The urinary nerve growth factor-to-creatinine and brain-derived neurotrophic factor-to-creatinine ratios are increased in patients with overactive bladder. These findings may have pathophysiological and clinical implications.

We demonstrated that β3AR is abundantly located in acetylcholine-containing nerve fibers. These findings have important consequences to understand the mechanism of action of β3AR agonists currently used for the treatment of OAB.

Overactive bladder syndrome (OAB) is a highly prevalent urinary dysfunction, with considerable economic and human costs. Clinical diagnosis of OAB is still based on subjective symptoms. A new accurate, objective and noninvasive test to diagnose OAB and assess therapeutic outcome is lacking. Recent studies in lower urinary tract (LUT) dysfunctions, particularly in OAB patients, indicate that urinary proteins (neurotrophins, prostaglandins, and cytokines), serum C reactive protein, and detrusor wall thickness are altered, and such changes could be used as biomarkers of the disease. Nowadays, increasing emphasis has been given to the role of urinary neurotrophins, namely nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF), as key players in some urinary dysfunctions. Although recently considered to be a bladder dysfunction biomarker, urinary NGF presents low sensitivity and specificity. Preliminary results suggest that BDNF may serve as a more efficient biomarker. Even though we have to wait for future studies to confirm the potential role of NGF and BDNF as OAB biomarkers, it is already clear that neurotrophins will contribute to elucidate the physiopathological basis of OAB. Herein are reviewed the latest advances in this new and exciting field, the detection and clinical application of emerging OAB biomarkers.

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Underactive bladder (UAB) is a multifactorial symptom complex often related to detrusor underactivity (DU). Although recognized as a common cause of lower urinary tract symptoms and with significant effects on quality of life, UAB/DU is largely underresearched. Herein, we review upto-date knowledge on the pathophysiological mechanisms of UAB/DU, with an emphasis on the relationship between UAB and bladder outlet obstruction (BOO). Original articles and reviews concerning UAB/DU were identified through a search of the PubMed/Medline and Scopus databases. DU can result from several pathological mechanisms, which can be categorized as idiopathic, neurogenic, myogenic, or functional. The main etiological factors of UAB/DU are aging, diabetes mellitus, neurogenic disorders, and BOO. Although conventional models focus primarily on efferent nerve and myogenic mechanisms, contemporary views highlight the importance of the afferent pathway. Specifically, recent findings in BOO showed that afferent dysfunction, such as altered expression of muscarinic and purinergic P2X 3 receptors or diminished urothelial ATP may play a role in the initial and reversible stages of DU, with potential diagnostic and therapeutic implications. K E Y W O R D S bladder outlet obstruction, detrusor underactivity, lower urinary tract symptoms, pathophysiology

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