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The human urinary bladder is subject to a unique and extraordinarily diverse array of congenital, inflammatory, metaplastic, and neoplastic abnormalities.  This book provides contemporary, comprehensive, and evidence-based practice information for pathologists, urologists, oncologists, and other medical professionals. In Bladder Pathology, a full spectrum of pathologic conditions that afflict the bladder and urothelium are described and lavishly illustrated. With its emphasis on diagnostic criteria and differential diagnoses, this book is of particular value to practicing pathologists-assisting in the pathologist's recognition, understanding, and accurate interpretation of the light microscopic findings in bladder specimens. Features and benefits of this new volume include: 1,741 high-quality, color illustrations and 112 tables to illustrate the wide range of pathologic and clinical features in the urinary tract An evidence-based approach to diagnosis and patient management for infectious, nonneoplastic, and neoplastic conditions Recent advances in the molecular genetics of the urinary bladder with discussion of their current or potential impact on diagnosis and personalized patient care With emphasis on the scientific validation of current diagnostic methods and their direct application in clinical practice, Bladder Pathology is a cutting-edge resource that not only offers comprehensive research and  clinical information for practicing surgical pathologists, urologists, oncologists, and their clinical colleagues, but also captures a genuine sense of excitement about recent advances in this vital, ever-evolving field.

Signalling epidermal growth The maintenance and regeneration of the adult bladder epithelium is poorly understood, yet it is clinically relevant to the development of urinary-tract infections and bladder cancer. A new study provides insight into the cellular and molecular mechanisms underlying the regenerative response to injury within the mammalian urinary bladder. On injury by bacterial infection or chemical agents, a Shh and Wnt signalling feedback circuit between basal cells of the urothelium and the stromal cells that underlie them leads to regenerative proliferation of the bladder epithelia. The maintenance and regeneration of the epithelium of the adult bladder is poorly understood yet it is a clinically relevant process during urinary tract infections and bladder cancer. This study provides insight into the cellular and molecular mechanisms underlying the regenerative response to injury within the mammalian urinary bladder. Upon injury by bacterial infection or chemical agents, a Shh and Wnt signalling feedback circuit between basal cells of the urothelium and the stromal cells that underlie them leads to regenerative proliferation of the bladder epithelia. Epithelial integrity in metazoan organs is maintained through the regulated proliferation and differentiation of organ-specific stem and progenitor cells. Although the epithelia of organs such as the intestine regenerate constantly and thus remain continuously proliferative 1 , other organs, such as the mammalian urinary bladder, shift from near-quiescence to a highly proliferative state in response to epithelial injury 2 , 3 , 4 . The cellular and molecular mechanisms underlying this injury-induced mode of regenerative response are poorly defined. Here we show in mice that the proliferative response to bacterial infection or chemical injury within the bladder is regulated by signal feedback between basal cells of the urothelium and the stromal cells that underlie them. We demonstrate that these basal cells include stem cells capable of regenerating all cell types within the urothelium, and are marked by expression of the secreted protein signal Sonic hedgehog (Shh). On injury, Shh expression in these basal cells increases and elicits increased stromal expression of Wnt protein signals, which in turn stimulate the proliferation of both urothelial and stromal cells. The heightened activity of this signal feedback circuit and the associated increase in cell proliferation appear to be required for restoration of urothelial function and, in the case of bacterial injury, may help clear and prevent further spread of infection. Our findings provide a conceptual framework for injury-induced epithelial regeneration in endodermal organs, and may provide a basis for understanding the roles of signalling pathways in cancer growth and metastasis.

Oxidative stress contributes to benign prostatic hyperplasia (BPH) pathogenesis, but its role in BPH with bladder diverticulum is unclear. This prospective cohort study compared 126 BPH patients at the Second Hospital of Harbin Medical University. The study involved two groups (n = 63 for each group): group A, comprising patients with BPH, and group B, consisting of BPH patients with bladder diverticulum. Ultrasound imaging and CT scans were employed to assess the features of BPH and bladder diverticulum, respectively. Various clinical parameters and oxidative stress biomarkers were compared between the groups. Group B exhibited significantly higher creatinine (101.8 ± 27.6 µmol/L vs. 56.1 ± 23.6 µmol/L, p < 0.0001), WBC counts (7.0 ± 1.9 vs. 4.2 ± 1.3 × 10⁹/L, p < 0.0001), residual urine volume (400.1 ± 252.0 mL vs. 150.7 ± 93.9 mL, p < 0.0001), and oxidative stress markers, including 8-OHdG (1.93 ± 0.58 vs. 1.70 ± 0.73 ng/mg creatinine, p = 0.014) and MDA (2.46 ± 0.57 vs. 2.03 ± 0.57 μmol/L, p < 0.0001). In group A, 8-OHdG positively correlated with residual urine volume (rho = 0.68) and nitric oxide with bladder wall thickness (rho = 0.70), while quality of life (QoL) negatively correlated with nitric oxide (rho = -0.76). In group B, oxidative stress markers correlated positively with BMI (e.g., homocysteine, rho = 0.69) and bladder wall thickness (e.g., nitric oxide, rho = 0.69), with QoL negatively correlated with uric acid (rho = -0.78). Bladder diverticulum in BPH patients is associated with elevated oxidative stress, increased inflammation, and impaired bladder function.

Podoplanin, D2-40, has been described in a variety of normal and neoplastic tissues. It is often used for highlighting lymphatics. We evaluated the expression of podoplanin in α-smooth muscle actinpositive myofibroblasts producing the suburothelial layer in tunica propria of the urinary bladder that have some similar features with telocytes. Our results showed that these cells demonstrate distinct D2-40 immunoreactivity from telocytes occurring in the renal pelvis and ureter. We observed positive reaction not only in bioptic specimens from women with interstitial cystitis, but also in a control group of women and men treated for pathological bladder lesion different from interstitial cystitis. It is interesting that identical staining reaction was observed in the ureters only exceptionally. In addition, we examined samples from myofibroblastic tumoriform lesions of soft tissue such as nodular fascitis and fibromatosis (desmoid) and we obtained negative results. It means that the so-called myofibroblasts of urinary bladder tunica propria have a unique immunophenotype that has probably not been described until now. Our findings suggest that D2-40 can be used as a complementary immunostainer to α-smooth muscle actin on urinary bladder biopsies from patients with interstitial cystitis. The role of D2-40 as an immunohistochemical marker is still being investigated.

Loss of bladder control is a challenging outcome facing patients with spinal cord injury (SCI). We report that systemic blocking of pro-nerve growth factor (proNGF) signaling through p75 with a CNS-penetrating small-molecule p75 inhibitor resulted in significant improvement in bladder function after SCI in rodents. The usual hyperreflexia was attenuated with normal bladder pressure, and automatic micturition was acquired weeks earlier than in the controls. The improvement was associated with increased excitatory input to the spinal cord, in particular onto the tyrosine hydroxylase-positive fibers in the dorsal commissure. The drug also had an effect on the bladder itself, as the urothelial hyperplasia and detrusor hypertrophy that accompany SCI were largely prevented. Urothelial cell loss that precedes hyperplasia was dependent on p75 in response to urinary proNGF that is detected after SCI in rodents and humans. Surprisingly, death of urothelial cells and the ensuing hyperplastic response were beneficial to functional recovery. Deleting p75 from the urothelium prevented urothelial death, but resulted in reduction in overall voiding efficiency after SCI. These results unveil a dual role of proNGF/p75 signaling in bladder function under pathological conditions with a CNS effect overriding the peripheral one.

Localized amyloidosis of the bladder is rare and often mimics bladder malignancy. It is typically associated with the extracellular deposition of monoclonal light chains, either κ or λ. The cause is unknown, but it is thought to be due to chronic inflammation/cystitis. To highlight the importance of localized urinary bladder amyloidosis as a rare mimicker of urothelial malignancy and elucidate its clinical, histopathologic, and cytopathologic manifestations. Cases of urinary bladder amyloidosis diagnosed during 2000-2023 were retrieved retrospectively from pathology archives. Electronic medical records, including cystoscopy findings and pathology slides including Congo red stain, were reviewed. Here we present 6 patients with localized urinary bladder amyloidosis. Four of the 6 patients were women, with ages ranging from 46 to 69 years, and a mean age of 58 years. Five of 6 patients presented with hematuria, while in 1 patient, bladder amyloidosis was discovered incidentally. Cystoscopy findings invariably were concerning for malignancy, with raised erythema in 5 patients and fungating mass protruding into the bladder lumen in 1 patient. Bladder biopsies and urine cytology were negative for malignancy in all cases. Congo red-positive amyloid deposits involved lamina propria with sparing of the detrusor muscle. In 5 cases, the deposits were typed as derived from the λ light chain, whereas no information was available for 1 patient. Subsequent clinical workup ruled out systemic amyloidosis. These cases of urinary bladder amyloidosis highlight the importance of considering rare amyloidosis in the differential diagnosis of hematuria and cystoscopy with a lesion mimicking malignancy.

Endometriosis is an uncommon condition, and its occurrence in the urachus is exceptionally rare. This case report highlights the extreme rarity of bladder endometriosis involving the urachal area. To the best of our knowledge, no such cases have been previously reported in the literature. The clinical presentation and imaging findings of this condition are extremely similar to those of urachal carcinoma, which makes the differential diagnosis particularly challenging. In this case, a 34-year-old woman presented with significant bladder irritative symptoms during menstruation. Imaging revealed a mass in the urachal region, but its characteristics remained uncertain. Cystoscopy showed only bladder compression, and the patient ultimately underwent robot-assisted laparoscopic partial cystectomy. Postoperative pathology confirmed the diagnosis of bladder endometriosis. This case underscores the importance of considering bladder endometriosis in the differential diagnosis of masses in the urachal area, particularly when they resemble urachal cancer. Early surgical intervention and histopathological confirmation are essential to prevent disease progression.

Background Diabetic cystopathy (DCP) is linked to bladder nerve conduction disorders, with diabetes-induced neuropathy impairing nerve signal transmission and causing bladder dysfunction. Myosin 5a, vital for neuronal transport, has been linked to neurological disorders, though its role in DCP remains unclear. The objective of this study was to investigate whether Myosin 5a plays a potential regulatory role in Diabetic Cystopathy. Methods Bladder strips from diabetic rats were use to assess heightened responsiveness to external stimuli. Urodynamic assessments were conducted to track the progression of bladder voiding dysfunction over time, following streptozotocin (STZ) injection. Single-cell RNA-Seq mining was employed to identify associations between Myosin 5a and bladder overactivity. Cellular and tissue analyses were performed to determine the co-localization of Myosin 5a with neurotransmitter-related proteins. The impact of Myosin 5a knockdown on ChAT and SP expression in bladder neurons was also evaluated. Additionally, Myosin 5a-deficient DBA mice were studied for voiding function and sensitivity to stimuli. Student's t-test (two-tailed) or Mann–Whitney’s U test analysis of variance was used to analyze the difference between groups. Results Bladder strips from diabetic rats exhibit increased responsiveness to external stimuli, with urodynamic assessments showing a progressive decline in bladder function, culminating in overactivity by the fourth week post-STZ injection. Co-localization of Myosin 5a with neurotransmitter-related proteins was observed, and the knockdown of Myosin 5a in bladder neurons led to a significant reduction in ChAT and SP expression. Myosin 5a-deficient DBA mice exhibited abnormal voiding function and reduced sensitivity to stimuli, along with significant downregulation of SLC17A9. Single-cell RNA-Seq analysis revealed a significant link between Myosin 5a and bladder overactivity, with Myosin 5a expression escalating in tandem with the severity of bladder dysfunction. Conclusions Myosin 5a's dysregulation in diabetic rats may worsen bladder overactivity, suggesting its potential as a therapeutic target for diabetic OAB.

Melanosis bladder refers to the urothelium of the bladder appearing black and velvety, with microscopic evaluation describing melanin deposition. Risk factors, pathogenesis and clinical implications are unknown because only sporadic cases are reported in the literature, both with and without the presence of urinary tract symptoms or malignancy. We report a case of melanosis bladder in a male patient with voiding urinary symptoms and an untreated hypospadias.

Diabetic bladder dysfunction (DBD) is a prevalent and multifactorial urological complication of diabetes, with pathogenesis driven by complex interactions between hyperglycemia‐induced oxidative stress, mitochondrial dysfunction, and bladder microenvironment dysregulation. Mitophagy, a selective autophagic process critical for mitochondrial quality control, has been linked to various metabolic diseases, but its precise role and the bidirectional interactions with the diabetic bladder microenvironment remain underexplored. This review outlines a novel, self‐reinforcing feedback loop central to DBD progression. In this cycle, hyperglycemia impairs both the PINK1/Parkin‐mediated mitophagy pathway and ubiquitin‐independent pathways like FUNDC1 under hypoxic conditions, leading to the accumulation of damaged mitochondria. Mitochondrial dysfunction then exacerbates microenvironmental damage through excessive mitochondrial reactive oxygen species (mtROS) production, release of damage‐associated molecular patterns (DAMPs), and activation of the NLRP3 inflammasome, which further drives inflammation, fibrosis, and extracellular matrix (ECM) remodeling. This aggravated microenvironment inhibits mitophagy, thereby accelerating the pathogenic cycle. Beyond elucidating this loop, this review suggests that targeting it offers a promising therapeutic strategy. A breakthrough in DBD treatment may necessitate a combined approach that both restores mitophagy and modulates the microenvironment. Additionally, this study critically reviews several promising, yet underexplored, interventions, including pharmacological mitophagy activation with urolithin A, NACHT, LRR, and PYD domains‐containing protein 3 (NLRP3) inflammasome inhibition via MCC950, and advanced techniques like nanoparticle‐mediated PINK1 mRNA delivery and CRISPR/Cas9‐based Parkin gene editing. Future research should incorporate spatial transcriptomics to resolve cellular heterogeneity, develop targeted nanodelivery systems, and establish mechanism‐driven, highly specific combination therapies to enable precision medicine for DBD. Highlights A novel bidirectional feedback loop connects mitophagy dysregulation with the deterioration of the diabetic bladder microenvironment. Hyperglycemia inhibits PINK1/Parkin‐mediated mitophagy, leading to ROS accumulation and fibrosis. Therapeutic synergy is achieved by simultaneously targeting both mitophagy and microenvironment modulation. Diabetic microenvironmental factors (hypoxia/AGEs/inflammation) impair mitophagy via FUNDC1 and lysosomal dysfunction. Spatial transcriptomics and nanodelivery systems are essential for advancing precision therapies in DBD. Hyperglycemia suppresses the PINK1/Parkin pathway, impairing mitophagy and triggering ROS accumulation. This activates NLRP3 inflammasome and AGEs‐RAGE axis, driving bladder inflammation and fibrosis. A bidirectional positive feedback loop forms between mitophagy dysregulation and microenvironment deterioration, accelerating diabetic bladder dysfunction.