Analysis of Bladder Dysfunction Etiology and Comorbid Disease Processes

Abstract Purpose of Review Lower urinary tract symptoms (LUTS), encompassing both storage and voiding dysfunction, frequently coexist with systemic metabolic, cardiovascular, neurological, and functional comorbidities. This review analyzes the pathophysiology, clinical manifestations, and management of LUTS in the context of diabetes, heart failure and hypertension, obstructive sleep apnea, fibromyalgia, multiple sclerosis, and Parkinson’s disease. Recent Findings Diabetic bladder dysfunction progresses through compensated and decompensated phases driven by oxidative stress, autonomic neuropathy, and advanced glycation end-product accumulation. Cardiovascular conditions promote nocturia and detrusor instability through neurohormonal activation and fluid redistribution. Obstructive sleep apnea induces nocturnal polyuria via atrial natriuretic peptide secretion and hypoxia-mediated bladder oxidative stress. Fibromyalgia contributes to overactive bladder through central sensitization and neurogenic inflammation. Multiple sclerosis and Parkinson’s disease cause neurogenic bladder dysfunction through demyelination and loss of dopaminergic inhibition, respectively. Summary LUTS reflect complex interactions between systemic disease and bladder dysfunction. Optimal management requires a multidisciplinary approach integrating systemic disease stabilization with targeted urological therapy.