BackgroundBladder outlet obstruction is a common urological condition. We aimed to summarize available evidences about bladder outlet obstruction-induced molecular and morphological alterations occurring in human bladder.MethodsWe performed a literature search up to December 2017 including clinical and preclinical basic research studies on humans. The following search terms were combined: angiogenesis, apoptosis, bladder outlet obstruction, collagen, electron microscopy, extracellular matrix, fibrosis, hypoxia, histology, inflammation, innervation, ischemia, pressure, proliferation, remodeling, suburothelium, smooth muscle cells, stretch, urothelium.ResultsWe identified 36 relevant studies. A three-stages model of bladder wall remodeling can be hypothesized involving an initial hypertrophy phase, a subsequent compensation phase and a later decompensation. Histological and molecular alterations occur in the following compartments: urothelium, suburothelium, detrusor smooth muscle cells, detrusor extracellular matrix, nerves. Cyclic stretch, increased hydrostatic and cyclic hydrodynamic pressure and hypoxia are stimuli capable of modulating multiple signaling pathways involved in this remodeling process.ConclusionsBladder outlet obstruction leads to progressive bladder tissue remodeling in humans. Multiple signaling pathways are involved.

Parkinson's disease (PD) is a common neurodegenerative disorder, and lower urinary tract (LUT) dysfunction is one of the most common autonomic disorders with an estimated incidence rate of 27-80%. Studies have shown that bladder dysfunction significantly influences quality-of-life (QOL) measures, early institutionalisation, and health economics. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1-GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post-void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double-blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add-on therapy with anticholinergics is required. Beta-3 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients' bladder-associated QOL. Neurourol. Urodynam. 35:551-563, 2016. © 2015 Wiley Periodicals, Inc.

BackgroundPercutaneous Tibial Nerve Stimulation (PTNS) has been proposed for the treatment of overactive bladder syndrome (OAB), non-obstructive urinary retention (NOUR), neurogenic bladder, paediatric voiding dysfunction and chronic pelvic pain/painful bladder syndrome (CPP/PBS). Despite a number of publications produced in the last ten years, the role of PTNS in urinary tract dysfunctions remains unclear. A systematic review of the papers on PTNS has been performed with the aim to better clarify potentialities and limits of this technique in the treatment of OAB syndrome and in other above mentioned urological conditions.MethodsA literature search using MEDLINE and ISI web was performed. Search terms used were “tibial nerve” and each of the already mentioned conditions, with no time limits. An evaluation of level of evidence for each paper was performed.ResultsPTNS was found to be effective in 37-100% of patients with OAB, in 41-100% of patients with NOUR and in up to 100% of patients with CPP/PBS, children with OAB/dysfunctional voiding and patients with neurogenic pathologies. No major complications have been reported.Randomized controlled trials are available only for OAB (4 studies) and CPP/PBS (2 studies). Level 1 evidence of PTNS efficacy for OAB is available. Promising results, to be confirmed by randomized controlled studies, have been obtained in the remaining indications considered.ConclusionsPTNS is an effective and safe option to treat OAB patients. Further studies are needed to assess the role of PTNS in the remaining indications and to evaluate the long term durability of the treatment. Further research is needed to address several unanswered questions about PTNS.

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Nosocomial urinary tract infections are a common complication in healthcare systems worldwide. A review of the literature was performed in June 2014 using the Medical Literature Analysis and Retrieval System Online (MEDLINE) database, through either PubMed or Ovid as a search engine, to identify publications regarding nosocomial urinary tract infections (NUTIs) definition, epidemiology, etiology and treatment.According to current definitions, more than 30% of nosocomial infections are urinary tract infections (UTIs). A UTI is defined 'nosocomial' (NUTI) when it is acquired in any healthcare institution or, more generally, when it is related to patient management. The origin of nosocomial bacteria is endogenous (the patient's flora) in two thirds of the cases. Patients with indwelling urinary catheters, those undergoing urological surgery and manipulations, long-stay elderly male patients and patients with debilitating diseases are at high risk of developing NUTIs. All bacterial NUTIs should be treated, whether the patient is harboring a urinary catheter or not. The length of treatment depends on the infection site. There is abundance of important guidance which should be considered to reduce the risk of NUTIs (hand disinfection with instant hand sanitizer, wearing non-sterile gloves permanently, isolation of infected or colonized catheterized patients). Patients with asymptomatic bacteriuria can generally be treated initially with catheter removal or catheter exchange, and do not necessarily need antimicrobial therapy. Symptomatic patients should receive antibiotic therapy. Resistance of urinary pathogens to common antibiotics is currently a topic of concern.