Impact of protease inhibitors on the evolution of urinary markers Subanalyses from an observational cross-sectional study
Impact of protease inhibitors on the evolution of urinary markers Subanalyses from an observational cross-sectional study
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DOI：
10.1097/md.0000000000004507
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发表时间：
2016-08-01
期刊：
影响因子：
1.6
通讯作者：
Negredo, E.
中科院分区：
文献类型：
--
作者：
Bonjoch, Anna;Puig, Jordi;Negredo, E.
肾损伤（定义为存在白蛋白尿、蛋白尿、糖尿[无高血糖症]、血尿和/或肾性低磷酸盐血症）是人类免疫缺陷病毒（HIV）感染患者的一个新问题，尽管关于蛋白酶抑制剂（PI）在这种情况下的作用的数据很少。为了确定接受PI的HIV感染患者队列中肾损伤的时间，我们报告了一项已发表的横断面研究的亚组分析结果。亚组分析仅纳入接受含PI方案治疗超过6个月的患者（共970例患者中的377例）。我们确定了相关因素，并构建了受试者工作特征曲线，以估计肾损伤的时间，这取决于所使用的PI。肾损伤患者的百分比为27.7%，地瑞那韦，洛匹那韦和阿扎那韦分别为27.9%和30%。至肾损伤的时间如下：阿扎那韦/利托那韦为229天（曲线下面积[AUC]，0.639;灵敏度，0.89;特异性，0.41）;阿扎那韦/利托那韦+替诺福韦332天（AUC，0.603;灵敏度，0.75;特异性，0.29）;非加强阿扎那韦为318天（AUC，0.581;灵敏度，0.89;特异性，0.29）;洛匹那韦/利托那韦为478天（AUC，0.566;灵敏度，0.864;特异性，0.44）;洛匹那韦/利托那韦+替诺福韦为1339天（AUC，0.667;灵敏度，0.86;特异性，0.77）;达芦那韦/利托那韦为283天（AUC，0.523;灵敏度，0.80;特异性，0.261）;地瑞那韦/利托那韦加替诺福韦为286天（AUC，0.446;灵敏度，0.789;特异性，0.245）。使用洛匹那韦/利托那韦而不使用替诺福韦是一个保护因素（比值比= 1.772; 95%CI，1.070-2.93; P = 0.026）。洛匹那韦/利托那韦组至肾损伤的时间最长。这些结果表明，需要肾脏监测，包括尿液样本，在接受PI为基础的方案，即使当替诺福韦不伴随使用的患者。
Kidney injury (defined as the presence of albuminuria, proteinuria, glycosuria [without hyperglycemia], hematuria, and/or renal hypophosphatemia) is an emerging problem in human immunodeficiency virus (HIV)-infected patients, although few data are available on the role of protease inhibitors (PIs) in this condition.To determine the time to kidney injury in a cohort of HIV-infected patients receiving a PI-containing regimen.We report the results of a subanalysis of a published cross-sectional study. The subanalysis included only patients receiving PI-containing regimens for more than 6 months (377 of the overall 970 patients). We determined associated factors and constructed receiver operating characteristic curves to estimate time to kidney injury depending on the PI used.The percentage of patients with kidney injury was 27.7% for darunavir, 27.9% for lopinavir, and 30% for atazanavir. Time to kidney injury was as follows: 229 days for atazanavir/ritonavir (area under the curve [AUC], 0.639; sensitivity, 0.89; specificity, 0.41); 332 days for atazanavir/ritonavir plus tenofovir (AUC, 0.603; sensitivity, 0.75; and specificity, 0.29); 318 days for nonboosted atazanavir (AUC, 0.581; sensitivity, 0.89; and specificity, 0.29); 478 days for lopinavir/ritonavir (AUC, 0.566; sensitivity, 0.864; and specificity, 0.44); 1339 days for lopinavir/ritonavir plus tenofovir (AUC, 0.667; sensitivity, 0.86; and specificity, 0.77); 283 days for darunavir/ritonavir (AUC, 0.523; sensitivity, 0.80; and specificity, 0.261); and 286 days for darunavir/ritonavir plus tenofovir (AUC, 0.446; sensitivity, 0.789; and specificity, 0.245). The use of lopinavir/ritonavir without tenofovir was a protective factor (odds ratio = 1.772; 95% CI, 1.070-2.93; P = 0.026).For all PIs, the percentage of patients with kidney injury exceeded 27%, irrespective of tenofovir use. The longest time to kidney injury was recorded with lopinavir/ritonavir. These results demonstrate the need for renal monitoring, including urine samples, in patients receiving a PI-based regimen, even when tenofovir is not used concomitantly.