BACKGROUND AIMS Treatment of hepatorenal syndrome-acute kidney injury (HRS-AKI), with terlipressin and albumin, provides survival benefit, but may be associated with cardiopulmonary complications. We analysed the predictors of terlipressin response and mortality using point-of-care echocardiography (POC-Echo), cardiac and renal biomarkers. APPROACH Between December 2021 and January 2023, patients with HRS-AKI were assessed with POC-Echo and lung ultrasound within 6h of admission, at the time of starting terlipressin(48h), and at 72h. Volume expansion was done with 20% albumin, followed by terlipressin infusion. Clinical data, POC-Echo data, and serum biomarkers were prospectively collected. Cirrhotic Cardiomyopathy(CCM) was defined per 2020 criteria. RESULTS One hundred and forty patients were enrolled [84% men, 59% alcohol-associated disease, mean MELDNa-25±standard deviation(SD) 5.6]. Median daily dose of infused terlipressin was 4.3(interquartile range:3.9-4.6)mg/day; mean duration-6.4± SD-1.9 days; complete response was in 62% and partial response in 11%. Overall mortality was 14% and 16% at 30 and 90 days, respectively. Cut-offs for prediction of terlipressin nonresponse were cardiac variables-[E/e'>12.5(indicating increased left filling pressures, C-statistic-0.774), e' velocity<7 cm/s (indicating impaired relaxation; C-statistic-0.791), >20.5% reduction in cardiac index at 72h(C-statistic-0.885); p<0.001] and pre-treatment biomarkers (Cystatin C>2.2 mg/l, C-statistic-0.640 and NT-ProBNP>350 pg/mL, C-statistic-0.655;p<0.050). About 6% of all HRS-AKI patients and 26% of patients with CCM had pulmonary edema. Presence of CCM(aHR1.9;CI-1.8-4.5,p=0.009) and terlipressin nonresponse (aHR 5.2;CI-2.2-12.2, p<0.001) were predictors of mortality independent of age, gender, obesity, DM-2, etiology and baseline creatinine. CONCLUSIONS Cirrhotic cardiomyopathy and reduction in cardiac index, reliably predict terlipressin non-response. CCM is independently associated with poor survival in HRS-AKI.

中文翻译：

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使用护理点超声心动图评估肝肾综合征-急性肾损伤中特利加压素相关患者的结局。

背景目的 用特利加压素和白蛋白治疗肝肾综合征-急性肾损伤（HRS-AKI）可提供生存益处，但可能与心肺并发症相关。我们使用护理点超声心动图 (POC-Echo)、心脏和肾脏生物标志物分析了特利加压素反应和死亡率的预测因素。方法 2021 年 12 月至 2023 年 1 月期间，HRS-AKI 患者在入院 6 小时内、开始使用特利加压素时（48 小时）和 72 小时接受 POC-Echo 和肺部超声评估。用20%白蛋白进行扩容，然后输注特利加压素。前瞻性收集临床数据、POC-Echo 数据和血清生物标志物。肝硬化心肌病 (CCM) 根据 2020 年标准定义。结果 纳入了 140 名患者[84% 为男性，59% 为酒精相关疾病，平均 MELDNa-25±标准差 (SD) 5.6]。输注特利加压素的中位每日剂量为4.3（四分位距：3.9-4.6）mg/天；平均持续时间-6.4±SD-1.9 天；完全缓解率为 62%，部分缓解率为 11%。30 天和 90 天的总体死亡率分别为 14% 和 16%。预测特利加压素无反应的截止点是心脏变量 - [E/e'>12.5（表明左充盈压增加，C 统计量 - 0.774），e' 速度 <7 cm/s（表明松弛受损；C 统计量 - 0.791), 72 小时心脏指数降低 >20.5% (C-statistic-0.885); p<0.001]和治疗前生物标志物（胱抑素 C>2.2 mg/l，C-统计量-0.640 和 NT-ProBNP>350 pg/mL，C-统计量-0.655；p<0.050）。大约 6% 的 HRS-AKI 患者和 26% 的 CCM 患者患有肺水肿。CCM 的存在（aHR1.9；CI-1.8-4.5，p=0.009）和特利加压素无反应（aHR 5.2；CI-2.2-12.2，p<0.001）是独立于年龄、性别、肥胖、DM-2 的死亡率预测因子、病因和基线肌酐。结论 肝硬化心肌病和心脏指数降低可以可靠地预测特利加压素无反应。CCM 与 HRS-AKI 患者的不良生存率独立相关。