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        膿毒癥性急性腎損傷患者T淋巴細(xì)胞內(nèi)三磷酸腺苷水平變化及其與腎功能轉(zhuǎn)歸的關(guān)系

        2016-05-16 01:45:16朱潮涌毛明鋒黃甘霖鮑曉紅
        中國(guó)全科醫(yī)學(xué) 2016年8期
        關(guān)鍵詞:急性腎損傷膿毒癥淋巴細(xì)胞

        朱潮涌,李 潔,毛明鋒,黃甘霖,鮑曉紅,金 烈

        323000浙江省麗水市中心醫(yī)院腎內(nèi)科

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        ·論著·

        朱潮涌,李 潔,毛明鋒,黃甘霖,鮑曉紅,金 烈

        323000浙江省麗水市中心醫(yī)院腎內(nèi)科

        【摘要】目的探討T淋巴細(xì)胞內(nèi)三磷酸腺苷T cell-iATP)水平預(yù)測(cè)膿毒癥并發(fā)急性腎損傷(AKI)患者預(yù)后的價(jià)值。方法前瞻性選擇2013年7月—2014年12月于麗水市中心醫(yī)院ICU、感染科及腎內(nèi)科住院的膿毒癥并發(fā)AKI患者69例為研究對(duì)象,分別于入組0、48、96 h檢測(cè)患者T cell-iATP水平。根據(jù)腎功能臨床轉(zhuǎn)歸情況將患者分為腎功能完全恢復(fù)組(18例)、腎功能部分恢復(fù)組(38例)、依賴透析組(4例)和死亡組(9例)。結(jié)果各組eGFR、功能衰竭臟器數(shù)量、AKI分期及0、48 hT cell-iATP水平比較,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。多分類Logistic回歸分析結(jié)果顯示,相對(duì)于預(yù)后不良(依賴透析或死亡),eGFR、功能衰竭臟器數(shù)量和48 hT cell-iATP水平為腎功能完全恢復(fù)、腎功能部分恢復(fù)的影響因素(P<0.05)。ROC曲線分析顯示,48 hT cell-iATP水平預(yù)測(cè)膿毒癥并發(fā)AKI患者預(yù)后的ROC曲線下面積為0.926(P<0.01),取48 hT cell-iATP臨界點(diǎn)為344.2 μg/L時(shí),靈敏度為92.3%,特異度為87.5%。結(jié)論T cell-iATP水平低的膿毒癥患者腎功能恢復(fù)良好,膿毒癥患者早期T cell-iATP水平是腎功能轉(zhuǎn)歸的預(yù)測(cè)指標(biāo)。

        【關(guān)鍵詞】膿毒癥;急性腎損傷;T 淋巴細(xì)胞; 臨床轉(zhuǎn)歸

        1對(duì)象與方法

        1.1研究對(duì)象前瞻性選擇2013年7月—2014年12月于麗水市中心醫(yī)院ICU、感染科及腎內(nèi)科住院的膿毒癥并發(fā)AKI患者69例為研究對(duì)象,均符合2001年美國(guó)胸科醫(yī)師學(xué)會(huì)(ACCP)和重癥醫(yī)學(xué)會(huì)(SCCM)膿毒癥的診斷標(biāo)準(zhǔn)[4];根據(jù)急性腎損傷網(wǎng)絡(luò)(AKIN)工作小組標(biāo)準(zhǔn)[5],1期25例,2期20例,3期24例。排除標(biāo)準(zhǔn):(1)年齡<18歲;(2)有慢性腎臟病史;(3)合并免疫缺陷性疾病、惡性腫瘤。

        1.2方法

        1.2.1臨床資料測(cè)量患者身高、體質(zhì)量,計(jì)算體質(zhì)指數(shù)(BMI)。檢測(cè)血清肌酐(Scr)水平,根據(jù)腎臟病飲食修正公式(MDRD)估算腎小球?yàn)V過(guò)率(eGFR),eGFR=186-1.154×Scr×年齡-0.203(女性則×0.742),記錄高血壓史、糖尿病史、細(xì)菌培養(yǎng)、功能衰竭臟器數(shù)及腎功能轉(zhuǎn)歸等臨床資料。

        1.2.3治療患者在治療原發(fā)病基礎(chǔ)上予抗感染、液體復(fù)蘇、控制血糖、營(yíng)養(yǎng)支持等綜合對(duì)癥治療,出現(xiàn)呼吸衰竭者予機(jī)械通氣治療,出現(xiàn)難治性高血鉀癥、Scr>3 mg/dl和/或尿素氮>100 mg/dl、尿量減少導(dǎo)致的液體超負(fù)荷中的1項(xiàng)及以上者予血液凈化治療。

        1.2.4腎功能臨床轉(zhuǎn)歸的判定患者入組后28 d進(jìn)行腎功能轉(zhuǎn)歸的判斷,eGFR正常判定為腎功能完全恢復(fù),eGFR持久下降但不需腎臟替代治療判定為腎功能部分恢復(fù),eGFR持久下降且需長(zhǎng)期腎臟替代治療判定為需依賴透析。根據(jù)腎功能臨床轉(zhuǎn)歸情況將患者分為腎功能完全恢復(fù)組(18例)、腎功能部分恢復(fù)組(38例)、依賴透析組(4例)和死亡組(9例)。

        2結(jié)果

        表2膿毒癥并發(fā)AKI患者預(yù)后影響因素的多分類Logistic回歸分析

        Table2MultivariableLogisticregressionanalysisoffactorsinfluencingtheprognosisofSIAKIpatients

        注:選擇預(yù)后不良(依賴透析或死亡)作為參照

        3討論

        作者貢獻(xiàn):朱潮涌進(jìn)行課題設(shè)計(jì)與實(shí)施、資料收集整理、撰寫論文、成文并對(duì)文章負(fù)責(zé);李潔、毛明鋒、黃甘霖、鮑曉紅進(jìn)行課題實(shí)施、評(píng)估、資料收集;金烈進(jìn)行質(zhì)量控制及審校。

        本文無(wú)利益沖突。

        參考文獻(xiàn)

        [1]Kribben A,Herget-Rosenthal S,Pietruck F,et al.Acute renal failure-an review[J].Dtsch Med Wochenschr,2003,128(22):1231-1236.

        [2]Bagshaw SM,Uchino S,Bellomo R,et al.Septic acute kidney injury in critically ill patients:clinical characteristics and outcomes[J].Clin J Am Soc Nephrol,2007,2(3):431-439.

        [3]Bagshaw SM,Lapinsky S,Dial S,et al.Acute kidney injury in septic shock:clinical outcomes and impact of duration of hypotension prior to initiation of antimicrobial therapy[J].Intensive Care Med,2009,35(5):871-881.

        [4]Levy MM,F(xiàn)ink MP,Marshall JC,et al.2001 SCCM/ESICM/ACCP/ATS/SIS international sepsis definitions conference[J].Intensive Care Med,2003,29(4):530-538.

        [5]Mehta RL,Kellum JA,Shah SV ,et al.Acute kidney injury network:report of an initiative to improve outcomes in acute kidney injury[J].Crit Care,2007,11(2):R31.

        [6]Dabrowski W,Kotlinska-Hasiec E,Schneditz D,et al.Continuous veno-venous hemofiltration to adjust fluid volume excess in septic shock patients reduces intra-abdominal pressure[J].Clin Nephrol,2014,82(1):41-50.

        [7]Zarbock A,Gomez H,Kellum JA.Sepsis-induced acute kidney injury revisited:pathophysiology,prevention and future therapies[J].Curr Opin Crit Care,2014,20(6):588-599.

        [8]Suh SH,Kim CS,Choi JS,et al.Acute kidney injury in paients with sepsis and septic shock:risk factors and clinical outcomes[J].Yonsei Med J,2013,54(4):965-972.

        [9]Hotchkiss RS,Nicholson DW.Apoptosis and caspases regulate death and inflammation in sepsis[J].Nat Rev Immunol,2006,6(11):813-822.

        [11]Schenk U,F(xiàn)rascoli M,Proietti M,et al.ATP inhibits the generation and function of regulatory T cells through the activation of purinergic P2X receptors[J].Sci Signal,2011,4(162):ra12.

        [12]Hotchkiss RS,Karl IE.The pathophysiology and treatment of sepsis[J].N Engl J Med,2003,348(2):138-150.

        [13]Devarajan P.Update on mechanisms of ischemic acute kidney injury[J].J Am Soc Nephrol,2006,17(6):1503-1520.

        [14]Martina MN,Noel S,Bandapalle S,et al.T lymphocytes and acute kidney injury:update[J].Nephron Clin Pract,2014,127(1-4):51-55.

        [15]Dai X,Zeng Z,F(xiàn)u C,et al.Diagnostic value of neutrophil gelatinase-associated lipocalin,cystatin C,and soluble triggering receptorexoressed on myeloid cells-1 in critically ill patients with sepsis-associated acute kindney injury[J].Crit Care,2015,19:223.

        [16]Huo W,Zhang K,Nie Z,et al.Kidney injury molecule-1 (KIM-1):a novel kidney-specific injury molecule playing potential double-edged functions in kidney injury[J].Transplant Rev (Orlando),2010,24(3):143-146.

        [17]Lahoud Y,Hussein O,Shalabi A,et al. Effects of phosphodiesterase-5 inhibitor on ischemic kidney injury during nephron sparing surgery: quantitative assessment by NGAL and KIM-1[J].World J Urol,2015,33(12):2053-2062.

        [18]Torregrosa I,Montoliu C,Urios A,et al. Urinary KIM-1, NGAL and L-FABP for the diagnosis of AKI in patients with acute coronary syndrome or heart failure undergoing coronary angiography[J].Heart Vessels,2015,30(6):703-711.

        [19]Wang XZ,Jin ZK,Tian XH,et al.Increased intracellular adenosine triphosphate level as an index to predict acute rejection in kidney transplant recipients[J].Transpl Immunol,2014,30(1):18-23.

        (本文編輯:吳立波)

        ZHUChao-yong,LIJie,MAOMing-feng,etal.

        DepartmentofNephrology,LishuiCentralHospital,Lishui323000,China

        【Abstract】ObjectiveTo investigate the value ofT cell-iATP level in the prediction of the prognosis of sepsis patients complicated with acute kidney injury (AKI).MethodsFrom July 2013 to December 2014,a total of 69 sepsis inpatients complicated with AKI in the ICU,the Department of Infectious Disease and Nephrology in Lishui Center Hosipital were enrolled in this prospective study.The levels ofT cell-iATP at 0 h,48 h and 96 h after onset of SIAKI were detected.According to the prognosis of acute kidney injury (AKI),the subjects were divided into four groups:complete renal recovery group(18 cases),partial renal recovery group(38 cases),dialysis dependency group(4 cases) and death group (9 cases).ResultsThe four groups were significantly different in estimated glomerular filtation rate(eGFR),the number of visceral organs with function failure,and numbers of patient in each stage of AKI and the levelsT cell-iATP at 0 and 48 h (P<0.05).Multivariable Logistic regression analysis indicated that eGFR,the number of visceral organ with function failure and the levels ofT cell-iATP(48 h)were influencing factors for the complete recovery and partial recovery of renal function (P<0.05),compared with unfavorable prognosis (dialysis dependency or death).ROC curve analysis showed that the AUC ofT cell-iATP(48 h) predicting the prognosis of sepsis patients complicated with AKI was 0.926(P<0.01),with a sensitivity and a specificity as 92.3% and 87.5% respectively at a critical point of 344.2 μg/L forT cell-iATP(48 h) level.ConclusionSepsis patients with lowerT cell-iATP level have better recovery of renal function,andT cell-iATP level of patients with early-stage sepsis may serve as a predictor for the renal function outcome.

        【Key words】Sepsis;Acute kidney injury;T lymphocyte;Clinical outcomes

        通信作者:金烈,323000浙江省麗水市中心醫(yī)院腎內(nèi)科;E-mail:carrol_506@hotmail.com

        【中圖分類號(hào)】R 631R 692.5

        【文獻(xiàn)標(biāo)識(shí)碼】A

        doi:10.3969/j.issn.1007-9572.2016.08.006

        (收稿日期:2015-04-22;修回日期:2016-01-12)

        ·膿毒癥性急性腎損傷專題研究·

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