Urine interleukin-6 is an early biomarker of acute kidney injury in children undergoing cardiac surgery.
Urine interleukin-6 is an early biomarker of acute kidney injury in children undergoing cardiac surgery.
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DOI：
10.1186/cc9289
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Faubel S
中科院分区：
文献类型：
--
作者：
Dennen P;Altmann C;Kaufman J;Klein CL;Andres-Hernando A;Ahuja NH;Edelstein CL;Cadnapaphornchai MA;Keniston A;Faubel S
白细胞介素-6（IL-6）是一种促炎细胞因子，在急性肾损伤（阿基）患者的血清中早期增加。本研究的目的是确定尿液IL-6是否是阿基的早期生物标志物并确定尿液IL-6的来源。许多蛋白质，包括细胞因子，被肾小球过滤，然后被近端小管内吞和代谢。由于近端小管损伤是阿基的标志，我们假设由于过滤的IL-6的近端小管代谢受损，尿IL-6将在阿基中增加。在接受心脏搭桥手术（CPB）的25例连续儿科患者中采集尿液。阿基定义为24小时血清肌酐升高50%（步枪（风险、损伤、失败、损失、终末期），R）。还研究了阿基和新鲜分离的近端小管的小鼠模型。AKI患者与无阿基患者相比，6小时尿IL-6升高（X2 = 8.1750; P < 0.0042）。尿IL-6 > 75 pg/mg鉴别阿基的敏感性为88%。为了评估增加的尿IL-6是否发生在功能性肾衰竭与结构性肾衰竭中，研究了呋塞米注射后肾前性氮质血症（无肾小管损伤）、缺血性阿基（肾小管损伤）和顺铂阿基（肾小管损伤）的小鼠模型。尿IL-6在肾前性氮质血症中没有显著增加，但在缺血性和顺铂阿基中增加。为了确定阿基中的尿液中是否出现循环IL-6，静脉内注射重组人（h）IL-6并收集尿液1小时;在缺血性阿基中尿液hIL-6增加，但在肾前性氮质血症中不增加。为了确定阿基对循环IL-6的影响，在静脉内注射后1小时测定血清hIL-6，并且在缺血性阿基中升高，但在肾前性氮质血症中不升高。为了直接检查IL-6代谢，将hIL-6加入到正常和缺氧分离的近端小管的培养基中;在正常与受损的缺氧近端小管的培养基中，hIL-6减少。阿基患者早期尿IL-6升高。动物研究表明，IL-6的近端小管代谢的失败导致血清和尿IL-6增加。导致血清IL-6升高的IL-6代谢受损可能导致与阿基相关的有害全身效应和死亡率升高。
Interleukin-6 (IL-6) is a proinflammatory cytokine that increases early in the serum of patients with acute kidney injury (AKI). The aim of this study was to determine whether urine IL-6 is an early biomarker of AKI and determine the source of urine IL-6. Numerous proteins, including cytokines, are filtered by the glomerulus and then endocytosed and metabolized by the proximal tubule. Since proximal tubule injury is a hallmark of AKI, we hypothesized that urine IL-6 would increase in AKI due to impaired proximal tubule metabolism of filtered IL-6. Urine was collected in 25 consecutive pediatric patients undergoing cardiac bypass surgery (CPB). AKI was defined as a 50% increase in serum creatinine at 24 hours (RIFLE (Risk, Injury, Failure, Loss, End stage), R). Mouse models of AKI and freshly isolated proximal tubules were also studied. Urine IL-6 increased at six hours in patients with AKI versus no AKI (X2 = 8.1750; P < 0.0042). Urine IL-6 > 75 pg/mg identified AKI with a sensitivity of 88%. To assess whether increased urine IL-6 occurs in functional versus structural renal failure, mouse models of pre-renal azotemia after furosemide injection (no tubular injury), ischemic AKI (tubular injury) and cisplatin AKI (tubular injury) were studied. Urine IL-6 did not significantly increase in pre-renal azotemia but did increase in ischemic and cisplatin AKI. To determine if circulating IL-6 appears in the urine in AKI, recombinant human (h)IL-6 was injected intravenously and urine collected for one hour; urine hIL-6 increased in ischemic AKI, but not pre-renal azotemia. To determine the effect of AKI on circulating IL-6, serum hIL-6 was determined one hour post-intravenous injection and was increased in ischemic AKI, but not pre-renal azotemia. To directly examine IL-6 metabolism, hIL-6 was added to the media of normal and hypoxic isolated proximal tubules; hIL-6 was reduced in the media of normal versus injured hypoxic proximal tubules. Urine IL-6 increases early in patients with AKI. Animal studies demonstrate that failure of proximal tubule metabolism of IL-6 results in increased serum and urine IL-6. Impaired IL-6 metabolism leading to increased serum IL-6 may contribute to the deleterious systemic effects and increased mortality associated with AKI.
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影响因子：
13.2
作者：
Kwon, O;Molitoris, BA;Kelly, KJ
通讯作者：
Kelly, KJ
影响因子：
13.6
作者：
Kielar, ML;John, R;Lu, CY
通讯作者：
Lu, CY
DOI：
10.1111/j.1432-1033.1988.tb14384.x
发表时间：
1988-11-01
期刊：
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子：
--
作者：
CASTELL, JV;GEIGER, T;HEINRICH, PC
通讯作者：
HEINRICH, PC
影响因子：
8.8
作者：
Parsons, PE;Eisner, MD;Wheeler, AP
通讯作者：
Wheeler, AP
影响因子：
3.1
作者：
Oberholzer, A;Souza, SM;Moldawer, LL
通讯作者：
Moldawer, LL