Structural, physiological or clinical outcomes to define urine output threshold in acute kidney injury,Critical Care

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Structural, physiological or clinical outcomes to define urine output threshold in acute kidney injury
Critical Care ( IF 8.8 ) Pub Date : 2024-12-18 , DOI: 10.1186/s13054-024-05195-5
Guido Dias Machado, Leticia Libório Santos, Alexandre Braga Libório

To the editor:

We read with interest the comments by Zhu and Li [1] regarding our article on evaluating various urine output (UO) thresholds and timeframes for defining acute kidney injury (AKI) [2]. The authors rightly emphasize that the core principle of AKI diagnosis is to reflect impaired excretion of metabolic waste. However, the concept of AKI must evolve in parallel with advancements in our understanding and the development of interventions to alter its natural progression and clinical impact.

From a physiological perspective, the traditional definition of oliguria (< 400 mL/24 h) is based on the assumption that a healthy adult excretes 600–800 mOsm of metabolic waste daily. At maximal urine concentration (1200 mOsm/L), at least 400 mL of urine is required for adequate waste excretion [3]. However, critically ill patients likely produce less metabolic waste and rarely achieve maximal urine concentration, making this physiological definition impractical in such contexts.

In our study, we also compared proposed UO thresholds to KDIGO standards for predicting progression to AKI stages 2/3, as measured by serum creatinine—a marker of metabolic waste. Our proposed criteria not only predicted hospital mortality but also outperformed KDIGO standards in predicting serum creatinine increases, a secondary outcome [2].

An accurate AKI definition is also essential to enable early interventions that can modify its course. Currently, these interventions are mostly preventive and include avoiding nephrotoxins, controlling hyperglycemia, monitoring serum creatinine and UO closely, and optimizing fluid balance and hemodynamics [4]. However, no studies have identified specific UO thresholds for initiating such measures. Future research should evaluate whether interventions targeting sensitive renal biomarkers—detectable before significant impairment in waste excretion—can effectively reduce AKI-related morbidity and mortality. If proven effective, we agree these biomarkers should be incorporated into AKI definitions.

As Zhu and Li pointed out [1], AKI stage 1—especially when based solely on UO—often does not correlate with increased mortality. Furthermore, there is limited evidence supporting the 0.5 mL/kg/h UO threshold as a definitive AKI marker for outcomes such as mortality, prolonged hospitalization, need for renal replacement therapy, or long-term morbidity. Additionally, no studies have demonstrated the efficacy of preventive or therapeutic interventions at this early stage.

Until higher UO thresholds are validated to guide AKI therapy or identify conditions associated with morbidity and mortality, overdiagnosing AKI poses risks of unnecessary costs and potential harm. This underscores the need for further research to define the optimal timing for AKI diagnosis, aiming to balance the benefits of early intervention with the financial, psychological, and clinical implications of the diagnosis.

Regarding timeframes, we computed a 3-h moving average for each hour, based on the mean UO within the preceding 3 h. Similarly, we calculated 6-, 12, and 24 h means using sliding windows.

No datasets were generated or analysed during the current study.

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Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Anders HJ. Acute kidney injury. Nat Rev Dis Primers. 2021;7(1):52. https://doi.org/10.1038/s41572-021-00284-z.
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A.B.L. was supported by Fundação Edson Queiroz and Conselho Nacional de Desenvolvimento Científico e Tecnológico (Grant No. 306377/2022-5).

Authors and Affiliations

Medical Sciences Postgraduate Program, Universidade de Fortaleza- UNIFOR, Fortaleza, Ceará, Brazil
Guido Dias Machado & Alexandre Braga Libório
Medical Program, Universidade de Fortaleza- UNIFOR, Fortaleza, Ceará, Brazil
Leticia Libório Santos

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A.B.L. wrote the letter. All authors have reviewed and approved the letter.

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Correspondence to Alexandre Braga Libório.

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Machado, G.D., Santos, L.L. & Libório, A.B. Structural, physiological or clinical outcomes to define urine output threshold in acute kidney injury. Crit Care 28, 410 (2024). https://doi.org/10.1186/s13054-024-05195-5

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Received: 25 November 2024
Accepted: 27 November 2024
Published: 18 December 2024
DOI: https://doi.org/10.1186/s13054-024-05195-5

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中文翻译：

定义急性肾损伤尿量阈值的结构、生理或临床结果

致编辑：

从生理学的角度来看，少尿的传统定义（< 400 mL/24 h）是基于健康的成年人每天排泄 600-800 mOsm 代谢废物的假设。在最大尿浓度（1200 mOsm/L）时，至少需要 400 mL 尿液才能充分排泄废物 [3]。然而，危重患者产生的代谢废物可能较少，并且很少达到最大尿浓度，因此在这种情况下，这个生理学定义是不切实际的。

在我们的研究中，我们还将提议的 UO 阈值与预测进展为 AKI 2/3 期的 KDIGO 标准进行了比较，通过血清肌酐（代谢废物的标志物）来衡量。我们提出的标准不仅预测了医院死亡率，而且在预测血清肌酐升高方面也优于 KDIGO 标准，这是次要结果 [2]。

准确的 AKI 定义对于实现可以改变其病程的早期干预也至关重要。目前，这些干预措施大多是预防性的，包括避免肾毒素、控制高血糖、密切监测血清肌酐和 UO，以及优化体液平衡和血流动力学 [4]。然而，没有研究确定启动此类措施的具体 UO 阈值。未来的研究应评估针对敏感肾脏生物标志物的干预措施（可在废物排泄显着损害之前检测到）是否可以有效降低 AKI 相关的发病率和死亡率。如果证明有效，我们同意这些生物标志物应纳入 AKI 定义。

正如 Zhu 和 Li 指出的那样 [1]，AKI 1 期（尤其是仅基于 UO 时）通常与死亡率增加无关。此外，有限的证据支持 0.5 mL/kg/h UO 阈值作为死亡率、住院时间延长、肾脏替代治疗需求或长期发病率等结局的确定性 AKI 标志物。此外，尚无研究证明预防或治疗干预在这个早期阶段的有效性。

在验证更高的 UO 阈值以指导 AKI 治疗或识别与发病率和死亡率相关的疾病之前，过度诊断 AKI 会带来不必要的成本和潜在危害的风险。这强调了进一步研究以确定 AKI 诊断的最佳时机的必要性，旨在平衡早期干预的益处与诊断的财务、心理和临床影响。

关于时间框架，我们根据前 3 小时内的平均 UO 计算了每小时的 3 小时移动平均线。同样，我们计算了 6 、 12 和 24 小时的平均值，即使用滑动窗。

在当前研究期间没有生成或分析数据集。

朱 L，林 J.AKI 的新定义：将重点从死亡转移到其他领域。暴击护理。2024;28(1):379.https://doi.org/10.1186/s13054-024-05170-0。

文章： PubMed PubMed Central Google Scholar
文章： PubMed PubMed Central Google Scholar
Sands JM，Layton HE。尿液浓度的生理学：更新。塞米尼·肾素。2009;29(3):178–95.https://doi.org/10.1016/j.semnephrol.2009.03.008。

论文： CAS PubMed， PubMed， Central Google Scholar
Kellum JA、Romagnani P、Ashuntantang G、Ronco C、Zarbock A、Anders HJ。急性肾损伤。Nat Rev Dis Primers.2021;7(1):52.https://doi.org/10.1038/s41572-021-00284-z。

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A.B.L. 得到了 Fundação Edson Queiroz 和 Conselho Nacional de Desenvolvimento Científico e Tecnológico 的支持（拨款编号 306377/2022-5）。

作者和单位

医学科学研究生课程，福塔莱萨大学- UNIFOR，巴西塞阿拉州福塔雷萨

圭多·迪亚斯·马查多 & 亚历山大·布拉加·利博里奥
Medical Program, Universidade de Fortaleza- UNIFOR, Fortaleza, Ceará, Brazil
Leticia Libório Santos

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Guido Dias MachadoView author publications

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Leticia Libório SantosView author publications

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Alexandre Braga LibórioView author publications

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A.B.L. wrote the letter. All authors have reviewed and approved the letter.

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Correspondence to Alexandre Braga Libório.

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