Renal Transplant in Patients With Abnormal Bladder: Impact of Causes on Graft Function and Survival.

OBJECTIVES: Successful kidney transplant depends partly on the normal physiologic functioning of the bladder, which involves effective urine storage and emptying. The bladder may become abnormal owing to various urologic and neuropathic disorders. Patients with abnormal bladders need careful management before and after transplant. In this study, we aimed to determine the outcomes of renal transplants in relation to various causes of abnormal bladder. MATERIALS AND METHODS: We conducted a retrospective review of 25 patients with abnormal bladder who received 30 renal transplants between 1990 and 2014. The patients were divided into neurologic and urologic groups based on the causes of abnormal bladder. Patient demographics, graft function, survival, and postoperative complications were compared. RESULTS: The most common urologic cause was posterior urethral valve (14 patients), while the most common neurologic cause was spina bifida (6 patients). There was no statistically significant difference in graft survival at 1, 3, and 5 years between patients with neurologic and urologic causes of abnormal bladder as well as at long-term follow-up. However, the mean estimated glomerular filtration rate at 1, 3, and 5 years was higher among patients with neurologic causes than in those with urologic causes, although the difference was statistically significant only at 1 year (61 ± 34 vs 37 ± 19 mL/min; P = .025). Stone formation was reported only in patients whose abnormal bladder had neurologic causes, and no incidence was reported in patients with urologic causes (20% vs 0%; P = .038). The incidence of other postoperative complications was not statistically significant between the 2 groups. CONCLUSIONS: With careful evaluation and proper preoperative correction of abnormal bladder dysfunction and optimization of the emptying and storage functions of the bladder, the causes of abnormal bladder did not appear to impact graft function and survival or overall rate of postoperative complications.

In vitro release of adenosine triphosphate from the urothelium of human bladders with detrusor overactivity, both neurogenic and idiopathic.

BACKGROUND: There is increased evidence to suggest a role for nonadrenergic-noncholinergic neurotransmission in the pathogenesis of bladder dysfunction. OBJECTIVE: In this set of experiments, we have assessed the contribution of the urothelium to purinergic activity by quantifying the amount of adenosine triphosphate (ATP) released from the urothelium of patients with idiopathic detrusor overactivity (IDO) and with neurogenic detrusor overactivity (NDO) and comparing these releases to those of controls. DESIGN, SETTING, AND PARTICIPANTS: Bladder tissue with urodynamically and clinically proven NDO (n=8) and IDO (n=8) were included in this study. The carefully dissected urothelium was stimulated by mechanically stretching as well as electrically stimulating and the ATP; thus, release was quantified. MEASUREMENTS: We used a Lucy Anthos 1 luminometre (Anthos Labtec Instruments GmBH, Wals, Austria) to perform the assay. The results were analysed using Stingray software (Dazdaq Ltd, Brighton, UK). RESULTS AND LIMITATIONS: Both mechanical stretch and electric field stimulation (EFS) led to increased ATP release in both sets of tissues with overactivity compared to the controls; this rise was even more significant for the IDO urothelium (2416.7±479.8 pmol/g [p<0.005]) than for the NDO urothelium (133.1±22.4 pmol/g [p<0.01]); values for the controls were 77.6±16.2 pmol/g. ATP release following mechanical stretch was more sensitive to tetrodotoxin in bladders with NDO compared to those with IDO as well as to the controls, with ATP levels falling from 233.5±20.7 pmol/g to 107.2±11.6 pmol/g, expressed as percentage of basal levels (p<0.002). The experiments were performed in vitro, and the female patients were a mix of peri- and postmenopausal states. CONCLUSIONS: These experiments suggested a significant rise in ATP release from the urothelium of bladders with NDO as well as those with IDO in comparison to controls. Most of the ATP released from bladders with NDO is primarily from neuronal sources.

Flat adenomas in a colonic bladder augmentation patch: cystoscopic removal using an endoscopic mucosal resection technique.

Bladder augmentation using colonic patches is being increasingly performed and a substantial risk of neoplasia in such patches has been reported. We present the case of a 62-year-old man who developed a large flat adenoma in the colonic mucosa of an augmented bladder. The adenoma was indigo-carmine dye sprayed and completely resected via a cystoscope using an endoscopic mucosal resection technique. We discuss how methods used at colonoscopy to detect and remove early neoplastic lesions may readily be employed during colonic patch surveillance at cystoscopy.