者的比例较未抗病毒组高，差异均有统计学意义(χ²＝15.174, P<0.001)；接受免疫抑制治疗后，抗病毒组与未抗病毒组肝损害的发生率分别为47.5%(19/40)及29.0 %(18/62)，差异无统计学意义(χ²＝3.369，P＝0.66)。

HBsAg阳性的肾病患者接受免疫抑制治疗时存在肝损伤高风险。在免疫抑制治疗期间，特别是前6个月，应加强对此类患者血清HBV-DNA载量及肝功能监测；CTX可能存在肝毒性及促进HBV活化的风险；预防性抗病毒治疗可明确抑制HBV-DNA复制，但似乎未能减少肝损伤事件发生率，需通过前瞻性研究证实该类患者预防性抗病毒治疗的价值。

To evaluate the risk of hepatitis B virus (HBV) activation in patients with glomerulonephritis (GN) receiving regular immunosuppressive therapy, and to provide data for more reasonable immunosuppressive therapeutic regimens in patients complicated with HBV infection.

Between January 2006 and December 2013, a total of 275 patients with GN were recruited, who were diagnosed by renal biopsy in the Affiliated Hospital to Guangdong Medical College, and divided into HBsAg positive group (102 cases) and HBsAg negative group (173 cases). HBsAg positive patients were further divided into Pred group, Pred+ CTX group, Pred+ AZA and/or TwHF group, whose incidences of liver injury were compared among them. HBsAg positive patients were also divided into antiviral group and non-antiviral group, whose incidences of liver injury were compared between them. The logistic regression statistical method was applied to analyze the risk factors for hepatitis activation.

The incidences of liver injury in HBsAg positive and negative groups were 32.4% (33/102) vs 7.6% (13/172), respectively, the difference of wghich was statistically significant (χ²=28.421, P<0.001). 78.4% of the liver injury in HBsAg positive patients occurred within 6 months after receiving immunosuppressive therapy. The incidence of liver injury in the Pred+ CTX group [66.7% (6/9)], was not significantly higher than those in the Pred group [37.8%(23/61)] and in the Pred+ AZA and/or TwHF group [25% (8/32)] (χ²=5.41, P=0.067). And it was found that the immunosuppression therapy regimen was a risk factor for HBV activation (OR=7.501, P=0.027). The baseline levels of ALT (t=3.133, P=0.03) and the percentage of patients with HBV-DNA copies over 10⁵/mL (χ²=15.174, P<0.001) were both higher in the antiviral group than in the non-antiviral group. After the immunosuppressive therapy treatment, the incidence of liver injury was not significantly higher in the antiviral group [47.5% (19/40)] than in the non-antiviral group [29% (18/62)] (P>0.05).

GN patients with positive HBsAg were at high risk for HBV activation during immunosuppressive therapy, especially in the first six months. So the serum HBV-DNA level and the liver function monitoring should be strengthened in these patients. CTX may expose HBsAg positive patients to the risks of HBV activation and hepatotoxicity.Prophylactic antiviral therapy can reduce HBV-DNA replication, but seems to fail in reducing the incidence of liver injury. More prospective studies are still needed to confirm the value of prophylactic antiviral therapy for GN patients with HBV infection.