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Although not so detrimental as other co\u2010morbidities, uropathy contributes to a significantly reduced quality\u2010of\u2010life in those affected. The purpose of this ICS\u2010RS report is to highlight clinical and basic research data to outline directions for further research and possible treatment approaches.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This report is based on a think tank presentation and discussion at the ICI\u2010RS 2011, original research data and literature research.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Clinical and experimental data confirm that detrusor overactivity, both neurogenic and myogenic, and changes in transmitter regulation leading to a hyper\u2010 excitability of the detrusor are the major findings in diabetic neuropathic bladders. These findings seem to be related to an earlier stage of DM, whereas detrusor underactivity appears to be linked to later stages of DM. Detrusor smooth muscle cells seem to be modulated directly by hyperglycemia. Data support the theory that hyperglycemia\u2010induced oxidative stress in the detrusor smooth muscle and that micro\u2010 and macrovascular events are also responsible for urologic complications of DM.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>DM causes bladder remodelling leading to uropathy in a mulitfactorial way. Future research should focus on the effects of DM as a function of time and develop novel animal models looking at defined aspects as well as interaction of different aspects\u2010 such as oxidative stress in neurogenic, myogenic and urothelial components and the role of inflammation and hypoxia caused by vascular complications. Neurourol. 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