Marios Stavropoulos

Background and Clinical Significance: Spontaneous renal forniceal rupture is an uncommon complication of obstructive uropathy and is classically associated with ureteric calculi rather than distal urinary retention. Bilateral retention-related rupture appears to be exceptionally rare and may be diagnostically challenging when renal function begins to improve after bladder decompression; Case Presentation: An 82-year-old man with a history of prostate cancer treated five years earlier with external beam radiotherapy and androgen deprivation therapy presented with acute abdominal pain radiating to both flanks and inability to void. Bedside ultrasonography showed urinary retention and bilateral hydronephrosis, and a 16-Fr Foley catheter drained 900 mL of urine. Admission evaluation showed severe acute kidney injury, microscopic hematuria, minimal leukocyturia, and elevated inflammatory markers. Post-obstructive diuresis developed after bladder decompression. CT urography with excretory-phase imaging on hospital day 3 demonstrated severe bilateral hydroureteronephrosis with bilateral renal forniceal rupture and associated urinomas, including a larger left-sided collection extending toward the psoas compartment. Bilateral percutaneous nephrostomies were placed on hospital day 4 for upper-tract diversion. Immediate nephrostography showed no active contrast extravasation. At one-month follow-up, combined CT and nephrostographic assessment confirmed complete resolution of the bilateral urinomas without persistent leak, and the nephrostomy tubes were removed; Conclusions: This case suggests that urinary retention in an older man with prior prostate radiotherapy may reflect radiation-associated outlet pathology and/or impaired detrusor function rather than simple prostate enlargement. Delayed-phase CT urography was essential for diagnosis, and active bilateral diversion was justified by bilateral rupture, acute kidney injury, and the extent of urinary extravasation. The report expands the limited PubMed-indexed literature on retention-related upper urinary tract rupture and supports cautious follow-up aimed at defining the underlying mechanism of retention.

Male infertility contributes substantially to couple infertility, and a large proportion of cases remain idiopathic. Dysbiosis within the gut, seminal, and urinary microbiomes has been associated with impaired semen parameters, reproductive tract inflammation, and oxidative stress. This narrative review, informed by a structured literature search, summarizes current evidence for the gut–testis axis and the androbactome in male infertility and discusses mechanistic pathways linking microbial imbalance to sperm dysfunction. Proposed mechanisms include immune activation, increased oxidative stress, endocrine and metabolic perturbations, and disruption of epithelial barriers, including the blood–testis barrier. Early clinical trials report that selected probiotic or synbiotic formulations may be associated with improvements in one or more World Health Organization (WHO) semen parameters and with reductions in oxidative or inflammatory biomarkers (surrogate laboratory endpoints; pregnancy and live-birth outcomes are rarely reported and remain unproven) in selected populations, such as idiopathic infertility and the post-varicocelectomy setting. Given patient heterogeneity, a personalized approach requires prespecified clinical phenotypes and measurable monitoring targets, rather than indiscriminate supplementation. At present, probiotics should be considered an adjunct rather than a stand-alone therapy. Well-designed, contamination-aware microbiome studies and adequately powered randomized trials with clinically meaningful endpoints, including pregnancy and live birth, are required before routine clinical implementation. This synthesis is intended to support personalized counseling and trial design by clarifying candidate phenotypes, appropriate monitoring endpoints, and realistic limitations of current evidence.

The relationship between chronic kidney disease (CKD) and renal cell carcinoma (RCC) is both bidirectional and multifactorial. Several risk factors, including hypertension, diabetes mellitus, obesity, and smoking, have been associated with an increased risk for the development of CKD and RCC. CKD may predispose individuals to RCC through various mechanisms, including renal cystic diseases or induced oxidative stress effects. Conversely, RCC can induce CKD through the direct effects of the tumor, after surgeries for the management of the tumor (either partial or radical nephrectomy), and through perioperative acute kidney injury. Furthermore, medical interventions, including immunotherapy or targeted therapies, may precipitate acute kidney injury, potentially leading to the development of CKD. The expression of several genes in renal tissues has been related to the remodeling of kidneys during end-stage kidney disease and with an increased risk of the development of preneoplastic lesions and tumors. The aim of this review is to update the knowledge of these relationships, highlight the pathophysiologic mechanisms, and identify the genes and molecular expressions involved in this pathway.

Prostate cancer (PCa) is the second most frequently diagnosed malignancy in men worldwide. Although traditionally considered a disease of older men, the incidence of early-onset PCa (diagnosis < 55 years) is steadily rising. Advances in screening and therapy have significantly improved survival, creating a growing cohort of younger survivors for whom post-treatment quality of life—notably reproductive function—is paramount. Curative treatments such as radical prostatectomy, pelvic radiotherapy, androgen-deprivation therapy (ADT), and chemotherapy often cause irreversible infertility via multiple mechanisms, including surgical disruption of the ejaculatory tract, endocrine suppression of spermatogenesis, direct gonadotoxic injury to the testes, and oxidative sperm DNA damage. Despite these risks, fertility preservation is frequently overlooked in pre-treatment counseling, leaving many patients unaware of their options. This narrative review synthesizes current evidence on how PCa therapies impact male fertility, elucidates the molecular and physiological mechanisms of iatrogenic infertility, and evaluates both established and emerging strategies for fertility preservation and restoration. Key interventions covered include sperm cryopreservation, microsurgical testicular sperm extraction (TESE), and assisted reproductive technologies (ART). Psychosocial factors influencing decision-making, novel biomarkers predictive of post-treatment spermatogenic recovery, and long-term offspring outcomes are also examined. The review underscores the urgent need for timely, multidisciplinary fertility consultation as a routine component of PCa care. As PCa increasingly affects men in their reproductive years, proactively integrating preservation into standard oncologic practice should become a standard survivorship priority.

Male infertility is an under-recognized global health burden. Accumulating evidence position the intestinal microbiota as a pivotal regulator of testicular function, underpinning the emerging gut microbiota–testis axis. This narrative review introduces the conceptual term “androbactome”, referring to gut microorganisms and microbial genes that are hypothesized to influence androgen biosynthesis, spermatogenesis, and broader reproductive endocrinology. The documented worldwide decline in sperm concentration heightens the urgency of clarifying microbe-mediated influences on male reproductive capacity. The synthesis of preclinical and clinical findings reveals four principal pathways by which dysbiosis compromises fertility: systemic inflammation, oxidative stress, endocrine disruption, and epigenetic alteration. Lipopolysaccharide-driven cytokinaemia, reactive oxygen species generation, hypothalamic–pituitary–gonadal axis suppression, and aberrant germ cell methylation collectively impair sperm quality and hormonal balance. Short-chain fatty acids, secondary bile acids, and indole derivatives emerge as pivotal messengers within this crosstalk. Therapeutic approaches targeting the androbactome, namely dietary optimization, probiotic or prebiotic supplementation, and fecal microbiota transplantation, have demonstrated encouraging improvements in sperm parameters and testosterone levels, yet the causal inference is constrained by predominantly cross-sectional designs and limited long-term safety data. Recognizing the androbactome as a modifiable determinant of male fertility may open new avenues for personalized diagnosis, risk stratification, and adjunctive therapy in regard to idiopathic infertility. The integration of multi-omics platforms to characterize microbial and metabolomic signatures promises to enrich diagnostic algorithms and guide precision interventions, but rigorously controlled longitudinal and interventional studies are required to secure a translational impact.

Background/Objectives: Benign prostatic hyperplasia (BPH) is a common urological condition that can significantly impair quality of life in aging men by causing lower urinary tract symptoms (LUTS), including nocturia, weak stream, and incomplete emptying. While pharmacotherapy and surgical approaches such as transurethral resection of the prostate (TURP) remain cornerstone treatments, minimally invasive surgical therapies (MISTs) have emerged to bridge the gap between long-term medication use and invasive surgery. This narrative review assesses Rezūm therapy (water vapor thermal therapy, WVTT) by examining its mechanism of action, clinical efficacy, safety profile, and place in the BPH treatment algorithm. Methods: This narrative review synthesizes evidence from randomized controlled trials (RCTs), prospective studies, real-world cohorts, and published systematic reviews with meta-analyses to provide a comprehensive evaluation of Rezūm therapy for BPH. Key outcomes assessed include changes in International Prostate Symptom Score (IPSS), urinary flow rates, retreatment rates, adverse events, and sexual function preservation. Results: Across multiple studies, Rezūm significantly reduces IPSS (typically by ≥50%) and increases peak urinary flow by 4–5 mL/s. These improvements are durable, with five-year follow-up data showing low retreatment rates of approximately 4–5% and sustained symptom relief. The procedure, performed under local or minimal anesthesia, has a favorable safety profile: most adverse events are mild or transient, and notable complications, such as bleeding requiring transfusion or persistent sexual dysfunction, are rare. Importantly, Rezūm preserves both erectile and ejaculatory function in most patients, setting it apart from many traditional surgical interventions associated with higher sexual side effect rates. Conclusions: Rezūm is an effective and minimally invasive alternative for men with moderate prostatic enlargement who desire durable symptom improvement while avoiding the morbidity and sexual side effects associated with more invasive surgery. Future research should aim to further refine patient selection and assess long-term outcomes in broader populations.

Male infertility is a prevalent condition affecting approximately 15% of couples worldwide. Recent evidence indicates that, beyond its immediate reproductive implications, male infertility may reflect broader health concerns. Large-scale cohort studies consistently show that men with poorer semen parameters have elevated all-cause mortality compared to fertile counterparts, with a dose-dependent pattern whereby more severe abnormalities correlate with a higher risk of early death. Proposed mechanisms linking infertility to reduced life expectancy encompass genetic, hormonal, and lifestyle factors. For instance, Klinefelter syndrome exemplifies a genetic cause of azoospermia that also predisposes to metabolic syndrome, diabetes, and certain malignancies. Low testosterone, a frequent finding in testicular dysfunction, is implicated in obesity, insulin resistance, and cardiovascular disease, all of which can shorten lifespan. Additionally, psychosocial stress and depression—commonly reported among infertile men—may contribute to health-compromising behaviors. Environmental exposures and socioeconomic factors further compound these risks. Collectively, these data underscore the importance of recognizing male infertility as an early indicator of potentially modifiable health vulnerabilities. A comprehensive evaluation of infertile men should therefore extend beyond fertility assessments to include screening for chronic diseases, hormonal imbalances, and mental health issues. Targeted surveillance for specific cancers (e.g., testicular and prostate) and early interventions—such as lifestyle modifications, appropriate hormonal therapies, and psychosocial support—can improve both reproductive outcomes and long-term well-being. Given these insights, male fertility assessment may serve as a valuable gateway to broader men’s healthcare, prompting proactive strategies that mitigate associated risks and potentially enhance longevity.

Background/Objectives: Benign prostatic hyperplasia (BPH) is among the most common conditions affecting men as they age, resulting in lower urinary tract symptoms (LUTS) that can profoundly impact quality of life. While historically attributed primarily to androgenic imbalances, current evidence implicates additional factors—particularly oxidative stress (OS) and chronic inflammation—in BPH pathogenesis. This review aims to synthesize research on the interplay between OS, inflammation, and hormonal regulation in BPH, emphasizing their clinical relevance and potential therapeutic implications. Methods: A comprehensive review of peer-reviewed literature was conducted focusing on mechanistic studies, clinical trials, and observational reports. Searches included data on ROS generation, antioxidant capacity, inflammatory mediators, and their contribution to pathological prostatic overgrowth. Potential interventions targeting OS—such as antioxidant supplementation, anti-inflammatory drugs, vitamin D receptor agonists, and phytotherapeutics—were also evaluated for their efficacy and safety profiles. Results: Chronic inflammation and OS were consistently identified within hyperplastic prostate tissue. Excessive ROS production, diminished antioxidant defense, and sustained cytokine release create a proproliferative and antiapoptotic environment, accelerating disease progression. Metabolic comorbidities (e.g., obesity, insulin resistance) further exacerbate these imbalances. Standard therapies (α-blockers and 5-ARIs) effectively relieve symptoms but do not directly address the oxidative–inflammatory axis. Emerging evidence suggests that pharmacological and dietary approaches targeting OS and inflammation may reduce prostate volume expansion and alleviate LUTS. Conclusions: Findings indicate that OS and inflammation are key contributors to BPH progression. Incorporating antioxidant and anti-inflammatory strategies alongside conventional treatments holds promise for improving clinical outcomes and patient quality of life. Future research should focus on validating OS-specific biomarkers and optimizing personalized therapy regimens.

Erectile dysfunction (ED) is a prevalent male sexual disorder characterized by the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance. While its etiology is multifactorial, encompassing vascular, neurological, hormonal, and psychological components, emerging evidence suggests a significant role for gut microbiota dysbiosis in its development. The gut microbiota influences various metabolic, inflammatory, and neuropsychological processes critical to erectile function. Dysbiosis can lead to systemic inflammation, endothelial dysfunction, hormonal imbalances, and altered neurotransmitter production, all of which are key factors in ED pathogenesis. This narrative review synthesizes current research on the association between gut microbiota alterations and ED, highlighting specific bacterial taxa implicated in ED through mechanisms involving inflammation, metabolic disturbances, and hormonal regulation. This review explores potential mechanisms linking gut microbiota and ED, including pro-inflammatory cytokines, gut barrier integrity disruption, metabolic disorders, psychological factors via the gut–brain axis, and hormonal regulation. Furthermore, the gut microbiota offers promising avenues for developing non-invasive biomarkers and therapeutic interventions such as probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation. Future research should focus on longitudinal studies, mechanistic explorations, and clinical trials to validate these findings and translate them into clinical practice. Understanding the interplay between the gut microbiota and erectile function could unveil novel diagnostic biomarkers and pave the way for innovative treatments targeting the microbiota, ultimately improving men’s sexual and overall health.

Background/Objectives: Varicoceles are a common contributor to male infertility, significantly impacting male-factor infertility cases. Traditional diagnostic methods often lack the sensitivity to detect the molecular and cellular disruptions caused by varicoceles, limiting the development of effective, personalized treatments. This narrative review aims to explore the advancements in proteomics and metabolomics as innovative, non-invasive diagnostic tools for varicocele-associated male infertility and their potential in guiding personalized therapeutic strategies. Methods: A comprehensive literature search was conducted using databases such as PubMed, Scopus, and Web of Science up to October 2024. Studies focusing on the application of proteomic and metabolomic analyses in varicocele-associated male infertility were selected. The findings were critically analyzed to synthesize current knowledge and identify future research directions. Results: Proteomic analyses revealed differentially expressed proteins in the sperm and seminal plasma of varicocele patients, revealing disruptions in pathways related to oxidative stress, mitochondrial dysfunction, apoptosis, and energy metabolism. Key proteins such as heat shock proteins, mitochondrial enzymes, and apoptotic regulators were notably altered. Metabolomic profiling uncovered specific metabolites in seminal plasma—such as decreased levels of lysine, valine, and fructose—that correlate with impaired sperm function and fertility potential. The integration of proteomic and metabolomic data provides a comprehensive molecular fingerprint of varicocele-induced infertility, facilitating the identification of novel biomarkers for early diagnosis and the development of personalized therapeutic interventions. Conclusions: Advances in proteomics and metabolomics have significantly enhanced our understanding of the molecular mechanisms underlying varicocele-associated male infertility. These “omics” technologies hold great promise for improving diagnostic accuracy and personalizing treatment, ultimately leading to better outcomes for affected men. Future large-scale clinical trials and validations are essential to confirm these biomarkers and facilitate their integration into routine clinical practice.