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Inheritance in overactive bladder syndrome

Nature Reviews Urology volume 20, pages 61–62 (2023)Cite this article

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Despite the high prevalence of overactive bladder (OAB) syndrome, its pathophysiology remains poorly understood. Twin studies offer a unique opportunity for studying the genetics of this disorder, but trials are limited by heterogeneous patient populations. Improved understanding of genetic factors in OAB will be vital to developing targeted management.

Despite the prevalence of lower urinary tract symptoms (LUTS) and urinary incontinence, the aetiology remains poorly understood. Results of major epidemiological studies, such as EPIC, have shown that LUTS are common in both men and women and increase with age, largely irrespective of the specific symptoms. Furthermore, the concept of overactive bladder (OAB) syndrome as a singular pathological entity is widely questioned1. Rather, a number of differing OAB syndromes are thought to exist2. Aetiology is likely to be multifactorial and various mechanisms have been hypothesized, including dysfunction of the detrusor muscle, bladder urothelium and central or peripheral nervous system. Confounders such as metabolic syndrome and the urinary microbiome are associated with OAB and might have important roles in modulating disease.

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Authors and Affiliations

  1. Department of Urology, Guy’s and St Thomas’ NHS Trust, London, UK

    Nicholas Raison, Sachin Malde & Arun Sahai

  2. Faculty and Life Sciences and Medicine, King’s College London, London, UK

    Nicholas Raison & Arun Sahai

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  1. Nicholas Raison
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  2. Sachin Malde
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  3. Arun Sahai
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Correspondence to Arun Sahai.

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Competing interests

S.M. declares an educational grant by Medtronic and speaker fees by Medtronic. A.S. declares educational grants by Medtronic, Boston scientific and Saluda Medical and speaker fees by Ferring, Allergan, Medtronic and Boston Scientific. N.R. declares no competing interests.

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Raison, N., Malde, S. & Sahai, A. Inheritance in overactive bladder syndrome. Nat Rev Urol 20, 61–62 (2023). https://doi.org/10.1038/s41585-022-00667-1

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  • DOI: https://doi.org/10.1038/s41585-022-00667-1

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