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. 2022 Sep 30:2:929743.
doi: 10.3389/fneph.2022.929743. eCollection 2022.

Urinary sodium excretion is low prior to acute kidney injury in patients in the intensive care unit

Affiliations

Urinary sodium excretion is low prior to acute kidney injury in patients in the intensive care unit

David Gomes de Morais et al. Front Nephrol. .

Abstract

Background: The incidence of acute kidney injury (AKI) is high in intensive care units (ICUs), and a better understanding of AKI is needed. Early chronic kidney disease is associated with urinary concentration inability and AKI recovery with increased urinary solutes in humans. Whether the inability of the kidneys to concentrate urine and excrete solutes at appropriate levels could occur prior to the diagnosis of AKI is still uncertain, and the associated mechanisms have not been studied.

Methods: In this single-center prospective observational study, high AKI risk in ICU patients was followed up for 7 days or until ICU discharge. They were grouped as "AKI" or "No AKI" according to their AKI status throughout admission. We collected daily urine samples to measure solute concentrations and osmolality. Data were analyzed 1 day before AKI, or from the first to the fifth day of admission in the "No AKI" group. We used logistic regression models to evaluate the influence of the variables on future AKI diagnosis. The expression of kidney transporters in urine was evaluated by Western blotting.

Results: We identified 29 patients as "No AKI" and 23 patients as "AKI," the latter being mostly low severity AKI. Urinary sodium excretion was lower in "AKI" patients prior to AKI diagnosis, particularly in septic patients. The expression of Na+/H+ exchanger (NHE3), a urinary sodium transporter, was higher in "AKI" patients.

Conclusions: Urinary sodium excretion is low before an AKI episode in ICU patients, and high expressions of proximal tubule sodium transporters might contribute to this.

Keywords: acute kidney injury; intensive care unit; kidney concentrating ability; kidney tubules; proximal; sodium–hydrogen exchanger 3.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer (GM) declared a shared affiliation to the handling editor, without collaboration with the authors at the time of review.

Figures

Figure 1
Figure 1
Flowchart of the study population selection. eGFR, estimated glomerular filtration rate; AKI, acute kidney injury.
Figure 2
Figure 2
Trajectories of variables over time in patients who developed AKI (from 3 days before AKI diagnosis (D-3) to 1 day before AKI diagnosis (D-1)), and with “No AKI” (over the first 5 days of ICU admission). Data from D-4 were not included in the graph because of the low number of patients (n=2). (A) Urinary sodium concentration; (B) Urinary sodium/urinary creatinine (uNa/uCr) ratio; (C) Fractional excretion of sodium; (D) Daily urinary sodium excretion; (E) Measured urinary osmolality; and (F) Serum creatinine.
Figure 3
Figure 3
Immunoblotting of the Na+/H+ exchanger (NHE3), collector duct sodium channel (ENaC), renal outer medullary potassium channel (ROMK), and aquaporin-2 (AQP2) expression in urine in “No AKI” and “AKI” patients, by exposure to sepsis or ischemia. In “AKI” patients, urine was collected 1 day before AKI diagnosis; in “No AKI” patients, pooled urine samples were collected from each patient from the first to the fifth day of ICU admission. Each continuous strip represents a different blot, and each blot contains samples from the “AKI” and “No AKI” patients to help with the visual comparison between the groups.

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