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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Severe hyponatremia (Na <120 mEq/L) carries a high risk of adverse outcomes, including osmotic demyelination syndrome due to overly rapid sodium correction. Although numerous algorithms have been proposed to guide diagnosis and treatment, most have not been validated in real-world clinical settings and fail to incorporate dynamic follow-up variables such as changes in urine output during therapy.
We conducted a retrospective cohort of hospitalized patients with severe hypotonic hyponatremia (<120 mEq/L) between 2016 and 2025. We assessed the performance of existing algorithms for etiologic diagnosis and for the prevention of rapid hyponatremia correction, defined as serum Na increase of >8 mEq/L within 24 h. The etiology of hyponatremia was determined retrospectively based on its clinical course and complementary studies. Additional clinical variables assessed included kidney free water clearance ([UNa+Uk]/SNa), UNa, Uosm, and water balance.
We included 475 patients with severe hyponatremia, with a median age of 59 years (IQR 22–91); 257 (54%) were women, 185 (39%) had AKI, and 71 (15%) received 3% hypertonic saline due to symptoms associated with hyponatremia. The etiology was multifactorial in most cases. Predisposing factors included cirrhosis in 356 (75%), CKD stages 3–4 in 266 (56%), and heart failure in 48 (10%) patients. Prior diuretic use was documented in 219 (46%).
We evaluated two diagnostic algorithms. The etiology of hyponatremia, as assessed by these algorithms within the first 24 hours after admission, could not be established in 375 patients (79%); in these cases, the real cause became evident only retrospectively, once the relationship between serum sodium changes, volume response, renal function trajectory, and/or loss of diuretic effect was observed.
Rapid correction within the first 24 hours occurred in 138 patients (29%). Initial and serial assessments of urinary sodium, urine osmolality, and renal free water clearance ([UNa+Uk]/SNa) were not associated with rapid correction. Diuresis during the first 12 hours was higher in patients with rapid correction (1.5 [IQR 0.6–2.6] vs. 0.9 [IQR 0.2–1.2] mL/kg/h; P<0.001).
Compared with a previous algorithm that predicted risk of rapid correction based on urinary sodium, a new model incorporating hourly urine output improved discrimination of rapid correction risk from 26% to 58%, with an AUC of 0.78 (95% CI, 0.72–0.86). In multivariate analysis, each 1 mL/kg/h increase in urine output was associated with an odds ratio of 1.17 (95% CI, 1.01–2.80; P<0.01) for rapid sodium correction.
In severe multifactorial hyponatremia, early diuresis within the first 12 hours of treatment emerged as a simple and inexpensive bedside marker of sodium overcorrection. Urinary indices were not associated with the rate of sodium correction. Given the frequent coexistence of CKD, cirrhosis, diuretic use, and sodium restriction, current diagnostic algorithms have limited applicability and should be adapted to real-world clinical practice. Hourly monitoring of urine output remains essential to prevent rapid sodium correction.
