Angiogenesis inhibition with bevacizumab, a monoclonal antibody against vascular endothelial growth factor A (VEGF-A), is an anticancer treatment associated with hypertension and renal glomerular toxicity referred to as a preeclampsia-like syndrome. In preeclampsia, podocyturia predates proteinuria and clinical features of preeclampsia, and is regarded as a biomarker of ongoing glomerular injury. Using a quantitative polymerase chain reaction of the podocyte-specific molecules nephrin, podocin, and VEGF-A in the urine, we examined whether podocyturia is present in bevacizumab-treated cancer patients, and whether it relates to proteinuria and the cumulative dose of bevacizumab. Urine samples were cross-sectionally collected from 43 bevacizumab-treated patients, 21 chemotherapy-treated patients, and 7 healthy controls. Urinary protein-to-creatinine ratio (mean and range) was 32.0 mg/mmol (5.2–284.4) in the bevacizumab group, compared with 11.4 mg/mmol (1.1–21.0) in the chemotherapy group and 7.4 mg/mmol (3.9–16.5) (P < .05) in healthy controls, whereas urinary albumin-to-creatinine ratio values in the three groups were, respectively, 18.9 mg/mmol (0.1–227.7), 1.5 mg/mmol (0.2–3.5), and 0.2 mg/mmol (0.1–0.4) (P < .05). The cumulative dose of bevacizumab ranged from 550 to 93,628 mg. Urinary podocin mRNA expression was undetectable in 59% of participants, urinary nephrin mRNA expression per mmol creatinine ranged from 0.0 to 5.3 and urinary VEGF-A mRNA expression from 0.0 to 2.7. Urinary nephrin mRNA expression did not correlate to the albumin-to-creatinine ratio or the cumulative dose of bevacizumab, whereas the latter correlated with the albumin-to-creatinine ratio (r = 0.77; P < .001). Our results demonstrate that the cumulative dose of bevacizumab is closely correlated with albuminuria but not with podocyturia as measured with the quantitative polymerase chain reaction technique, challenging the feasibility of this measurement to monitor ongoing glomerular injury in patients chronically treated with bevacizumab.

贝伐单抗是一种针对血管内皮生长因子A（VEGF-A）的单克隆抗体，可抑制血管生成，是一种与高血压和肾小球毒性相关的抗癌治疗，称为先兆子痫样综合征。在先兆子痫中，足癣早于蛋白尿和先兆子痫的临床特征，并且被认为是正在进行的肾小球损伤的生物标志物。使用尿液中足细胞特异性分子nephrin，podocin和VEGF-A的定量聚合酶链反应，我们检查了在贝伐单抗治疗的癌症患者中是否存在足癣，以及是否与蛋白尿和贝伐单抗的累积剂量有关。从43名贝伐单抗治疗的患者，21名化疗治疗的患者和7名健康对照中横断面收集尿液样品。P  <.05）在健康对照组中，而三组中尿白蛋白与肌酐的比值分别为18.9 mg / mmol（0.1-227.7），1.5 mg / mmol（0.2-3.5）和0.2 mg /毫摩尔（0.1–0.4）（P  <.05）。贝伐单抗的累积剂量为550至93,628 mg。在59％的参与者中未检测到尿podocin mRNA表达，每mmol肌酐的尿nephrin mRNA表达范围为0.0至5.3，而尿VEGF-A mRNA表达范围为0.0至2.7。尿肾素mRNA表达与白蛋白/肌酐比值或贝伐单抗的累积剂量无关，而后者与白蛋白/肌酐比值相关（r = 0.77; P <.001）。我们的结果表明，用定量聚合酶链反应技术测定，贝伐单抗的累积剂量与白蛋白尿密切相关，而与足底尿不相关，这挑战了用该方法来监测用贝伐单抗长期治疗的患者正在进行的肾小球损伤的可行性。