Deng Ying-Hao, Liu Qian, Luo Xiao-Qin
Health Management Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Department of Pediatrics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
BMC Nephrol. 2025 Aug 11;26(1):449. doi: 10.1186/s12882-025-04392-w.
Pediatric Acute Kidney Injury (AKI) is an increasingly prevalent global health concern that extends far beyond a transient clinical event, posing a significant risk for long-term kidney dysfunction. This review consolidates current knowledge on the pathophysiological transition from pediatric AKI to Chronic Kidney Disease (CKD), critically evaluating the mechanisms of maladaptive repair, the utility of biomarkers, and the state of long-term surveillance strategies. The progression to CKD is driven by maladaptive repair, a process where the kidney's healing mechanisms become dysregulated following a severe or prolonged insult. This pathological cascade involves persistent inflammation, endothelial dysfunction, tubular epithelial cell cycle arrest, and the activation of myofibroblasts, culminating in irreversible interstitial fibrosis and nephron loss. The kidneys of preterm infants and neonates are particularly vulnerable; preterm infants may have incomplete nephrogenesis, leading to a reduced nephron endowment, while neonates exhibit functional immaturity. An AKI during these critical early periods can have a disproportionately large impact, amplifying the lifetime risk for hypertension and accelerated CKD. Evidence confirms that pediatric AKI survivors face a substantially increased risk of incident CKD, hypertension, and proteinuria, even when serum creatinine levels return to baseline. Current diagnostic tools, reliant on creatinine, are insensitive and lag behind the actual injury, hindering timely intervention. While novel biomarkers show promise for early AKI detection, their ability to predict the transition to CKD remains an area of active investigation. Major conclusions from this review highlight that pediatric AKI must be reframed as a sentinel event that necessitates a long-term approach to kidney health. However, care is often fragmented, a challenge compounded by a lack of pediatric-specific, evidence-based follow-up guidelines. Future progress depends on dedicated research into the unique aspects of maladaptive repair in developing kidneys, the validation of predictive biomarkers, and the development of targeted, age-appropriate therapies.
小儿急性肾损伤（AKI）是一个日益普遍的全球健康问题，其影响远不止于短暂的临床事件，还对长期肾功能障碍构成重大风险。本综述整合了当前关于小儿AKI向慢性肾脏病（CKD）病理生理转变的知识，批判性地评估了适应性修复不良的机制、生物标志物的效用以及长期监测策略的现状。向CKD的进展是由适应性修复不良驱动的，这一过程中，肾脏在遭受严重或长期损伤后，其愈合机制会失调。这种病理级联反应包括持续炎症、内皮功能障碍、肾小管上皮细胞周期停滞以及肌成纤维细胞的激活，最终导致不可逆的间质纤维化和肾单位丢失。早产儿和新生儿的肾脏尤其脆弱；早产儿可能存在肾发生不全，导致肾单位数量减少，而新生儿则表现出功能不成熟。在这些关键的早期阶段发生的AKI可能产生不成比例的重大影响，增加终生患高血压和加速性CKD的风险。有证据证实，小儿AKI幸存者即使血清肌酐水平恢复到基线，发生CKD、高血压和蛋白尿的风险也会大幅增加。目前依赖肌酐的诊断工具不敏感，且滞后于实际损伤，阻碍了及时干预。虽然新型生物标志物在早期AKI检测方面显示出前景，但其预测向CKD转变的能力仍是一个活跃的研究领域。本综述的主要结论强调，小儿AKI必须被重新定义为一个哨兵事件，需要对肾脏健康采取长期方法。然而，护理往往是零散的，由于缺乏针对儿科的、基于证据的随访指南，这一挑战更加复杂。未来的进展取决于对发育中肾脏适应性修复不良的独特方面进行专门研究、验证预测性生物标志物以及开发有针对性的、适合年龄的治疗方法。
