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轻度肝功能障碍的生化证据可识别出伴有可逆性肾功能障碍的失代偿性心力衰竭患者。

Biochemical evidence of mild hepatic dysfunction identifies decompensated heart failure patients with reversible renal dysfunction.

机构信息

Cardiovascular Division, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina.

出版信息

J Card Fail. 2013 Nov;19(11):739-45. doi: 10.1016/j.cardfail.2013.10.005. Epub 2013 Oct 17.

DOI:10.1016/j.cardfail.2013.10.005
PMID:24263117
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3884639/
Abstract

BACKGROUND

Differentiation of HF-induced renal dysfunction (RD) from irreversible intrinsic kidney disease is challenging, likely related to the multifactorial pathophysiology underlying HF-induced RD. In contrast, HF-induced liver dysfunction results in characteristic laboratory abnormalities. Given that similar pathophysiologic factors are thought to underlie both conditions, and that the liver and kidneys share a common circulatory environment, patients with laboratory evidence of HF-induced liver dysfunction may also have a high incidence of potentially reversible HF-induced RD.

METHODS AND RESULTS

Hospitalized patients with a discharge diagnosis of HF were reviewed (n = 823). Improvement in renal function (IRF) was defined as a 20% improvement in estimated glomerular filtration rate (eGFR). An elevated international normalized ratio (INR; odds ratio [OR] 2.8; P < .001), bilirubin (BIL; OR 2.2; P < .001), aspartate aminotransferase (AST; OR 1.8; P = .004), and alanine aminotransferase (ALT; OR 2.1; P = .001) were all significantly associated with IRF. Among patients with baseline RD (eGFR ≤45 mL min(-1) 1.73 m(-2)), associations between liver dysfunction and IRF were particularly strong (INR: OR 5.7 [P < .001]; BIL: OR 5.1 [P < .001]; AST: OR 2.9 [P = .005]; ALT: OR 4.8 [P < .001]).

CONCLUSIONS

Biochemical evidence of mild liver dysfunction is associated with reversible RD in decompensated HF patients. In the absence of methodology to directly identify HF-induced RD, signs of HF-induced dysfunction of other organs may serve as an accessible method by which HF-induced RD is recognized.

摘要

背景

HF 引起的肾功能障碍(RD)与不可逆的固有肾脏疾病的区分具有挑战性,这可能与 HF 引起的 RD 背后的多因素病理生理学有关。相比之下,HF 引起的肝功能障碍会导致特征性的实验室异常。鉴于认为相似的病理生理因素可能是这两种情况的基础,并且肝脏和肾脏具有共同的循环环境,因此具有 HF 引起的肝功能障碍实验室证据的患者也可能具有较高的潜在可逆转 HF 引起的 RD 发生率。

方法和结果

回顾性分析了因 HF 出院诊断的住院患者(n=823)。肾功能改善(IRF)定义为估计肾小球滤过率(eGFR)提高 20%。国际标准化比值(INR;优势比[OR]2.8;P<.001)、胆红素(BIL;OR 2.2;P<.001)、天门冬氨酸氨基转移酶(AST;OR 1.8;P=.004)和丙氨酸氨基转移酶(ALT;OR 2.1;P=.001)升高均与 IRF 显著相关。在基线 RD 患者(eGFR≤45 mL min(-1) 1.73 m(-2))中,肝功能障碍与 IRF 之间的关联尤其强烈(INR:OR 5.7[P<.001];BIL:OR 5.1[P<.001];AST:OR 2.9[P=.005];ALT:OR 4.8[P<.001])。

结论

失代偿性 HF 患者轻度肝功能障碍的生化证据与可逆性 RD 相关。在没有直接识别 HF 引起的 RD 的方法的情况下,其他器官的 HF 引起的功能障碍的迹象可能是识别 HF 引起的 RD 的一种可行方法。

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本文引用的文献

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Eur J Heart Fail. 2013 Jun;15(6):599-601. doi: 10.1093/eurjhf/hft060. Epub 2013 Apr 19.
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Lack of significant renal tubular injury despite acute kidney injury in acute decompensated heart failure.尽管急性失代偿性心力衰竭患者发生急性肾损伤,但无明显肾小管损伤。
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Worsening renal function defined as an absolute increase in serum creatinine is a biased metric for the study of cardio-renal interactions.将血清肌酐的绝对升高定义为肾功能恶化,这是一种用于研究心肾相互作用的有偏差的指标。
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