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首页> 美国卫生研究院文献>American Journal of Physiology - Renal Physiology >Comparison of serum creatinine and serum cystatin C as biomarkers to detect sepsis-induced acute kidney injury and to predict mortality in CD-1 mice
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Comparison of serum creatinine and serum cystatin C as biomarkers to detect sepsis-induced acute kidney injury and to predict mortality in CD-1 mice

机译：比较血清肌酐和半胱氨酸蛋白酶抑制剂C作为生物标记物检测败血症诱导的急性肾损伤并预测CD-1小鼠死亡率的生物标志物

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Acute kidney injury (AKI) dramatically increases sepsis mortality, but AKI diagnosis is delayed when based on serum creatinine (SCr) changes, due in part, to decreased creatinine production. During experimental sepsis, we compared serum cystatin C (sCysC), SCr, and blood urea nitrogen (BUN) to inulin glomerular filtration rate (iGFR) before or 3–18 h after cecal ligation and puncture (CLP)-induced sepsis in CD-1 mice. sCysC had a faster increase and reached peak levels more rapidly than SCr in both sepsis and bilateral nephrectomy (BiNx) models. sCysC was a better surrogate of iGFR than SCr during sepsis. Combining sCysC with SCr values into a composite biomarker improved correlation with iGFR better than any biomarker alone or any other combination. We determined the renal contribution to sCysC handling with BiNx. sCysC and SCr were lower post-BiNx/CLP than post-BiNx alone, despite increased inflammatory and nonrenal organ damage biomarkers. Sepsis decreased CysC production in nephrectomized mice without changing body weight or CysC space. Sepsis decreased sCysC production and increased nonrenal clearance, similar to effects of sepsis on SCr. sCysC, SCr, and BUN were measured 6 h postsepsis to link AKI with mortality. Mice with above-median sCysC, BUN, or SCr values 6 h postsepsis died earlier than mice with below-median values, corresponding to a substantial AKI association with sepsis mortality in this model. sCysC performs similarly to SCr in classifying mice at risk for early mortality. We conclude that sCysC detects AKI early and better reflects iGFR in CLP-induced sepsis. This study shows that renal biomarkers need to be evaluated in specific contexts.
机译：急性肾损伤（AKI）极大地增加了败血症的死亡率，但是当基于血清肌酐（SCr）的变化而导致AKI的诊断被延迟时，部分原因是肌酐的产生减少。在实验性脓毒症期间，我们比较了盲肠结扎和穿刺（CLP）诱导的CD-脓毒症发作前或之后3–18 h，血清半胱氨酸蛋白酶抑制剂C（sCysC），SCr和血尿素氮（BUN）与菊粉肾小球滤过率（iGFR） 1只小鼠。在脓毒症和双侧肾切除术（BiNx）模型中，sCysC的增加速度都比SCr更快，并且达到峰值的速度更快。在脓毒症期间，sCysC比iCr更好地替代了iGFR。将sCysC和SCr值组合到复合生物标志物中比单独使用任何生物标志物或任何其他组合更好地改善了与iGFR的相关性。我们确定了肾脏对BiNx处理sCysC的贡献。尽管炎症和非肾脏器官损伤的生物标志物增加，但sCysC和SCr在BiNx / CLP后比单独的BiNx低。脓毒症降低了肾切除小鼠的CysC产量，而没有改变体重或CysC空间。脓毒症降低了sCysC的产生并增加了非肾清除率，类似于脓毒症对SCr的影响。 sCysC，SCr和BUN在癫痫发作后6小时测量，以将AKI与死亡率联系起来。 sCysC，BUN或SCr值高于中值的小鼠在癫痫发作后6 h死亡的时间早于中值低于sCysC，BUN或SCr的小鼠，这与该模型中脓毒症死亡率与AKI的相关性相当。在对有早期死亡风险的小鼠进行分类时，sCysC的表现与SCr相似。我们得出的结论是，sCysC可以及早发现AKI，并在CLP引起的败血症中更好地反映iGFR。这项研究表明，需要在特定情况下评估肾脏生物标志物。

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