Department of Pediatric Gastroenterology, Nephrology and Metabolic Diseases, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Institute of Medical Biometry and Informatics, University of Heidelberg, Heidelberg, Germany.
PLoS One. 2020 Oct 27;15(10):e0240446. doi: 10.1371/journal.pone.0240446. eCollection 2020.
The uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (pCS) accumulate in patients with chronic kidney disease (CKD) as a consequence of altered gut microbiota metabolism and a decline in renal excretion. Despite of solid experimental evidence for nephrotoxic effects, the impact of uremic toxins on the progression of CKD has not been investigated in representative patient cohorts. In this analysis, IS and pCS serum concentrations were measured in 604 pediatric participants (mean eGFR of 27 ± 11 ml/min/1.73m2) at enrolment into the prospective Cardiovascular Comorbidity in Children with CKD study. Associations with progression of CKD were analyzed by Kaplan-Meier analyses and Cox proportional hazard models. During a median follow up time of 2.2 years (IQR 4.3-0.8 years), the composite renal survival endpoint, defined as 50% loss of eGFR, or eGFR <10ml/min/1.73m2 or start of renal replacement therapy, was reached by 360 patients (60%). Median survival time was shorter in patients with IS and pCS levels in the highest versus lowest quartile for both IS (1.5 years, 95%CI [1.1,2.0] versus 6.0 years, 95%CI [5.0,8.4]) and pCS (1.8 years, 95%CI [1.5,2.8] versus 4.4 years, 95%CI [3.4,6.0]). Multivariable Cox regression disclosed a significant association of IS, but not pCS, with renal survival, which was independent of other risk factors including baseline eGFR, proteinuria and blood pressure. In this exploratory analysis we provide the first data showing a significant association of IS, but not pCS serum concentrations with the progression of CKD in children, independent of other known risk factors. In the absence of comorbidities, which interfere with serum levels of uremic toxins, such as diabetes, obesity and metabolic syndrome, these results highlight the important role of uremic toxins and accentuate the unmet need of effective elimination strategies to lower the uremic toxin burden and abate progression of CKD.
尿毒症毒素硫酸吲哚酚(IS)和对甲酚硫酸盐(pCS)在慢性肾脏病(CKD)患者中由于肠道微生物群代谢改变和肾脏排泄减少而积累。尽管有确凿的实验证据表明其具有肾毒性作用,但尿毒症毒素对 CKD 进展的影响尚未在代表性患者队列中进行研究。在这项分析中,在前瞻性心血管合并症在儿童 CKD 研究中,对 604 名儿科参与者(平均 eGFR 为 27 ± 11 ml/min/1.73m2)入组时测量了血清中 IS 和 pCS 的浓度。通过 Kaplan-Meier 分析和 Cox 比例风险模型分析了与 CKD 进展的关联。在中位随访时间为 2.2 年(IQR 4.3-0.8 年)期间,360 名患者(60%)达到了复合肾脏生存终点,定义为 eGFR 下降 50%,或 eGFR <10ml/min/1.73m2 或开始肾脏替代治疗。对于 IS 和 pCS,IS 水平最高与最低四分位组的中位生存时间较短(1.5 年,95%CI [1.1,2.0]与 6.0 年,95%CI [5.0,8.4])和 pCS(1.8 年,95%CI [1.5,2.8]与 4.4 年,95%CI [3.4,6.0])。多变量 Cox 回归显示 IS 与肾脏生存显著相关,但 pCS 无此关联,这与其他危险因素独立相关,包括基线 eGFR、蛋白尿和血压。在这项探索性分析中,我们提供了第一个数据,表明 IS 但不是 pCS 血清浓度与儿童 CKD 进展显著相关,独立于其他已知危险因素。在没有合并症的情况下,尿毒症毒素的血清水平会受到干扰,如糖尿病、肥胖和代谢综合征,这些结果突出了尿毒症毒素的重要作用,并强调了需要有效的清除策略来降低尿毒症毒素负担并减缓 CKD 进展。