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Abstract

Benign bladder pathology resulting from prostatic hypertrophy or other causes is a significant problem associated with ageing in humans. This condition is characterized by increased bladder mass, decreased urinary flow rate, decreased compliance, and these and other changes in bladder function often subject patients to increased risk of urinary tract infection. While the physiologic attributes of benign bladder pathology have been extensively described in humans and in various animal model systems, the biochemical and molecular genetic bases for that pathology have only recently been investigated in detail. Studies demonstrate that mitochondrial energy production and utilization are severely impaired in bladder smooth muscle during benign bladder disease, and to a large extent this realization has provided a rational basis for understanding the characteristic alterations in urinary flow and compliance in bladder tissue. Recent investigations targeting the detailed molecular basis for impaired mitochondrial function in the disease have shown that performance of the organellar genetic system, and to a large extent that of relevant portions of the nuclear genetic system as well, is severely aberrant in bladder tissue. In this article, we discuss the physiologic aspects of benign bladder disease, summarize biochemical evidence for the altered mitochondrial energy metabolism that appears to underlie bladder pathology, review the structure and function of the mitochondrial genetic system, and discuss molecular genetic studies of that system which have begun to provide a mechanistic explanation for the biochemical and physiological abnormalities that characterize the disease. We also discuss areas for further research which will be critically important in increasing our understanding of the detailed causes of benign bladder pathology.

Learning From Heart Failure: How Will We Lead Bladder Failure Into the Future?

“…Furthermore, although there are currently no pharmacologic agents that directly affect mitochondrial biogenesis in heart failure, this article shows current advances in the development of heart failure therapies, including mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial pore transition proteins. A similar relationship between the bladder and mitochondrial function was described previously in a study of bladder failure [ 4 , 5 ]. However, researchers in the field of bladder failure seem to have much work to do in the future.…”

Risk factors for urinary tract infection in children with urinary urgency

“…The incidence of UTI in children with overactive bladder may be higher in those who usually perform holding maneuvers to postpone voiding compared to those who do not use these maneuvers ( 2 , 15 ). In the present study, the association between the practice of holding maneuvers and UTI did not achieve statistical significance (p=0.097; OR = 1.64; 95%CI: 0.940 - 2.864).…”

“…Holding maneuvers could redirect urine from the urethra into the bladder, increasing urinary stasis and predisposing the child to recurrent UTI. Straining to void can lead to hypertrophy of the bladder wall and decreased perfusion of the detrusor ( 15 ), which could lead to a reduction of the specific factors in the bladder that protect against UTI. Nevertheless, no statistically significant association was found between this symptom and UTI in the present study.…”