Increasing evidence suggested the multifactorial nature of nocturia, but the true pathogenesis of this condition still remains to be elucidated. Contemporary clinical medications are mostly symptom based, aimed at either reducing nocturnal urine volume or targeting autonomic receptors within the bladder to facilitate urine storage. The day–night switch of the micturition pattern is controlled by circadian clocks located both in the central nervous system and in the peripheral organs. Arousal threshold and secretion of melatonin and vasopressin increase at night-time to achieve high-quality sleep and minimize nocturnal urine production. In response to the increased vasopressin, the kidney reduces the glomerular filtration rate and facilitates the reabsorption of water. Synchronously, in the bladder, circadian oscillation of crucial molecules occurs to reduce afferent sensory input and maintain sufficient bladder capacity during the night sleep period. Thus, nocturia might occur as a result of desynchronization in one or more of these circadian regulatory mechanisms. Disrupted rhythmicity of the central nervous system, kidney and bladder (known as the brain–kidney–bladder circadian axis) contributes to the pathogenesis of nocturia. Novel insights into the chronobiological nature of nocturia will be crucial to promote a revolutionary shift towards effective therapeutics targeting the realignment of the circadian rhythm.

越来越多的证据表明夜尿症具有多因素性质，但这种情况的真正发病机制仍有待阐明。现代临床药物大多基于症状，旨在减少夜间尿量或靶向膀胱内的自主神经受体以促进尿液储存。排尿模式的昼夜转换由位于中枢神经系统和外周器官的生物钟控制。夜间褪黑激素和加压素的觉醒阈值和分泌增加，以实现高质量的睡眠并最大限度地减少夜间尿液的产生。作为对加压素增加的反应，肾脏降低肾小球滤过率并促进水的重吸收。同时，在膀胱中，关键分子的昼夜节律振荡发生，以减少传入感觉输入并在夜间睡眠期间保持足够的膀胱容量。因此，夜尿可能是由于这些昼夜节律调节机制中的一种或多种不同步而发生的。中枢神经系统、肾脏和膀胱（称为脑-肾-膀胱昼夜轴）的节律中断是夜尿症发病机制的原因。对夜尿症时间生物学性质的新见解对于促进向针对昼夜节律重新调整的有效疗法的革命性转变至关重要。