College of Pharmacy, Sunchon National University, Republic of Korea.
National Institute of Transplantation Foundation, Los Angeles, CA, United States.
Transpl Immunol. 2019 Aug;55:101206. doi: 10.1016/j.trim.2019.04.001. Epub 2019 Apr 19.
Hematological abnormalities after transplantation are complications that may arise after renal transplantation, of which thrombocytopenia is associated with increased risk of bleeding and other complications. The development of thrombocytopenia is affected by various clinical conditions, and the stromal-derived factor 1 (SDF1) and platelet factor 4 (PF4) genes are known to be involved in the production or destruction of platelets. The purpose of this study was to investigate the prevalence of posttransplant thrombocytopenia and its association with other clinical conditions and genetic polymorphisms of SDF1 and PF4 genes a long time after transplantation.
This is a retrospective study that includes a total of 305 kidney transplant (KT) recipients between 2008 and 2012 at St. Vincent Medical Center, Los Angeles, CA. In this study, posttransplant thrombocytopenia was defined as a 30% reduction in platelet count from the baseline in the first week or a decrease of <100 (×10/μL) within 1 year after KT. The subjects were divided into posttransplant thrombocytopenia and control groups. The chi-square test, t-test, and logistic regression were used for the analyses.
In the first week, 65 patients had a 30% reduction in platelet count (21.3%). Gender, simultaneous kidney-pancreas transplantation, induction therapy (IT), and only alleles of rs2297630 of SDF1, among the SDF1 and PF4 genes, showed statistically significant differences. The rs2297630 alleles were consistently significant risk factors (non G vs. G: odds ratio = 0.445; 95% confidence interval, 0.224-0.884; p = .021) in the multiple logistic regression. In the 1-year study, 61 patients (20.0%) had platelet counts of <100 × 10/μL and had statistically significant differences in patients who had delayed graft function and induction therapy.
In this study, non-G group of rs2297630 in SDF1 significantly increased the risk of post-transplant thrombocytopenia in the first week of kidney transplantation.
移植后血液学异常是肾移植后可能出现的并发症，其中血小板减少与出血等并发症的风险增加有关。血小板减少的发生受多种临床情况的影响，基质衍生因子 1（SDF1）和血小板因子 4（PF4）基因已知参与血小板的产生或破坏。本研究旨在探讨移植后血小板减少的发生率及其与其他临床情况以及 SDF1 和 PF4 基因多态性的关系。
这是一项回顾性研究，共纳入 2008 年至 2012 年在加利福尼亚州洛杉矶圣文森特医疗中心接受肾移植（KT）的 305 例患者。本研究中，移植后血小板减少定义为血小板计数在第 1 周内从基线水平下降 30%或在 KT 后 1 年内下降 <100（×10/μL）。将受试者分为移植后血小板减少组和对照组。采用卡方检验、t 检验和逻辑回归进行分析。
在第 1 周，有 65 例患者血小板计数下降 30%（21.3%）。SDF1 和 PF4 基因中，性别、同时进行肾胰联合移植、诱导治疗（IT）以及仅 SDF1 的 rs2297630 等位基因存在统计学差异。rs2297630 等位基因在多因素逻辑回归分析中始终是显著的危险因素（非 G 对 G：比值比=0.445；95%置信区间，0.224-0.884；p=0.021）。在 1 年的研究中，有 61 例（20.0%）患者血小板计数<100×10/μL，在发生延迟移植物功能和诱导治疗的患者中存在统计学差异。
在本研究中，SDF1 的 rs2297630 非 G 组在肾移植后第 1 周显著增加了移植后血小板减少的风险。
