Mechanisms of Action for Diabetic Bladder Dysfunction — State of the Art

Purpose of Review Diabetes (DM) is a common cause of lower urinary tract symptoms (LUTS), known as diabetic bladder dysfunction (DBD).

The phenotype for DBD is described in the literature with considerable heterogeneity and includes poor sensation, increased compliance, detrusor underactivity, urinary retention, weak stream, hesitancy, but also urgency incontinence, and, for many, detrusor overactivity.

Progress has been made in understanding DBD, yet a unified phenotype or classification system for DBD remains elusive.

Much remains unknown about the underlying mechanisms.

Recent Findings No classification scheme to phenotype DBD has been proposed.

Evidence from recent literature suggests four primary drivers: detrusor smooth muscle dysfunction, urothelial dysfunction, autonomic neurologic dysfunction, and circulating and systemic factors such as inflammation, oxidative stress, and microvascular damage.

It is likely that these drivers have multi-factorial causes and inter-relate in complex ways.

Recent findings in animal models lend new support to detrusor smooth muscle dysfunction as well as inflammation.

Reports utilizing next-generation sequencing have begun to appear in the DBD literature and promise further insight.

Summary DBD currently lacks a unified classification scheme and a clear mechanism.

The advent of new, more translatable large animal models and next-generation sequencing promises many exciting new tools and models that more closely translate to human disease.