Reply to ‘Revisiting the complex interactions in nocturnal polyuria: insights on OSA, ADH and ANP’

Abstract

Lin, Lin and Wu provide insightful comments regarding our article¹ on the physiological mechanisms linking obstructive sleep apnoea (OSA) with nocturia (Vrooman, O. P. J. et al. Nocturia and obstructive sleep apnoea. Nat. Rev. Urol. 21, 735–753; 2024), which are thought-provoking (Lin, Y.-H., Lin, K.-J. & Wu, C.-T. Revisiting the complex interactions in nocturnal polyuria: insights on OSA, ADH and ANP. Nat. Rev. Urol. https://doi.org/10.1038/s41585-025-01028-4; 2025)². We agree that benign prostatic hyperplasia (BPH) can contribute to nocturia through bladder outlet obstruction, leading to increased intravesical pressure and impaired bladder compliance³. Indeed, these events can result in detrusor overactivity and reduced voided volumes during nocturnal urination. However, as highlighted in our Review¹, nocturia is a multifactorial condition, and alternative mechanisms influencing urine production should be considered. Specifically, nocturnal polyuria, which can coexist with lower urinary tract dysfunction in BPH, is increasingly recognized as a considerable contributor to nocturia in the ageing population⁴.

We acknowledge the Correspondence authors’ focus on the interplay between atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) in influencing nocturnal urine production². The antagonistic effects of ANP on ADH-driven water reabsorption in the renal collecting ducts provide valuable mechanistic insight into treatment resistance observed with ADH analogues such as desmopressin⁵. This process is particularly relevant in patients with OSA, in whom negative intrathoracic pressures and intermittent hypoxia promote ANP secretion, counteracting ADH-mediated water retention⁶. Thus, incorporating ANP measurements into clinical evaluation might improve management of nocturnal polyuria in this patient population⁷. Nevertheless, certain challenges should be considered. ANP levels peak at night owing to negative intrathoracic pressures, so the optimal time for measurement remains uncertain. Morning samples might not accurately reflect nocturnal surges given the short half-life of ANP⁸.