Reply: Chronic kidney disease after liver transplantation: Accurate measurement, early acute kidney injury, and renal-protective strategies.

Pranjal Kashiv, Khushboo Saxena, Manish Ramesh Balwani, Vivek B Kute
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Abstract

In this article, we comment on the article by Sessa et al published in the recent issue of the World Journal of Transplantation, who revisit the three-decade single centre cohort of Muñoz-Serrano et al and conclude that chronic kidney disease (CKD) after liver transplantation (LT) is a modifiable determinant of long-term survival rather than an unavoidable consequence of calcineurin inhibitor exposure. We share their central position and welcome the weight they give to perioperative acute kidney injury (AKI), to calcineurin inhibitor minimisation through basiliximab induction and mycophenolate, and to the disciplined control of hypertension and metabolic disease. Our intention is to carry the argument one step further, because three problems lie beneath the literature they assemble and constrain what any inventory of risk factors can deliver. The first is metrological. Almost every reported association, including the signal attached to female sex, and the reported incidence itself, which varies according to the definition of CKD applied, the time point of ascertainment and whether creatinine-based or measured filtration is used, derive from creatinine-based estimates of glomerular filtration, a measure the same authors concede performs poorly in patients who are sarcopenic, oedematous and metabolically deranged. The second concerns timing, since the most powerful and most modifiable determinant of chronic injury is the passage from early AKI to fixed nephropathy, a transition that draws surveillance away from isolated tacrolimus trough concentrations, which did not predict one year disease in the index cohort, towards intrapatient variability and time within the therapeutic range. The third is therapeutic, because the prevailing synthesis omits the sodium glucose cotransporter 2 inhibitors, agents with established renal benefit in non-transplant CKD populations that deserve formal evaluation after LT. Measured accurately, protected early and evaluated pharmacologically, the kidney of the liver transplant recipient is more defensible than current practice assumes.

回复:肝移植后慢性肾病:准确测量,早期急性肾损伤,肾脏保护策略。
在这篇文章中,我们对Sessa等人发表在最近一期《世界移植杂志》上的文章进行了评论,他们重新审视了Muñoz-Serrano等人30年的单中心队列,并得出结论,肝移植(LT)后慢性肾脏疾病(CKD)是长期生存的可改变决定因素,而不是钙调磷酸酶抑制剂暴露的不可避免的后果。我们分享他们的中心地位,并欢迎他们给予围手术期急性肾损伤(AKI)的重视,通过basiliximab诱导和霉酚酸盐最小化钙调磷酸酶抑制剂,以及高血压和代谢性疾病的严格控制。我们的目的是进一步推进这一论点,因为在他们收集的文献之下存在三个问题,并限制了任何风险因素清单所能提供的内容。首先是计量学。几乎所有报道的关联,包括与女性相关的信号,以及报道的发病率本身,根据所应用的CKD的定义、确定的时间点以及是否使用基于肌酐的或测量的滤过,都来自基于肌酐的肾小球滤过的估计,同一作者承认,这种测量方法在肌肉减少、水肿和代谢紊乱的患者中表现不太好。第二个问题是时间,因为慢性损伤最强大和最可改变的决定因素是从早期AKI到固定肾病的过渡,这一转变将监测从孤立的他克莫司谷浓度转移到患者体内的变异性和治疗范围内的时间,他克莫司谷浓度在指数队列中不能预测一年的疾病。第三种是治疗性的,因为目前流行的合成方法忽略了葡萄糖共转运蛋白2钠抑制剂,这种药物在非移植性CKD人群中具有确定的肾脏益处,值得在lt后进行正式评估。准确测量、早期保护和药理学评估表明,肝移植受体的肾脏比目前的实践假设更具有防御性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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