Toxicology Unit, University of Salamanca, Salamanca, Spain.
Institute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain.
BMJ Open. 2020 Mar 8;10(3):e032918. doi: 10.1136/bmjopen-2019-032918.
Tobacco causes kidney damage that can progress to chronic kidney disease. However, the diagnostic parameters used in clinics are not effective in identifying smokers at risk. Our first objective is to more effectively detect subclinical renal damage in smokers. In addition, we hypothesise that tobacco consumption can predispose smokers to renal damage on exposure to other potentially nephrotoxic events (drugs, diagnostic procedures and so on). We will test this hypothesis in our second objective by investigating whether certain predisposition markers (GM2 ganglioside activator protein (GM2AP), transferrin and t-gelsolin) are able to detect smokers who are predisposed to kidney damage. Finally, in our third objective, we will study whether smoking cessation reduces subclinical and/or predisposition to renal damage.
For our first objective, a prospective cross-sectional study will be carried out with patients from a primary healthcare centre. The influence of tobacco on renal damage, in patients both with and without additional risk factors, will be studied using a panel of early biomarkers (albuminuria, N-acetyl-beta-D-glucosaminidase, kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin). For our second objective, a prospective longitudinal study will be carried out with patients recruited for our first objective. We will study whether certain predisposition biomarkers (GM2AP, transferrin and t-gelsolin) are able to detect smokers predisposed to renal damage. For our third objective, a prospective longitudinal study will be carried out with patients from a smoking cessation unit. We will study the evolution of the markers described above following smoking cessation.
The study has been approved by the Clinical Research Ethics Committee of the Healthcare Area of Salamanca. All study participants will sign an informed consent form in compliance with the Declaration of Helsinki and the WHO standards for observational studies. Results will be presented at conferences and submitted to peer-reviewed journals.
NCT03850756.
烟草会导致肾脏损伤，进而发展为慢性肾脏病。然而，临床中使用的诊断参数并不能有效地识别有风险的吸烟者。我们的首要目标是更有效地检测吸烟者的亚临床肾脏损伤。此外，我们假设烟草的摄入会使吸烟者在接触其他潜在的肾毒性物质（药物、诊断程序等）时更容易发生肾脏损伤。在第二个目标中，我们将通过研究某些易感性标志物（神经节苷脂激活蛋白（GM2AP）、转铁蛋白和 t-凝胶蛋白）是否能够检测到易受肾脏损伤影响的吸烟者，来验证这一假设。最后，在第三个目标中，我们将研究戒烟是否能降低亚临床和/或易感性肾脏损伤的风险。
为了实现我们的第一个目标，将对来自初级保健中心的患者进行前瞻性横断面研究。使用一组早期生物标志物（蛋白尿、N-乙酰-β-D-氨基葡萄糖苷酶、肾损伤分子-1 和中性粒细胞明胶酶相关脂质运载蛋白）研究烟草对伴有和不伴有其他危险因素的患者的肾脏损伤的影响。为了实现我们的第二个目标，将对第一个目标中招募的患者进行前瞻性纵向研究。我们将研究某些易感性标志物（GM2AP、转铁蛋白和 t-凝胶蛋白）是否能够检测到易受肾脏损伤影响的吸烟者。为了实现我们的第三个目标，将对戒烟单位的患者进行前瞻性纵向研究。我们将研究戒烟后上述标志物的变化情况。
该研究已获得萨拉曼卡医疗保健区临床研究伦理委员会的批准。所有研究参与者都将签署一份知情同意书，以符合赫尔辛基宣言和世界卫生组织的观察性研究标准。研究结果将在会议上公布，并提交给同行评议的期刊。
NCT03850756。
