2025 Southeastern Residency Conference

Title: Evaluation of Desmopressin in Preventing Overcorrection of Hyponatremia Among Patients with Renal Dysfunction


Authors: Kelsea Mabie, Tara Kennell, Rajarshi Patel, Brooke Smith, Aaron Chase, Kelli Henry


Background: Hyponatremia is a common cause for hospital and intensive care unit (ICU) admission. Treatment strategies vary based on patient presentation and the presumed cause of hyponatremia, but center around sodium repletion, fluid balance management, and discontinuation of offending agents. Increasing serum sodium must be done in a slow, controlled fashion to prevent overcorrection which may cause adverse neurological effects, including osmotic demyelination syndrome (ODS). One method to prevent sodium overcorrection includes administering desmopressin to decrease free water loss via the kidneys, avoiding hemoconcentration and rapid increase in sodium. Studies have demonstrated desmopressin is a useful agent for this indication; however, there is limited evidence on the efficacy of desmopressin in the setting of renal dysfunction.  


Methods: This was a single center, retrospective cohort study at an academic medical center that received exemption from the institutional review board. Adult patients with a serum sodium <125 mEq/L who received one or more doses of intravenous (IV) desmopressin during their admission were included. Patients were excluded if they received desmopressin for a diagnosis of diabetes insipidus or hemorrhage. The primary outcome was the difference in rate of sodium overcorrection (>8 mEq/L) 24 hours after the first desmopressin dose in patients with renal dysfunction compared to those without renal dysfunction. Renal dysfunction was defined as creatinine clearance less than 30 mL/min. Secondary outcomes included rate of correction before and after desmopressin, proportion of patients achieving a sodium correction of 5–10 mEq/L within 24 hours of presentation, and rate of overcorrection at 24 and 48 hours after presentation. Outcomes were assessed with chi-squared, t-test, and Mann-Whitney U as appropriate. All patient demographics were categorized using mean and standard deviation or median and interquartile range.


Results: Sixty-five patients were included in this study with 14 patients (21.5%) having renal dysfunction. Forty-three (66.2%) patients were male, 54 (83.1%) were admitted to the ICU, and 17 (26.2%) received a home medication associated with hyponatremia. Baseline variables including age, sex, ICU admission, renal function, baseline sodium, weight, and fluid status were well-balanced between groups. Patients in the renal dysfunction group received significantly more milliequivalents of sodium through IV fluids compared to those without renal dysfunction (90.7 vs 284.2 mEq, p=0.001), which was primarily driven by 0.9% sodium chloride administration. There was no difference in the primary outcome of rate of overcorrection 24 hours after administration of desmopressin (9.8 vs 21.4%, p=0.476). The mean change in sodium 24 hours after desmopressin was similar between groups (2.43 vs 3 mEq/L, p=0.691), with no difference in rate of overcorrection at 24 hours (9.8 vs 28.6%, p=0.173) or 48 hours (5.9 vs 14.3%, p=0.632) after admission. Correction within goal range was similar between groups at 24 hours after admission (51.0 vs 50.0%, p=1.000) and after desmopressin administration (17.6 vs 28.6%, p=0.597). There were no differences in safety outcomes. 


Conclusion: Our study did not demonstrate a difference in overcorrection of sodium after desmopressin in those with impaired versus normal renal function. Overall, there was a low incidence of overcorrection, though this study was likely underpowered. The results did not reach statistical significance however, the observed differences in sodium overcorrection rates could suggest that renal dysfunction may not influence the clinical response to desmopressin. Future studies are warranted to determine the effect of renal dysfunction on safety and efficacy of desmopressin.