Medicine and Pharmacology

Abstract: Urothelial carcinoma of the bladder remains challenging to assess in real time. Standard tools such as white-light cystoscopy and urine cytology are essential but have recognized limitations, particularly for carcinoma in situ and for repeated, long-term surveillance in non-muscle-invasive bladder cancer (NMIBC). Conventional risk models also show imperfect performance in contemporary practice, contributing to both overtreatment and delayed escalation in biologically aggressive disease. Long non-coding RNAs (lncRNAs) are emerging as attractive biomarkers because of their context-specific expression and their detectability in urine, including within extracellular vesicles/exosomes that protect RNA from degradation. Urinary lncRNAs show promise as non-invasive tools for hematuria triage and diagnostic support, risk stratification for recurrence and progression, and treatment guidance in selected settings. Repeatedly studied candidates include UCA1 and several exosomal/uEV-associated lncRNAs (e.g., TERC, SNHG16), while multi-lncRNA panels and combined strategies (including integration with established urine tests such as NMP22) may stabilize performance across biological and pre-analytical variability. Evidence also supports the concept of longitudinal “molecular response” monitoring using liquid-based lncRNA readouts, although truly predictive, treatment-interaction evidence remains limited. Across studies, performance is strongly influenced by the urine compartment analyzed (pellet/sediment, cell-free urine, or uEVs/exosomes) and by pre-analytical handling and normalization choices. lncRNA assays are unlikely to replace cystoscopy in the near term, but they have clear potential as decision-support tests that complement clinical risk assessment, cytology, and other urine-based platforms. This work synthesizes mechanistic and clinically annotated evidence on lncRNAs in bladder cancer, with an emphasis on urine-based and urinary extracellular vesicle (uEV)/exosomal assays. The search strategy covered publications from 1 January 2015 to 30 December 2025, with emphasis on most recent clinically relevant studies, and included mechanistic studies with functional validation, liquid biopsy/urine studies, and evidence syntheses.

Abstract: Subarachnoid hemorrhage (SAH) induces a sympathetic surge and systemic inflammation that may impair renal perfusion and glomerular integrity. Although the vagus nerve is central to autonomic and anti-inflammatory regulation, its relationship to renal structural injury in severe SAH is unclear. This study evaluated whether electrophysiological vagal CAP amplitude correlates with glomerular integrity in an experimental SAH model. Nineteen rabbits were assigned to control (n = 5), sham (n = 5), and SAH groups (n = 9). SAH was induced by daily cisterna magna injections of autologous blood for three days, and animals were followed for 14 days; those that did not survive to the 14-day endpoint formed the SAH-Nonsurvivor subgroup (n = 4). Vagal compound action potential (CAP) amplitude (mV) was recorded electrophysiologically and used as the principal physiologic readout of vagal nerve integrity. Renal tissue and perirenal parasympathetic ganglia were analyzed histologically and stereologically to quantify degenerated neurons and atrophic glomeruli (per mm³). Vagal CAP amplitude decreased from 1.42 ± 0.36 mV in controls to 0.34 ± 0.11 mV in the SAH-Nonsurvivor subgroup (p < 0.001), while atrophic glomeruli increased from 4 ± 1 to 98 ± 11 per mm³. Degenerated neuronal density peaked in the SAH-Nonsurvivor subgroup (98 ± 19 per mm³). Vagal CAP amplitude was inversely correlated with glomerular injury (Spearman ρ = –0.89, p < 0.001). In this small exploratory study, reduced vagal CAP amplitude was associated with greater glomerular injury after severe SAH. These hypothesis-generating findings warrant confirmation in larger, adequately powered studies before any physiologic or translational interpretation can be made.

Abstract: Introduction: The optimal surgical approach for elderly bladder cancer patients remains controversial. We compared perioperative morbidity and short-term outcomes in patients aged ≥75 years undergoing open radical cystectomy (ORC) versus robotic-assisted radical cystectomy (RARC). Methods: A retrospective, multicenter cohort study was performed including 179 patients aged ≥75 years, of whom 101 underwent RARC between 2021 and 2025, and 78 underwent ORC between 2016 and 2020. After 1:1 propensity score matching, 138 patients were analyzed to assess perioperative complications and oncological outcomes, adjusting for age, body mass index (BMI), pathological stage, comorbidities, prior chemotherapy, and type of urinary diversion. Perioperative complications and oncological outcomes were subsequently compared between the two groups. Results: Following propensity score matching, RARC was associated with longer operative time (332 vs. 247 min; p< 0.001) but resulted in significantly lower blood loss (310 vs. 743 mL; p< 0.001), reduced transfusion rates, shorter length of hospital stay (p< 0.001), and fewer overall intraoperative complications (8.7% vs. 18.8%; p=0.04). Patients undergoing RARC also experienced lower rates of any complications (43.4% vs. 62.3%; p=0.02), major complications (Clavien–Dindo III–V: 11.6% vs. 27.5%; p=0.03), and postoperative mortality (1.4% vs. 2.9%; p< 0.001) compared with ORC. In multivariate analysis, surgical approach independently predicted major complications, with RARC conferring a significantly lower risk (OR 0.75; 95% CI 0.51–0.88; p=0.04). Analysis of the learning curve showed a significant reduction in major complications over time for RARC (OR 0.68; 95% CI 0.53–0.93; p=0.01) but not for ORC. Conclusion: RARC offers superior perioperative outcomes, including reduced blood loss, shorter hospitalization, and lower rates of major complications, without compromising oncological control. These data support RARC as a safe and effective option for elderly patients undergoing radical cystectomy.

Abstract: Background/Objectives: Transurethral resection of bladder tumors (TURBT) is the standard for diagnosing and treating non-muscle-invasive bladder cancer. For lateral bladder wall tumors, obturator nerve stimulation can trigger sudden adductor contractions, raising the risk of perforation, hemorrhage, incomplete resection, and poor specimen quality. We evaluated the impact of obturator nerve block (ONB) on specimen quality and perioperative complications. Methods: In this single-center retrospective study, patients with lateral wall tumors treated by TURBT between October 2022 and December 2024 were divided into an ONB group (spinal anesthesia plus ONB) and a non-ONB group (spinal anesthesia alone). Specimen quality, perioperative complications, and 12-month recurrence were analyzed. Results: Of 219 patients (135 ONB, 84 non-ONB), high-quality specimens were more frequent with ONB (71.1% vs. 35.7%, p &lt; 0.001). No perforations occurred with ONB versus 5 (6.0%) without (p = 0.008); hematuria (11.1% vs. 28.6%, p = 0.002) and 12-month recurrence (4.4% vs. 16.7%, p = 0.005) were also lower. Conclusions: ONB added to spinal anesthesia during TURBT for lateral wall tumors was associated with improved specimen quality and fewer perioperative complications. The lower recurrence rate should be considered hypothesis-generating, given the retrospective design and lack of multivariate adjustment; prospective studies are needed.

Abstract: Testicular torsion is a urological emergency that requires prompt diagnosis and surgical intervention to preserve testicular viability. Bilateral orchidopexy is widely regarded as the definitive treatment for the prevention of recurrence [1,2]. We report two rare cases of recurrent testicular torsion despite prior surgical fixation. Both patients had previously undergone orchidopexy and presented with acute scrotal pain. Surgical exploration confirmed torsion in both cases, despite macroscopically intact fixation sutures. Intraoperative findings suggested that recurrence was not due to suture failure but rather to the insufficient restriction of testicular mobility related to the initial fixation technique. Revision orchidopexy with modified multi-point fixation was performed, resulting in successful detorsion and the preservation of testicular perfusion. These cases highlight that orchidopexy does not universally prevent recurrent torsion and emphasize the critical importance of the surgical technique, including the suture placement, orientation, and number of fixation points. Increased awareness of potential re-torsion is essential, even in previously pexied patients. Improved standardization of fixation techniques may help reduce the risk of recurrence.

Abstract: Background: Nephrogenic diabetes insipidus (NDI) is a rare disorder characterized by renal resistance to arginine vasopressin, most commonly caused by pathogenic variants in the AVPR2 gene. While X-linked NDI classically affects males, heterozygous females may exhibit variable clinical expression. Certain AVPR2 variants are associated with partial NDI and milder phenotypes. Methods: We conducted a retrospective family study of a multigenerational Greek pedigree with suspected hereditary NDI. Clinical, biochemical, and pedigree data were collected through chart review and family interviews. Genetic analysis was performed using whole exome sequencing and variant interpretation followed ACMG/AMP guidelines. Results: Fourteen individuals across four generations were evaluated. Molecular analysis identified a familial AVPR2 (NM_000054.7):c.964C>T (p.Pro322Ser) missense variant in three males and three females, with heterozygous status suspected in two deceased females, segregating in an X-linked pattern. Hemizygous males exhibited a broad phenotypic spectrum, ranging from partial NDI with later onset to severe early-onset disease with urinary tract complications. Heterozygous females showed variable expression, from asymptomatic carriers to mildly symptomatic individuals. The variant co-segregated with disease and, based on ACMG criteria, it was classified as pathogenic. Conclusions: This study expands the phenotypic spectrum associated with the AVPR2 p.Pro322Ser variant and highlights marked intrafamilial variability in both hemizygous males and heterozygous females. These findings underscore the role of modifying factors in disease expression and emphasize the importance of genetic diagnosis for early management and family counseling in NDI.

Abstract: Background/Objectives: Clomiphene citrate (CC) is widely used off-label for male infertility despite limited evidence and inconsistent guideline recommendations. Although previous studies suggest variability in clinical practice, real-world data on prescribing patterns, patient selection, monitoring, and treatment success definitions remain limited. This study assessed CC prescribing patterns among urologists and identified factors associated with its use. Methods: A national, cross-sectional, web-based survey was conducted among urologists in Türkiye between November and December 2025. Of 1,558 invited participants, 421 responded (27.0%), and 402 were included in the final analysis. The questionnaire was based on European Association of Urology and American Urological Association guidelines, refined through expert consensus, and pilot-tested. Multivariable logistic regression identified independent predictors of CC use. Results: CC was used by 39.3% of respondents and was independently associated with private practice (odds ratio [OR] = 2.90, p &lt; 0.001), greater professional experience (OR = 2.18, p = 0.002), and higher infertility case volume (OR = 2.27, p = 0.001). Substantial heterogeneity was observed in patient selection, dosing, monitoring, and success definitions. Treatment goals mainly focused on surrogate laboratory outcomes, including semen parameters and testosterone levels, rather than pregnancy and live birth. An indication paradox was identified for hypogonadotropic hypogonadism, and 31.6% of clinicians reported not routinely providing risk counseling. Conclusions: CC prescribing for male infertility remains heterogeneous and mainly driven by clinician experience rather than standardized protocols. The reliance on surrogate outcomes highlights a gap between evidence and practice, emphasizing the need for standardized frameworks and clearer guidance on patient selection, monitoring, and counseling.

Abstract: The Kidney Disease: Improving Global Outcomes (KDIGO) classification of chronic kidney disease (CKD) is based on the cause of disease, the category of estimated glomerular filtration rate (eGFR), and the category of albuminuria. This framework is indispensable for risk stratification, yet it does not always identify the functional and hemodynamic mechanism that maintains the current filtration level and drives future progression. In particular, a normal or only moderately reduced eGFR does not exclude relative hyperfiltration of the remaining nephrons, and albuminuria reflects not only glomerular barrier injury but also the limited capacity of the proximal tubule to endocytose and metabolically process filtered proteins. In this conceptual review, we propose a functional-hemodynamic extension of the KDIGO CGA model: Cause + GFR + Albuminuria + Functional Renal Reserve + Blood Pressure. Within this framework, functional renal reserve (FRR) is considered a dynamic stress test of nephron reactivity, whereas blood pressure acts as an essential hemodynamic and therapeutic modifier that influences the safety, sequencing, and intensity of renoprotection. Detailed antihypertensive treatment is beyond the scope of this article; the KDIGO 2021 recommendation of a target systolic blood pressure below 120 mmHg in adults with CKD and elevated blood pressure, when tolerated and measured in a standardized manner, is used as a clinical reference point. A central element of the proposed algorithm is FRR. A zero or negative FRR under standardized testing may indicate an "actionable hyperfiltration phenotype": a clinically meaningful state in which total eGFR does not reflect the true workload imposed on individual nephrons. Depending on the combination of urinary albumin-to-creatinine ratio, eGFR, FRR, blood pressure, metabolic phenotype, and tubular overload markers, the proposed approach may support RAAS-blockade-first, SGLT2-inhibitor-first, early dual therapy, or staged triple renoprotection. A mechanistic distinction is also emphasized. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) directly inhibit proximal tubular sodium and glucose reabsorption, but their key anti-hyperfiltration effect is mediated by increased sodium delivery to the macula densa, restoration of tubuloglomerular feedback, and increased afferent arteriolar tone. By contrast, renin-angiotensin-aldosterone system inhibitors (RAASi) predominantly modulate the efferent/postglomerular compartment and may improve downstream peritubular perfusion, a mechanism potentially relevant to albumin and protein handling by the proximal tubule. The proposed model does not replace KDIGO; rather, it adds physiological phenotyping to the existing risk map. More precise evaluation of proteinuria, including the albumin-to-total-protein ratio, first-morning urine sampling, low-molecular-weight proteins, and tubular markers, may prevent misclassification of physiological, orthostatic, postglomerular, or tubular proteinuria as progressive glomerular CKD. The model requires prospective validation but may help develop practical algorithms for personalized renoprotection, particularly in patients with low or moderate albuminuria, normal or moderately reduced eGFR, diabetes, obesity, hypertension, solitary kidney, reduced nephron mass, or an uncertain progression trajectory.

Abstract: Background: Eukaryotic translation elongation factor 1 alpha 1(EEF1A1) primarily participates in protein synthesis by binding aminoacyl-tRNA complexes to facilitate peptide chain elongation on ribosomes. Its expression and functional roles exhibit significant heterogeneity across various malignancies, exerting dual regulatory effects as both an oncogene and a tumor suppressor. This study aims to investigate the potential prognostic value and tumor-suppressive role of EEF1A1 in Kidney renal clear cell carcinoma (KIRC). Methods: We analyzed the differential expression of EEF1A1 in KIRC and its correlation with patient prognosis based on TCGA, GEO, and HPA databases. The STRING and GEPIA databases were utilized to perform functional enrichment analysis of its interacting proteins and co-expressed genes. The xCell algorithm was employed to assess the correlation between EEF1A1 and immune cell infiltration, immune checkpoints, and immunomodulatory molecules. Furthermore, drug sensitivity analysis was conducted to evaluate its clinical application potential. Finally, the expression of EEF1A1 in 786-0 and A498 cell lines were validated via qRT-PCR and Western Blotting. Furthermore, CCK-8, wound healing, and Transwell migration/invasion assays were performed to evaluate cell proliferation, migration, and invasion, respectively. Results: EEF1A1 was significantly downregulated in KIRC tissues and cell lines, and its expression level was closely associated with clinicopathological features and prognosis of patients. GO, KEGG, and GSEA enrichment analyses revealed that low EEF1A1 expression is intimately linked to immunosuppressive pathways. Further immunological analysis confirmed significant correlations between EEF1A1 and various immune cell infiltrates, immune checkpoints, tumor-infiltrating lymphocytes, and immunomodulatory molecules. Moreover, cells with high EEF1A1 expression exhibited increased sensitivity to anti-tumor drugs, with expression levels negatively correlated with inhibitory activity (IC50). Finally, overexpression of EEF1A1 significantly inhibited the proliferation, migration, and invasion of clear cell renal cell carcinoma cells. Conclusion: EEF1A1 is downregulated in KIRC and functions as a tumor suppressor. It correlates with TNM stage, grade, and prognosis, and is involved in immune and metabolic pathways. EEF1A1 serves as a prognostic biomarker and indicator of immune microenvironment and drug sensitivity, providing potential targets for advanced KIRC treatment.

Abstract: Background and Objectives: Stress urinary incontinence (SUI) is a common condition among women and is frequently associated with impaired sexual function and increased sexual distress. Pelvic floor muscle training (PFMT) is considered a first-line conservative treatment for SUI; however, its effects on female sexual function remain incompletely understood. The present study aimed to evaluate the impact of PFMT on sexual function, sexual distress, and pelvic floor muscle performance in women with SUI. Materials and Methods: This prospective controlled observational study included sexually active women with clinically confirmed SUI and female sexual dysfunction. Participants were allocated either to a control group (Group A) or to a supervised 12-week PFMT program (Group B). Sexual function and distress were assessed using the Female Sexual Function Index (FSFI) and the Female Sexual Distress Scale–Revised (FSDS-R), respectively. Pelvic floor muscle performance was evaluated using Peritron perineometry, including peak vaginal squeeze pressure, endurance, and resting tone. Objective severity of SUI was assessed using the one-hour pad test. Results: A total of 102 women completed the study, including 44 in the control group and 58 in the PFMT group. After 12 weeks, women undergoing PFMT demonstrated significant improvements in urinary continence, pelvic floor muscle strength, and sexual function compared with controls (all p < 0.01). Mean FSFI total score increased from 21.5 ± 2.5 to 26.6 ± 3.3, while the proportion of women with clinically significant sexual distress decreased from 100% to 58.6%. Peak vaginal squeeze pressure and endurance also improved significantly following PFMT. Conclusions: PFMT significantly improves sexual function, reduces sexual distress, and enhances pelvic floor muscle performance in women with SUI. These findings support the integration of PFMT into the comprehensive management of women with SUI and associated sexual dysfunction.

Abstract: Background/Objectives: Vesicoureteral reflux (VUR) is an important pediatric urologic condition in which accurate grading on voiding cystourethrography (VCUG) may influence counseling, surveillance, antimicrobial prophylaxis, and surgical decision-making. Visual grading is partly subjective, particularly around the grade III-IV boundary. This review mapped the available evidence on AI-based pediatric VUR assessment on VCUG, with emphasis on diagnostic performance, clinician comparison, AI-assisted interpretation, and implementation gaps. Methods: A computer-assisted scoping evidence map was conducted using an exported screening dataset containing 500 records and an extraction dataset containing 13 included studies. Studies were classified as direct VCUG-based VUR grading, low/high-grade classification, AI-assisted clinician interpretation, or indirect clinical prediction. Because the exported files did not document independent duplicate screening, full-text verification, or database-specific deduplication, the synthesis was designed as an evidence map rather than a formal diagnostic meta-analysis. Results: Thirteen studies published between 2019 and 2025 were included. Reported AI performance was generally promising but heterogeneous. The strongest externally validated Deep-VCUG study reported external AUC values of 0.944 for unilateral reflux and 0.924 for bilateral reflux. A qVUR model achieved AUC 0.84 and improved grading reliability 3.6-fold. A multicenter VCUG-DAM study showed marked improvement in clinician AUC with AI support. Direct AI-versus-clinician evidence remained limited. Conclusions: AI may support pediatric VCUG interpretation by improving grading consistency and high-grade VUR recognition. However, current evidence does not establish autonomous superiority over radiologists. AI should currently be considered a decision-support tool rather than a replacement for expert clinician interpretation.

Abstract: Background/Objectives:Urothelial carcinoma remains one of the most surveillance-intensive malignancies in urologic oncology because, particularly in the non-muscle-invasive setting, it combines prolonged survivorship with frequent recurrence and the need for repeated cystoscopic reassessment. Conventional follow-up based on cystos-copy and urinary cytology is clinically entrenched but limited by invasiveness, patient discomfort, recurrent health-care utilization, and the well-recognized low sensitivity of cytology for low-grade disease. . Methods: The purpose of this paper is to review available literature regarding urinary biomarkers used in urothelial cancer from 2017 to 2026. . Results:The studied literature consistently shows that modern urinary bi-omarker platforms, particularly Xpert Bladder Cancer Monitor, Bladder EpiCheck, ADXBLADDER, and Cxbladder-derived assays, generally outperform conventional cy-tology in sensitivity while often preserving very high negative predictive value for clinically consequential recurrence, especially high-grade disease. In the Xpert litera-ture, overall sensitivity repeatedly exceeded that of cytology, while high-grade sensi-tivity and high-grade NPV were particularly favorable. Bladder EpiCheck similarly showed strong diagnostic and clinical utility, especially in the setting of atypical cytol-ogy and high-grade exclusion. ADXBLADDER and Cxbladder studies broadened the translational narrative by supporting less invasive, risk-adapted pathways, although neither primary haematuria data nor surveillance data yet justify universal replace-ment of cystoscopy. Results:Contemporary urinary biomarkers should not yet be in-terpreted as stand-alone substitutes for cystoscopy across all urothelial carcinoma set-tings. However, the cumulative evidence strongly supports their use as clinically meaningful adjuncts for high-grade recurrence exclusion, interpretation of equivocal findings, and selective cystoscopy de-intensification within personalized surveillance pathways.

Abstract: Prostate cancer is formed of a hetergeneous population with different biological properties.They initially form a small part of the normal stromal microenviroment, but are able through cell to cell contact and via exsomes, small nanoparticles containing DNA, mRNA, microRNA, long non-coding RNA, enzymes, chemokines and cytokines are transform the normal stromal cells into tumour associated cells to create an immunosuppressive environment as well as inhibiting the antitumour immune response. Matrix metalloproteinases are able to degrade not only the basement mnbrane but also the extracelular matrix allowing the exosomes to disseminate via the circulation. They are organotrophic, homing in to specific tissues such as bone. Here they create the premetastatic niche devoid of cancer cells and cause an immunosuppressive environement as well as inducing changes in the host cells, producing myeloid derived suppressor cells of which some migrate to the primary tumour inhibiting the antitumour immune response further. Prostate cancer cells can disseminate even before the cancer is detected and thus escape curative therapy. If they survive the shear forces of the circulation and the antitumour immune response they are able to implant in the premetastatic niche transforming it into the metastatic niche. Here they enter a latent state or dormancy which may last for months or years, but later can “awake” to form metastasis. This review critically analyzes the celular and molecular mechanisms which produce this process from celular aspects to the signaling pathways responsable for this process. Multiple mechanisms are involved in a coordinated fashion to permit the survival of the cancer cells; from celular changes in host cells and immunomodulation via chemokines and cytokines. It emphasizes the role of microRNA and long non-coding RNA in this process, and that patients with higher Gleason scores have a worse prognosis in terms of biochemical free survial at ten years. Therefore, a precisión medical approach may improve the biochemical free survival rate without affecting the role of these signaling pathways in normal cells. This includes the modulation of interleukin expresion,elimination of exosomes or the inhibition of important enzymes such as MMP-2 thus mitigating the residual recurrence risk that persists with conventional therapy.

Abstract: Erectile dysfunction (ED) affects one in five men, with moderate to severe forms disproportionately prevalent among men with type 2 diabetes mellitus (T2DM). First-line phosphodiesterase 5 inhibitors (PDE5i) fail in 30-35% of men, and no single non-invasive treatment reliably restores penetrative function in this refractory population. This retrospective case series reports a multimodal protocol in 71 hypogonadal men (38 euglycemic, 33 T2DM) with moderate to severe ED (Erection Hardness Score [EHS] ≤2) refractory to maximum-dose PDE5i. All men received shockwave therapy, class IV laser, therapeutic ultrasound, therapeutic exercise, daily tadalafil, testosterone cypionate, and counseling addressing psychological contributors to ED. Men with T2DM also received tirzepatide (Mounjaro, 2.5-7.5 mg weekly) over the 3-4 month treatment period. Every man improved from an EHS ≤2 to ≥3, restoring penetrative intercourse, with 68% of euglycemic men and 58% of men with T2DM reaching EHS 4. Arizona Sexual Experience Scale scores improved by a median of 6 points in both groups, and PROMIS-10 scores improved, with baseline between-group differences eliminated after treatment. Despite greater baseline severity, men with T2DM achieved equivalent post-treatment sexual function. In this group, hemoglobin A1c fell from 9.2% to 6.2%, with 58% transitioning from the diabetic to the prediabetic range. Both groups lost fat while gaining skeletal muscle and grip strength, with larger changes in men with T2DM, indicating that concurrent testosterone and resistance exercise counteracted the muscle loss typically associated with incretin therapy. These findings suggest that refractory ED, particularly with diabetes and hypogonadism, may require simultaneous intervention across multiple pathophysiologic domains rather than sequential escalation of single-modality treatments. Prospective controlled trials are needed to confirm these findings and determine the contribution of each component.

Abstract: Hard flaccid syndrome (HFS) is an emerging condition of male sexual dysfunction characterized by a persistent semi-rigid penis in the flaccid state, altered penile sensation, erectile dysfunction, and pelvic or perineal pain. Single-modality treatments have shown limited success, and multimodal protocols have been reported only in single-patient case studies. Our objective was to conduct a retrospective analysis of clinical outcomes from an integrative multimodal rehabilitation protocol in men with HFS. Thirty-two men with HFS completed a comprehensive protocol combining class IV laser therapy, dry needling, radial pressure wave shockwave therapy, therapeutic ultrasound, biofeedback training, manual therapy, therapeutic exercise, behavioral coaching, and oral tadalafil. Patient-reported outcomes were collected at treatment initiation and completion. The main outcome measures were Erection Hardness Scale (EHS), penile satisfaction, PROMIS Sexual Interest, and PROMIS Global Health Physical and Mental Component scores. In this case series, median EHS increased from 2 to 4 and median penile satisfaction increased from 2 to 5 (both P<0.01). All 32 patients achieved EHS ≥3 by treatment end, compared with 8 of 32 (25%) at baseline. PROMIS Sexual Interest, Physical Component, and Mental Component scores all improved significantly (P<0.01). Common comorbid features included low back pain (53%), hip or groin pain (38%), pelvic floor pain (31%), and urinary symptoms (28%). In this retrospective case series, multimodal treatment produced substantial improvements in erectile function and sexual quality of life in men with HFS, supporting an integrative model in which musculoskeletal and end organ pathologies initiate the syndrome and are amplified by central and peripheral nervous system contributions.

Abstract: Dengue remains a major public health problem in tropical and subtropical regions, particularly in Latin America. Acute kidney injury (AKI) is one of the severe complications associated with dengue and has been linked to worse clinical outcomes, including prolonged hospitalization, need for renal replacement therapy, and increased mortality. This review aimed to summarize the available evidence on the epidemiology, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of dengue-associated AKI, while also providing an overview of the literature from Latin America. This manuscript was developed as a narrative review. For the Latin America-specific overview, a focused structured search was conducted in PubMed, ScienceDirect, Cochrane Library, LILACS, and Web of Science, including studies published up to December 2025. The available data suggest that AKI in dengue is multifactorial, involving plasma leakage, renal hypoperfusion, endothelial dysfunction, tubular injury, rhabdomyolysis, thrombotic microangiopathy, and inflammatory renal damage. Clinically, AKI has been associated with oliguria, proteinuria, elevated serum creatinine, renal replacement therapy, and higher mortality. Only four eligible indexed studies from Latin America were identified in our search, all from Brazil, with small sample sizes and incomplete reporting of renal outcomes; however, additional unpublished or non-indexed local data may exist. In summary, dengue-associated AKI is a relevant complication of severe dengue, but the evidence available from Latin America remains limited. These findings highlight the need for improved renal surveillance and standardized reporting in dengue-endemic settings across Latin America.

Abstract: Background/Objectives: Penile rehabilitation (PR) techniques are claimed to counteract chronic degenerative processes of cavernous tissue such as penile hypoxia, neurovascular damage, and cavernous fibrosis. The objective of this umbrella review is to synthesize findings from existing meta-analyses to evaluate the efficacy of traditional and emerging PR strategies, providing an evidence-based roadmap for clinical management after surgery for prostate cancer. Methods: Conducted in accordance with PRIOR guidelines, a comprehensive literature search of PubMed, The Cochrane Library, and Scopus was performed through April 2026. The review included primarily systematic reviews and meta-analyses investigating pharmacological, physical, surgical, and regenerative interventions for post-prostatectomy erectile dysfunction (ED). Methodological quality was independently assessed using standardized tools. Results: PDE5 inhibitors (PDE5-is) significantly improve erectile function during active treatment, yet evidence supporting their role in promoting spontaneous, "unassisted" recovery remains limited. Vacuum erectile devices demonstrate high efficacy for assisted intercourse but show minimal impact on returning to baseline function compared to placebo. Penile prosthesis (PP) implantation maintains robust efficacy with exceptionally high satisfaction rates (83–85%), proving independent of prior pelvic surgery. Although early-phase trials suggest clinical potential for regenerative therapies like low-intensity extracorporeal shockwave therapy, platelet-rich plasma, and stem cell interventions, the evidence is currently undermined by substantial heterogeneity in study protocols and concerns regarding methodological quality. Conclusions: PR following radical prostatectomy remains a complex challenge characterized by poor evidence. While PDE5-Is are established first-line therapy for assisted function, PP remains the most reliable definitive treatment for refractory ED cases. Regenerative approaches show promise but remain investigational until standardized protocols and large-scale trials are established.

Abstract: Background and hypothesis. Sodium–glucose cotransporter 2 inhibitors (SGLT2i) provide consistent cardiorenal benefits; however, tissue-level mechanisms remain insufficiently characterized. We investigated whether SGLT2i were associated with longitudinal remodeling of organ-specific adipose depots in patients with chronic kidney disease (CKD). Methods. In this observational study cohort (ADIPO-CKD; NCT07309094), adults with CKD stages 1–4 underwent clinical, biochemical and ultrasound imaging assessment at baseline (T0) and 8-month follow-up (T8). Thus, epicardial (EAT) and perirenal adipose tissue (PRAT) thickness were measured. Changes over time between patients under SGLT2i treatment and those without (Non-SGLT2i) were assessed using repeated-measures ANOVA and multivariable linear regression models adjusted for age, sex, baseline estimated glomerular filtration rate (eGFR), diabetes status, concomitant glucagon-like peptide 1 (GLP-1) receptor agonist therapy, body mass index (BMI) and visceral fat area (VFA) changes. Results. Among 189 CKD patients (50 SGLT2i and 139 non-SGLT2i), SGLT2i therapy was associated with significant reductions in PRAT (1.28±0.70 to 0.91±0.61 cm; ΔPRAT −0.37 cm; p<0.002) and EAT (0.57±0.27 to 0.36±0.14 cm; ΔEAT −0.21 cm; p<0.012), whereas no significant changes were observed in the Non-SGLT2i group. In multivariable models, SGLT2i exposure remained independently associated with ΔPRAT (β=0.447; 95% CI 0.211–0.682; p<0.001; R²=0.371) and ΔEAT (β=0.061; 95% CI 0.009–0.113; p<0.021; R²=0.053), including adjustment for changes in BMI and VFA. These findings were accompanied by trends toward improvement in renal function and systemic inflammation biomarkers in the SGLT2i group, although these changes did not reach statistical significance. In a secondary analysis, dapagliflozin was significantly associated with PRAT reduction, whereas a significant association was found between empagliflozin and EAT decrease. Conclusions. In CKD stages 1–4, SGLT2i use was independently associated with reductions in EAT and PRAT. These findings support a potential link between organ-specific adipose tissue and cardiorenal disease; however, given the observational design, these results should be interpreted as associative and hypothesis-generating. Dedicated mechanistic and adequately powered studies are warranted to determine their clinical relevance.

Abstract: Background: Neurogenic bladder in children is a major cause of progressive upper urinary tract deterioration and chronic kidney disease if not diagnosed and managed early. High intravesical pressure, recurrent urinary tract infections, and vesicoureteral reflux are key contributors to renal damage, particularly in resource-limited settings. This study aims to evaluate the clinical course of pediatric patients with neurogenic bladder in Sana’a city, Yemen. Patients and Methods: This multicentric cross-sectional descriptive study was conducted between January and December 2024 across multiple hospitals and specialized clinics in Sana’a city. Children aged 2–15 years with confirmed neurogenic bladder were included. Data collected comprised demographic characteristics, etiology, neurological and lower urinary tract manifestations, management strategies, history of urinary tract infections, renal function parameters, and imaging findings. Renal function was assessed using serum creatinine and estimated glomerular filtration rate, while radiological evaluation was based on ultrasound. Results: A total of 54 children were included, with a mean age of 8.60 ± 3.18 years; 53.7% were females. Myelomeningocele was the most common etiology (57.4%). All patients presented with lower urinary tract symptoms and recurrent urinary tract infections. Hydronephrosis was present in all patients, and vesicoureteral reflux was detected in 92.6%, predominantly bilateral. Renal impairment was universal, with 90% of patients diagnosed with chronic kidney disease and 5.6% requiring regular dialysis. Clean intermittent catheterization was underutilized, while indwelling catheterization and vesicostomy were frequently employed. Conclusion: Pediatric neurogenic bladder in Yemen is associated with a high burden of renal morbidity, largely due to delayed diagnosis and suboptimal early bladder management. Early detection, timely initiation of clean intermittent catheterization, and structured multidisciplinary follow-up are essential to preserve renal function and prevent progression to chronic kidney disease.

Abstract: Background/Objectives: Immunoglobin A nephropathy (IgAN) is a type of chronic kidney disease (CKD) and the most common cause of kidney failure in patients <40 years of age. Previous economic models in CKD have generally defined health states solely by the progression of CKD. This manuscript presents an alternative method which also considers the level of proteinuria in a CKD patient. Methods: A cohort-level state transition model was developed comparing the health benefits of sparsentan, a dual endothelin angiotensin receptor antagonist, to irbesartan, an angiotensin receptor blocker, in IgAN. Within four UP/C (proteinuria) states, patients are assigned to three sub-health states according to CKD stage. Patients with end-stage renal disease are grouped together irrespective of UP/C, and are stratified instead by renal replacement therapy modality. Transition matrices are derived from a combination of data from PROTECT, a clinical trial comparing sparsentan to irbesartan, and the UK RaDaR registry. Health-related quality of life data from a general CKD population is used as a proxy. Results: Patients with IgAN who were modelled to receive treatment with sparsentan had estimated total undiscounted life years of 25.5 years, a gain of 0.9 years in comparison with irbesartan. Patients were also more likely to spend more time in earlier CKD stages while pre-ESRD. This translated to significant quality adjusted life year gains for patients treated with sparsentan in comparison with irbesartan. Conclusions: This study presents a new structure for health economic models in IgAN that more comprehensively captures the effect of proteinuria in combination with CKD progression. This new approach ultimately allows for the more robust implementation of clinical trial data in IgAN and estimates of the cost-effectiveness of new treatments.