脓毒败血症中血肌酐生成减少

指导意见：减少肠内毒物的生成和吸收：短期禁食蛋白质，灌肠或导泻，口服新霉... 细菌进入血循环成为败血症或脓毒败血症。

临床上常应用血清肌酐水平来检验测定和评估急性肾脏毁伤(cute kidney injury,aki)和慢性肾脏疾病(hronic kidney disease,ckd),但众所周知的是,血清肌酐在早期的发现及准确评估急性肾脏毁伤方面是受到限定的。在aki中,因为患者不成能保持恒定状况,所以血肌酐水平不克不及准确的反应肾小球率过滤。此外血肌酐还受到肾小管分泌肌酐的影响和很多非肾脏因素的影响,例如:由肌肉及肝脏产生,由胃肠道排除等。在重症患者中,脓毒败血症仍然是个棘手的问题,特别是那些归并有aki的患者其灭亡率大大增长。所以早期发现及准确评价aki对于有脓毒败血症的患者十分重要。本文中作者发现,路程经过过程结扎住及刺破盲肠诱导小鼠发生脓败毒血症同时兴两侧肾脏切掉,血中测得升高的标记物主要来自非肾器官毁伤所释放,如:天冬氨酸转氨酶(ast)、丙氨酸转氨酶(alt)、乳酸脱氢酶(ldh)和肿瘤坏死因子α(tnf-α)。然而上面所说的小鼠血肌酐水平却显著低于仅有脓毒血症而未切掉双肾和切掉双肾未传染脓毒血症的小鼠。在上面所说的实验的基础上,加用氯喹来减少非肾器官组织毁伤在血中所产生的标记物,反而增长了血肌酐水平。在体重,血细胞比容和细胞外液容积恒定的前提下,传染脓毒败血症并行双肾切掉的小鼠肌酐的生成显著减低。本文的发现具有重大的临床意义,血肌酐生成减少的成果就是引起血肌酐水平在脓毒败血症归并肾脏毁伤中的作用极其微弱,恰是因为其生成减少从而让咱们远远地低估了肾脏现实毁伤的紧张程度。虽然血肌酐在临床研究中被广泛的施用,但要是仅只施用血肌酐水平来评估肾脏毁伤,对于脓毒败血症和脓毒败血症归并aki的患者的治疗效果也将有可能不克不及被确证。临床研究脓毒败血症需要其他更多的终点指标,例如毁伤害生命物标记物,灭亡率和患病率等。咱们可以从本文中看出,脓毒败血症减少了肌酐的产生,使传染脓毒败血症后肌酐水平不克不及反映患者真实肾脏毁伤的情况,极大地限定了早期发现及诊断急性肾脏毁伤。这就可以部分地解释血肌酐水平反应的滞后性和早期在临床上的聊胜于无的作用。此文研究给了咱们很大的启迪,咱们需要找到新的有生命的物质学标记物来更好证实肾脏早期的损害,特别是在脓毒败血症中的肾脏毁伤的早期发现、诊断及治疗,改善患者的预后。j am soc nephrol 20:1217? 1221,2009.doi:10.1681/asn.2008060617reduced production of creatinine limits its use as 马克er of kidney injury in sepsisabstract:abstract although diagnosis and staging of acute kidney injury uses serum creatinine,acute changes in creatinine lag behellond both renal injury and recovery.the risk for mortality increases when acute kidney injury accompanies sepsis;therefore,we sought to explore the limitations of serum creatinine in thellos setting.in mice,induction of sepsis by cecal ligation and puncture in bilaterally nephrectomized mice increased markers of nonrenal organ injury and serum tnf-α.serum creatinine,however,was significantly lower in septic animals than in animals subjected to bilateral nephrectomy and sham cecal ligation and puncture.under these conditions treatment with chloroquine decreased nonrenal organ injury markers but paradoxically increased serum creatinine.sepsis dramatically decreased production of creatinine in nephrectomized mice,without changes in body weight,hematocrit,or extracellular fluid volume.in conclusion,sepsis reduces production of creatinine,whelloch blunts the increase in serum creatinine after sepsis,potentially limiting the early detection of acute kidney injury.thellos may partially explain why small absolute increases in serum creatinine levels are associated with poor clinical outcomes.these data support the need for new biomarkers that provide better measures of renal injury,especially in patients with sepsis.