Copeptin improves prediction of treatment response in children with monosymptomatic nocturnal enuresis
Clara Odilia Sailer1,2, Odile Gaisl1,2, Svetlana Beglinger3
1Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Insights
Plasma copeptin ratio effectively predicts desmopressin treatment response in children with monosymptomatic nocturnal enuresis (MNE). A lower evening/morning copeptin ratio indicates a better response, aiding individualized MNE therapy.
Area of Science:
- Pediatric Nephrology
- Endocrinology
- Urology
Background:
- Monosymptomatic nocturnal enuresis (MNE) affects many children.
- Desmopressin is a primary treatment, but response varies.
- Predictors for desmopressin efficacy in MNE are lacking.
Purpose of the Study:
- To evaluate plasma copeptin as a predictor of desmopressin treatment response in children with MNE.
- To establish if plasma copeptin ratio can guide individualized MNE treatment.
Main Methods:
- Prospective observational study of 28 children with MNE.
- Baseline assessment included wet nights, plasma copeptin (morning/evening), and serum sodium.
- Desmopressin treatment (120-240 µg/day) for 12 weeks.
Main Results:
- Eighteen of 28 children responded to desmopressin.
- A plasma copeptin ratio cutoff of 1.34 predicted response (AUC 70.6%, P = .07).
- Lower copeptin ratios correlated with better treatment outcomes; serum sodium did not predict response.
Conclusions:
- Plasma copeptin ratio is a promising predictor of desmopressin response in pediatric MNE.
- This marker can help identify children likely to benefit from desmopressin.
- Plasma copeptin ratio may improve individualized treatment strategies for MNE.
Objective:
One of the main medical treatment options for monosymptomatic nocturnal enuresis (MNE) is the vasopressin analog desmopressin. But not all children respond to desmopressin treatment, and no reliable treatment predictor has yet been established. We hypothesize that plasma copeptin, a surrogate marker for vasopressin, can be used to predict treatment response to desmopressin in children with MNE.
Design/Methods:
In this prospective observational study, we included 28 children with MNE. At baseline, we assessed the number of wet nights, morning, and evening plasma copeptin, and plasma sodium and started treatment with desmopressin (120 µg daily). Desmopressin was increased to 240 µg daily if clinically necessary. The primary endpoint was reduction in the number of wet nights following 12 weeks of treatment with desmopressin using plasma copeptin ratio (evening/morning copeptin) at baseline.
Results:
Eighteen children responded to desmopressin treatment at 12 weeks, while 9 did not. A copeptin ratio cutoff of 1.34 (sensitivity 55.56%, specificity 94.12%, area under the curve 70.6%, P = .07) was best at predicting treatment response, with a lower ratio indicating a better treatment response. In contrast, neither the number of wet nights at baseline (P = .15) nor serum sodium (P = .11) alone or in combination with plasma copeptin improved outcome prediction.
Conclusions:
Our results indicate that, of our investigated parameters, plasma copeptin ratio is the best predictor for treatment response in children with MNE. Plasma copeptin ratio could thus be useful to identify children with the highest benefit of desmopressin treatment and improve individualized treatment of MNE.
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