Alkaff Firas F, Kremer Daan, Niekolaas Tessa M, van den Born Jacob, Rimbach Gerald, Tseng Tzu-Ling, Berger Stefan P, Bakker Stephan J L, de Borst Martin H
Division of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.
Division of Pharmacology and Therapy, Department of Anatomy, Histology, and Pharmacology, Faculty of Medicine Universitas Airlangga, Jl. Mayjen Prof Dr. Moestopo No 47, Surabaya, East Java, 60131, Indonesia.
Sci Rep. 2024 Jan 27;14(1):2283. doi: 10.1038/s41598-024-52635-x.
We investigated whether urinary vascular non-inflammatory molecule-1 (vanin-1), a promising early-onset tubular injury marker, correlates with other established tubular injury markers and is associated with graft failure in kidney transplant recipients (KTR). We measured 24 h urinary vanin-1 excretion in 656 KTR (age 53 ± 13 years, 43% female, estimated glomerular filtration rate (eGFR) 53 ± 21 mL/min/1.73 m) who had undergone kidney transplantation ≥ 1 year. The median 24 h urinary vanin-1 excretion was 145 [51-331] pmol/24 h. 24 h urinary vanin-1 excretion correlated weakly but significantly with other tubular injury markers (ρ = 0.14, p < 0.001 with urinary liver-type fatty acid binding protein, ρ = 0.13, p = 0.001 with urinary post-translationally modified fetuin-A protein, and ρ = 0.10, p = 0.011 with plasma neutrophil gelatinase-associated lipocalin) and with eGFR (ρ = - 0.13, p = 0.001). During a median follow-up of 7.4 [4.9-8.0] years, 94 (14%) KTR developed death-censored graft failure. In multivariable Cox regression analyses, 24 h urinary vanin-1 excretion was not associated with an increased risk of death-censored graft failure (adjusted hazard ratio [95% confidence interval] = 0.96 [0.86-1.07], p = 0.5). In conclusion, our findings do not support the role of urinary vanin-1 as a biomarker of graft failure after kidney transplantation.
我们研究了尿血管非炎症分子-1（血管生成素-1），一种很有前景的早期肾小管损伤标志物，是否与其他已确立的肾小管损伤标志物相关，以及是否与肾移植受者（KTR）的移植失败有关。我们测量了656例肾移植≥1年的KTR（年龄53±13岁，43%为女性，估计肾小球滤过率（eGFR）53±21 mL/min/1.73 m²）的24小时尿血管生成素-1排泄量。24小时尿血管生成素-1排泄量的中位数为145[51-331]pmol/24小时。24小时尿血管生成素-1排泄量与其他肾小管损伤标志物呈弱但显著的相关性（与尿肝型脂肪酸结合蛋白的相关系数ρ=0.14，p<0.001；与尿翻译后修饰胎球蛋白-A蛋白的相关系数ρ=0.13，p=0.001；与血浆中性粒细胞明胶酶相关脂质运载蛋白的相关系数ρ=0.10，p=0.011），并与eGFR相关（ρ=-0.13，p=0.001）。在中位随访7.4[4.9-8.0]年期间，94例（14%）KTR发生了去除死亡因素后的移植失败。在多变量Cox回归分析中，24小时尿血管生成素-1排泄量与去除死亡因素后的移植失败风险增加无关（调整后的风险比[95%置信区间]=0.96[0.86-1.07]，p=0.5）。总之，我们的研究结果不支持尿血管生成素-1作为肾移植后移植失败生物标志物的作用。
