Neurourology and urodynamics · 2026
Response to Letter to the Editor on "Unveiling 'Idiopathic' Nocturia: The Central Role of Sleep-Induced Hypogonadism and ANP-Mediated Hemodynamics".
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Song Qi-Xiang, Sinha Sanjay, Vahabi Bahareh, Kanai Anthony, Fry Christopher, Tyagi Pradeep, Musco Stefania, Robinson Dudley, Drake Marcus J, Abrams Paul, Wein Alan, Chapple Christopher R
Аннотация
BACKGROUND: We respond to the comments of Lin et al. on our Think Tank review of potential therapeutic avenues for idiopathic nocturia.
METHODS: Evidence was synthesized from relevant literature on OSA-associated nocturia, testosterone decline with sleep-induced hypogonadism, and natriuresis-mediated impairment of aquaporin (AQP)-dependent water reabsorption.
RESULT: We first clarify that our review was confined to idiopathic nocturia. We also note that "occult OSA" should more accurately be termed undiagnosed OSA, and that the associated nocturia should be classified as secondary rather than idiopathic. Nonetheless, we acknowledge the value of the proposed sleep-induced hypogonadism hypothesis, while emphasizing that the causal link between OSA-related testosterone decline and nocturia remains unestablished and that available evidence is currently male-specific. We further recognize that natriuresis attributed to atrial natriuretic peptide may impair aquaporin-mediated water reabsorption; however, existing evidence pertains mainly to renal tubular aquaporins, whereas our review focused on bladder urothelial aquaporins and transvesical water reabsorption, a largely unexplored extrarenal mechanism.
CONCLUSIONS: We are grateful to Lin et al. for their letter, which raises additional mechanisms as critical drivers of nocturia. We believe that cross-disciplinary research into OSA-associated secondary nocturia is warranted to translate these mechanistic insights into clinical benefit.
METHODS: Evidence was synthesized from relevant literature on OSA-associated nocturia, testosterone decline with sleep-induced hypogonadism, and natriuresis-mediated impairment of aquaporin (AQP)-dependent water reabsorption.
RESULT: We first clarify that our review was confined to idiopathic nocturia. We also note that "occult OSA" should more accurately be termed undiagnosed OSA, and that the associated nocturia should be classified as secondary rather than idiopathic. Nonetheless, we acknowledge the value of the proposed sleep-induced hypogonadism hypothesis, while emphasizing that the causal link between OSA-related testosterone decline and nocturia remains unestablished and that available evidence is currently male-specific. We further recognize that natriuresis attributed to atrial natriuretic peptide may impair aquaporin-mediated water reabsorption; however, existing evidence pertains mainly to renal tubular aquaporins, whereas our review focused on bladder urothelial aquaporins and transvesical water reabsorption, a largely unexplored extrarenal mechanism.
CONCLUSIONS: We are grateful to Lin et al. for their letter, which raises additional mechanisms as critical drivers of nocturia. We believe that cross-disciplinary research into OSA-associated secondary nocturia is warranted to translate these mechanistic insights into clinical benefit.