Carollo Caterina, Benfante Alida, Sorce Alessandra, Montalbano Katia, Cirafici Emanuele, Calandra Leonardo, Geraci Giulio, Mulè Giuseppe, Scichilone Nicola
Unit of Nephrology and Dialysis, Hypertension Excellence Centre, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90133 Palermo, Italy.
Department of Health Promotion Sciences, Maternal and Infant Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90133 Palermo, Italy.
Life (Basel). 2025 Apr 29;15(5):720. doi: 10.3390/life15050720.
Acute kidney injury (AKI) has emerged as a significant complication in patients with coronavirus disease 2019 (COVID-19). The pathophysiology of COVID-19-associated AKI is multifactorial, involving both direct viral effects on renal cells and indirect mechanisms such as systemic inflammation and cytokine storms. This highlights the critical need for early detection and effective management strategies to mitigate kidney injury and improve patient outcomes. The aim of our study is to assess the potential predictive role of inflammatory biomarkers in determining the risk of developing COVID-19-associated AKI in patients with and without pre-existing CKD.
This study included 84 patients stratified by pre-existing chronic kidney disease (CKD) status. Demographic, clinical, and laboratory data were collected, including vital signs, hematological profiles, renal function markers, inflammatory biomarkers, coagulation parameters, and treatments. Outcomes such as acute kidney injury (AKI) and in-hospital mortality were documented.
In patients with pre-existing CKD, IL-6 and NLR demonstrated high predictive accuracy for AKI onset. In patients without pre-existing CKD, white blood cell (WBC) count emerged as a significant predictor of AKI onset.
The differential roles of IL-6, NLR, and WBC in predicting AKI onset highlight distinct physiopathological pathways influenced by COVID-19. In CKD+ patients, chronic inflammation and immune dysregulation are key drivers of AKI, with IL-6 and NLR serving as robust markers of this inflammatory state. In contrast, in CKD- patients, AKI may be more influenced by acute inflammatory responses and infectious factors, as reflected by WBC count.
急性肾损伤（AKI）已成为2019冠状病毒病（COVID-19）患者的一种重要并发症。COVID-19相关AKI的病理生理学是多因素的，涉及病毒对肾细胞的直接作用以及全身炎症和细胞因子风暴等间接机制。这凸显了早期检测和有效管理策略对于减轻肾损伤和改善患者预后的迫切需求。我们研究的目的是评估炎症生物标志物在确定有无慢性肾脏病（CKD）的患者发生COVID-19相关AKI风险中的潜在预测作用。
本研究纳入84例根据既往慢性肾脏病（CKD）状态分层的患者。收集人口统计学、临床和实验室数据，包括生命体征、血液学指标、肾功能标志物、炎症生物标志物、凝血参数和治疗情况。记录急性肾损伤（AKI）和住院死亡率等结局。
在既往有CKD的患者中，IL-6和中性粒细胞与淋巴细胞比值（NLR）对AKI发病具有较高的预测准确性。在既往无CKD的患者中，白细胞（WBC）计数是AKI发病的重要预测指标。
IL-6、NLR和WBC在预测AKI发病中的不同作用突出了受COVID-19影响的不同病理生理途径。在CKD+患者中，慢性炎症和免疫失调是AKI的关键驱动因素，IL-6和NLR是这种炎症状态的有力标志物。相比之下，在CKD-患者中，AKI可能更多地受急性炎症反应和感染因素的影响，白细胞计数反映了这一点。
