Zaragoza Jose J, Gómez-Fregoso Juan A, Hernández-Barajas Eduardo M, Andrade-Jorge Zarahi, de Leon Juarez Correa-, Granado Rolando Claure-Del, Padilla-Armas Jorge L, Ornelas-Ruvalcaba R Lizzete, Cabrera-Aguilar J Said, Chávez-Alonso Gael, Villalvazo-Maciel Estefania, Orozco-Chan Carlos E, Cárdenas-Mercado Carlos B, Rodríguez-García Gonzalo, Navarro-Blackaller Guillermo, Medina-González Ramón, Gallardo-González Alejandro Martínez, Alcantar-Vallin Luz, Abundis-Mora Gabriela J, García-García Guillermo, Chávez-Iñiguez Jonathan S
Intensive Care Unit, Hospital H+ Queretaro, Mexico.
Nephrology Service, Hospital Civil de Guadalajara Fray Antonio Alcalde, Guadalajara, Jalisco, Mexico.
Clin Kidney J. 2024 Dec 18;18(2):sfae419. doi: 10.1093/ckj/sfae419. eCollection 2025 Feb.
Consequences of hypernatremia in akute kidney injury (AKI-hyperNa) is poorly understood. We analyzed the risk of major adverse kidney events (MAKE) in comparison with AKI and normal serum sodium (AKI-normalNa). Such data could help in understanding this complex interaction.
In this retrospective cohort we compared the AKI-hyperNa with the AKI-normalNa regarding the risk of MAKE, which include death, new dialysis requirement, and worsening kidney function (≥25% decrease in estimated glomerular filtration rate), at 10 (MAKE10) and at 30-90 days (MAKE30-90) using multivariate logistic regression and area under the curve (AUC) analysis. The association between serum sodium levels (per 1 mEq/l increase) and the number of days with hypernatremia was also compared.
A total of 357 patients were included (78 with AKI-hyperNa and 279 with AKI-normalNa). Compared to the AKI-normalNa, AKI-hyperNa were predominantly male (73% versus 59%), experienced hypernatremia for a longer duration (3 days versus 0 days), and took 5 days to normalize serum sodium levels. After multivariate regression analysis, the AKI-hyperNa group had higher risk of MAKE10 [odds ratio (OR) 5.7, confidence interval (CI) 2.5 to 12.89, < 0.001] with an AUC of 0.79. Also its components such as mortality and decreased estimated glomerular filtration rate (OR 2.13, CI 1.11 to 4.07, = 0.021 and OR 20.14, CI 7.69 to 10.03, = 0.001, respectively). A similar trend was found for MAKE30-90 (OR 4.17, CI 1.73 to 10.03, ≤ 0.001). A gradual increase in serum sodium was associated with a higher risk of MAKE (OR 1.07, CI 1.04 to 1.11, ≤ 0.001), as was the number of days spend with hypernatremia (OR 1.51, CI 1.22 to 1.87, = 0.001).
In this cohort, AKI-hyperNa compared with AKI-normalNa had a fivefold risk of short- and long-term MAKE. This event was more frequently observed as serum sodium increased and it was closely related to the number of days that hypernatremia persisted.
急性肾损伤合并高钠血症（AKI-高钠血症）的后果尚不清楚。我们分析了与急性肾损伤和正常血清钠水平（AKI-正常钠）相比的主要不良肾脏事件（MAKE）风险。这些数据有助于理解这种复杂的相互作用。
在这项回顾性队列研究中，我们使用多因素逻辑回归和曲线下面积（AUC）分析，比较了AKI-高钠血症组与AKI-正常钠组在10天（MAKE10）和30-90天（MAKE30-90）时发生MAKE的风险，MAKE包括死亡、新的透析需求和肾功能恶化（估计肾小球滤过率下降≥25%）。还比较了血清钠水平每升高1 mEq/L与高钠血症天数之间的关联。
共纳入357例患者（78例AKI-高钠血症患者和279例AKI-正常钠患者）。与AKI-正常钠组相比，AKI-高钠血症组男性占比更高（73%对59%），高钠血症持续时间更长（3天对0天），血清钠水平恢复正常需要5天。多因素回归分析后，AKI-高钠血症组发生MAKE10的风险更高[比值比（OR）5.7，置信区间（CI）2.5至12.89，P<0.001]，AUC为0.79。其组成部分如死亡率和估计肾小球滤过率下降也是如此（OR分别为2.13，CI 1.11至4.07，P=0.021和OR 20.14，CI 7.69至10.03，P=0.001）。MAKE30-90也有类似趋势（OR 4.17，CI 1.73至10.03，P≤0.001）。血清钠逐渐升高与MAKE风险增加相关（OR 1.07，CI 1.04至1.11，P≤0.001），高钠血症持续天数也是如此（OR 1.51，CI 1.22至1.87，P=0.001）。
在该队列中，与AKI-正常钠相比，AKI-高钠血症发生短期和长期MAKE的风险高出五倍。随着血清钠升高，这种情况更常出现，且与高钠血症持续天数密切相关。
