Acute kidney injury induced by aristolochic acid in patients with primary glomerular nephritis

Abstract

Background: 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. Methods: 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. Results: 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. Conclusion: 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.