The aberrant circadian rhythm of arginine vasopressin secretion is generally accepted as one of the main factors underlying the pathophysiology of monosymptomatic nocturnal enuresis. This is also the rationale behind treatment with desmopressin. However, not all children share the same pathophysiology, hence not all children respond to desmopressin treatment. Measurements of AVP levels could theoretically indicate which children may be candidates for adequate desmopressin response, but AVP has a rather short half-life and is difficult to measure. Copeptin is cleaved from the precursor of AVP and is more stable. The exact physiological role of the molecule is under discussion. Copeptin has emerged as a surrogate for AVP level measurements.
The first study showing lower levels of copeptin in children with MNE originates from 2013 (1). The authors demonstrated lower levels of copeptin in children with monosymptomatic nocturnal enuresis. Recently, Hara et al (2) measured copeptin levels on 32 children and related the levels to desmopressin. The authors were able to document that pretreatment levels of copeptin are associated with good response to desmopressin. This seems rational, because children with lower AVP levels during nighttime probably benefit from reduction in urine volumes produced during sleep.
Identifying a biomarker as predictor of desmopressin response can be of clinical importance, since clinicians could possibly tailor the treatment for individual patients by a simple measurement, avoiding the trial-and-error approach. However, as the pathophysiology of enuresis is complex and factors beyond the AVP secretion profile are often of importance, we are still far from being able to direct treatment based on single biomarkers. Another issue to be resolved is the time when copeptin has to be measured to optimize its predictive value.
The results from these studies seem promising, but larger scale studies are needed before copeptin measurements can be implemented in daily practice.
