Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine , Nanjing , China.
Ren Fail. 2014 Apr;36(3):367-71. doi: 10.3109/0886022X.2013.868359. Epub 2013 Dec 17.
Acute kidney injury induced by aristolochic acid (AA) might occur in patients with chronic glomerular nephritis (CGN). In this study, the clinical and pathological features of patients with acute aristolochic acid nephropathy (AAN) superimposing CGN (AAN-CGN) were investigated.
Eighteen patients diagnosed as acute AAN were included in this retrospective study, from January 2001 to December 2009. According to the pre-existing CGN, 13 patients were identified as the AAN-CGN group, and 5 isolated AAN patients as the control group. Clinical and pathological features were compared between the two groups.
In the AAN-CGN group, six patients complained with gastrointestinal symptoms, such as nausea, vomiting, or loss of appetite. The rest of seven cases were asymptomatic or minimally uncomfortable, who were found with elevated serum creatinine (Scr) in the follow up of CGN. Compared with the control group, the patients in AAN-CGN group had higher levels of serum uric acid, urine n-acetyl-β-d-glucosaminidase, and urine protein excretion (366.2 ± 122.8 vs. 218.0 ± 125.8 μmol/L, p = 0.037; 9.74 ± 4.4 vs. 1.38 ± 1.01 g/d, p = 0.001; 61.2 ± 21.9 vs. 27.4 ± 15.8 μ/g ċ cr, p = 0.007, respectively). In addition to, the AAN-CGN patients had an absolutely prominent percentage of macromolecule substance in the urine protein electrophoresis (25.0 ± 6.32 vs. 15.8 ± 7.8%, p = 0.029). The occurrence of hypokalemia and excretion of aminoaciduria were lower than that in the control group. Pathologically, 84.6% of patients were found with tubular brush border dropping, 30.8% with naked tubular basement membrane, and 15.4% with different stages of vascular lesion. There were no statistical differences in the above-mentioned pathological parameters between the two groups. In the follow-up, 10 patients with AAN-CGN recovered with normal Scr, accounting for 76.9%, which was better than the recovery in the control group.
Patients with acute AAN-CGN manifested with a great mass of urine protein excretion, low incidence of hypokalemia and aminoaciduria, however, the tubular-interstitial lesions were similar to the isolated AAN.
马兜铃酸（AA）引起的急性肾损伤可能发生在慢性肾小球肾炎（CGN）患者中。在这项研究中，我们研究了急性马兜铃酸肾病（AAN）合并 CGN（AAN-CGN）患者的临床和病理特征。
本回顾性研究纳入了 18 名被诊断为急性 AAN 的患者，时间为 2001 年 1 月至 2009 年 12 月。根据预先存在的 CGN，13 名患者被确定为 AAN-CGN 组，5 名孤立性 AAN 患者为对照组。比较两组患者的临床和病理特征。
在 AAN-CGN 组中，有 6 名患者有胃肠道症状，如恶心、呕吐或食欲不振。其余 7 例无症状或症状轻微，在 CGN 的随访中发现血清肌酐（Scr）升高。与对照组相比，AAN-CGN 组患者的血尿酸、尿 N-乙酰-β-D-氨基葡萄糖苷酶和尿蛋白排泄量更高（366.2 ± 122.8 与 218.0 ± 125.8 μmol/L，p=0.037；9.74 ± 4.4 与 1.38 ± 1.01 g/d，p=0.001；61.2 ± 21.9 与 27.4 ± 15.8 μ/g·cr，p=0.007）。此外，AAN-CGN 患者尿蛋白电泳中大分子物质的百分比绝对显著（25.0 ± 6.32 与 15.8 ± 7.8%，p=0.029）。低钾血症和氨基酸尿的发生率低于对照组。病理上，84.6%的患者有肾小管刷状缘脱落，30.8%的患者有裸露的肾小管基底膜，15.4%的患者有不同阶段的血管病变。两组间上述病理参数无统计学差异。随访中，10 例 AAN-CGN 患者的 Scr 恢复正常，占 76.9%，优于对照组。
急性 AAN-CGN 患者表现为大量蛋白尿排泄，低钾血症和氨基酸尿发生率低，但肾小管间质病变与孤立性 AAN 相似。
