Revisiting the complex interactions in nocturnal polyuria: insights on OSA, ADH and ANP

Abstract

Notably, a similar vicious cycle can occur in men with benign prostatic hyperplasia (BPH). BPH-induced bladder outlet obstruction leads to increased bladder pressure, impaired bladder compliance and, ultimately, nocturia². In such circumstances, the overlapping contributions of impaired ADH secretion and heightened ANP activity could complicate the therapeutic landscape. In clinical practice, ADH analogues (such as desmopressin) are frequently used to address ADH deficiency-associated nocturnal polyuria. These treatments are effective but often fail in a subset of patients owing to several factors, including heterogeneous pathophysiological mechanisms underlying nocturnal polyuria³.

Our hypothesis that ANP antagonizes ADH-driven water reabsorption in patients with OSA⁴ provides a mechanistic insight into reported treatment resistance³. Incorporating ANP measurement into clinical evaluation could refine the treatment paradigm for nocturnal polyuria.