Molecular Characteristics of Underactive Bladder

Abstract

Underactive bladder (UAB) is a common urological problem in elderly patients presenting with urinary retention and lower urinary tract symptoms. UAB causes chronic urinary retention or a large post-void residual urine which is usually difficult to manage. Treatment of UAB is a challenge to urologists. The underlying pathophysiology has not been completely elucidated. Molecular diagnosis for the clinical characteristics of UAB is important for us to understand the pathogenesis and develop new therapeutic modalities. The urodynamic finding of UAB might be detrusor acontractility of low contractility and is often termed detrusor underactivity. UAB is frequently encountered in elderly patients with chronic medical or neurological diseases. The pathophysiology of UAB may involve neurogenic, myogenic, and bladder outlet pathologies. Recent studies also reveal that increased suburothelial inflammation and altered sensory protein expressions in bladder mucosa were prominent in patients with UAB. Impaired urothelial signaling and sensory transduction pathways might be associated with impaired bladder sensation as well as impaired detrusor contractility. In addition, the bladder outlet obstruction, inflammation, or bladder ischemia-induced oxidative stress might also decrease the energy of the detrusor and result in UAB. Neurogenic inhibition, myogenic factor, and psychogenic inhibition might also be the causes for UAB. This article reviews recent researches on the pathophysiology and molecular characteristics of UAB. Neurogenic, myogenic, urotheliogenic, bladder outlet, and psychogenic factors might all contribute to UAB. Comprehensive clinical investigations and basic researches may provide a better understanding and effective treatment for this common but difficult bladder disorder.