Aims In healthy volunteers, the kidney deploys compensatory post-diuretic sodium reabsorption (CPDSR) following loop diuretic-induced natriuresis, minimizing sodium excretion and producing a neutral sodium balance. CPDSR is extrapolated to non-euvolemic populations as a diuretic resistance mechanism; however, its importance in acute decompensated heart failure (ADHF) is unknown. Methods and results Patients with ADHF in the Mechanisms of Diuretic Resistance cohort receiving intravenous loop diuretics (462 administrations in 285 patients) underwent supervised urine collections entailing an immediate pre-diuretic spot urine sample, then 6-h (diuretic-induced natriuresis period) and 18-h (post-diuretic period) urine collections. The average spot urine sodium concentration immediately prior to diuretic administration [median 15 h (13–17) after last diuretic] was 64 ± 33 mmol/L with only 4% of patients having low (<20 mmol/L) urine sodium consistent with CPDSR. Paradoxically, greater 6-h diuretic-induced natriuresis was associated with larger 18-h post-diuretic spontaneous natriuresis (r = 0.7, P < 0.001). Higher pre-diuretic urine sodium to creatinine ratio (r = 0.37, P < 0.001) was the strongest predictor of post-diuretic spontaneous natriuresis. In a subgroup of patients (n = 43) randomized to protocol-driven intensified diuretic therapies, the mean diuretic-induced natriuresis increased three-fold. In contrast to the substantial decrease in spontaneous natriuresis predicted by CPDSR, no change in post-diuretic spontaneous natriuresis was observed (P = 0.47). Conclusion On a population level, CPDSR was not an important driver of diuretic resistance in hypervolemic ADHF. Contrary to CPDSR, a greater diuretic-induced natriuresis predicted a larger post-diuretic spontaneous natriuresis. Basal sodium avidity, rather than diuretic-induced CPDSR, appears to be the predominant determinate of both diuretic-induced and post-diuretic natriuresis in hypervolemic ADHF.

中文翻译：

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代偿性利尿剂后肾钠重吸收不是急性心力衰竭利尿剂抵抗的主要机制

目标 在健康志愿者中，肾脏在袢利尿剂诱导的利尿钠排泄后进行代偿性利尿剂后钠重吸收 (CPDSR)，最大限度地减少钠排泄并产生中性钠平衡。CPDSR 作为利尿剂抵抗机制外推至非血容量正常的人群；然而，它在急性失代偿性心力衰竭 (ADHF) 中的重要性尚不清楚。方法和结果 利尿剂抵抗机制中的 ADHF 患者接受静脉袢利尿剂（285 名患者 462 次给药）接受监督尿液收集，需要立即采集利尿剂前的尿液样本，然后 6 小时（利尿剂诱导的排尿期）和18 小时（利尿期后）尿液收集。利尿剂给药前的平均现场尿钠浓度[最后一次利尿剂后中位 15 小时 (13-17)] 为 64 ± 33 mmol/L，只有 4% 的患者尿钠偏低 (<20 mmol/L)与 CPDSR。矛盾的是，利尿剂诱导的 6 小时尿钠排泄增多与利尿剂后 18 小时的自发尿钠排泄增多有关（r = 0.7，P < 0.001）。利尿剂前尿钠与肌酐比值较高（r = 0.37，P < 0.001）是利尿剂后自发性尿钠排泄的最强预测因素。在随机接受方案驱动的强化利尿剂治疗的患者亚组 (n = 43) 中，利尿剂诱导的利尿钠排泄的平均数增加了三倍。与 CPDSR 预测的自发性尿钠排泄显着减少相反，未观察到利尿剂后自发性尿钠排泄的变化（P = 0.47）。结论 在人群水平上，CPDSR 不是高血容量性 ADHF 中利尿剂抵抗的重要驱动因素。与 CPDSR 相反，更大的利尿剂诱导的尿钠排泄预示着更大的利尿剂后自发尿钠排泄。基础钠亲和力，而不是利尿剂诱导的 CPDSR，似乎是高血容量性 ADHF 中利尿剂诱导和利尿剂后钠尿的主要决定因素。