Assessment of Acute Kidney Injury in Neurologically Injured Patients Receiving Hypertonic Sodium Chloride: Does Chloride Load Matter?

Abstract

Background: Increasing evidence suggests that large-volume infusions of 0.9% sodium chloride (NaCl) for resuscitation are associated with hyperchloremic metabolic acidosis, renal vasoconstriction, and increased risk of acute kidney injury (AKI). Patients with neurological injury may require hypertonic NaCl for therapeutic hypernatremia, treatment of cerebral salt wasting, hyponatremia, or elevated intracranial pressure. Consequently, this increased exposure to chloride may result in an increased risk for development of AKI. Objective: The primary aim of this study was to describe the risk for development of AKI in neurologically injured patients receiving large volumes of intravenous hypertonic NaCl. Methods: This single-center, retrospective study looked at neurologically injured patients who received hypertonic NaCl and sodium acetate. Data were collected to assess renal function, hyperchloremia, and acidemia. Receiver operating characteristic (ROC) curve analysis was used to determine the predictive association between the amount of daily and overall chloride exposure and development of AKI. Results: A total of 301 patients were screened, and of those, 142 were included. Of the 142 patients included, 13% developed AKI, and 38% developed hyperchloremia. Additionally, 32% of patients were switched from NaCl to sodium acetate after an average of 3.4 ± 1.5 days of NaCl therapy. The ROC curve demonstrated that if patients received greater than 2055 mEq of chloride over 7 days, they were more likely to develop AKI (sensitivity 72%, specificity 70%; P = 0.002; area under the curve = 0.7). Conclusion and Relevance: Neurologically injured patients receiving hypertonic sodium therapy with a high chloride load are at risk of developing hyperchloremia and AKI.

The dynamic relationship between serum chloride and cardiorenal syndrome

“…Moreover, it was shown that chloride availability in the renal tubules can modulate renal vasoactivity; low chloride perfusion of diminishes tubular response to vasopressors (Quilley et al, 1993). In line with those observations, more recent clinical studies have suggested that high chloride load could be associated with an increased risk of acute kidney injury (Sigmon et al, 2019;Yunos et al, 2012). Therefore, it is conceivable that various biological impacts of serum or tubular concentrations of chloride represent a less well known territory with potential clinical implications.…”

Reply: Assessment of Acute Kidney Injury in Neurologically Injured Patients Receiving Hypertonic Sodium Chloride: Does Chloride Load Matter?

“…We thank Gueret et al 1 for their comments on our recent article and acknowledge that we too understand that our retrospective study cannot answer all the issues regarding acute kidney injury (AKI) caused by hyperchloremia in the neurologically injured patient population. 1,2 The question posed regarding the risk of AKI in the neurologically injured population only stimulates more questions and research opportunities. We chose to use the acute kidney injury network (AKIN) criteria based on a previous study assessing AKI caused by hyperchloremia in a similar patient population.…”

“…We thank Gueret et al 1 for their comments on our recent article and acknowledge that we too understand that our retrospective study cannot answer all the issues regarding acute kidney injury (AKI) caused by hyperchloremia in the neurologically injured patient population. 1,2…”

Comment: Assessment of Acute Kidney Injury in Neurologically Injured Patients Receiving Hypertonic Sodium Chloride: Does Chloride Load Matter?

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We are interested in the article written by Sigmon et al 1 The authors concluded that hypertonic sodium therapy with high chloride load, for neurologically injured patients, increases risk of developing hyperchloremia and acute kidney injury (AKI). However, we have questions.The authors defined AKI as change in serum creatinine of 0.3 mg/dL or an increase to 1.5 times baseline.

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“…5 Finally, this study gives us some answers on the relationship between chloride load and AKI in neurologically injured patients. 1 However, a few elements are missing to arrive at a conclusion, particularly the amount of hypertonic saline received by patients. It is like the chicken and the egg question: Is AKI a result of the amount of hypertonic saline solution or patients' injury severity?…”