A man in his early 40s presented with acute right flank pain, vomiting and dysuria. Ultrasonography demonstrated an obstructing right upper ureteric calculus with a contralateral renal calculus. CT urography revealed fine, serpiginous contrast-opacified tubular channels extending from the right renal pelvis into the retroperitoneum without evidence of urinoma. Delayed excretory phase imaging demonstrated convergence towards the para-aortic region, consistent with pyelolymphatic backflow rather than collecting system rupture. The imaging pattern reflected markedly elevated intrarenal pressure and prompted urgent decompression. The patient underwent bilateral ureteric stenting followed by definitive endourological management with complete symptomatic resolution. Early recognition of this radiological entity prevents misdiagnosis and guides appropriate pressure-relieving intervention.

Failed ureteroscopic access (FA) in unstented patients remains a significant clinical challenge. We aimed to identify preoperative clinical, laboratory, and CT-based predictors of FA, determine optimal cutoff values, and develop a clinically applicable risk-stratification model. This prospective cohort study enrolled 141 consecutive patients with ureteral stones undergoing unstented ureteroscopy (83 semi-rigid, 58 flexible) at a tertiary center (January 2024-January 2025). Preoperative demographics, pain characteristics, inflammatory markers (TLC, ESR, CRP, procalcitonin), and NCCT parameters (stone size, density, ureteral wall thickness [UWT], perinephric fat stranding [PFS] grade, hydronephrosis grade, HU of hydronephrosis, renal parenchymal thickness) were compared between successful access (SA, n = 112) and failed access (FA, n = 29) groups. Firth's penalized logistic regression, ROC analysis with DeLong comparison, and decision curve analysis (DCA) were performed. FA occurred in 29 patients (20.6%). UWT demonstrated the highest discriminatory power (AUC 0.965; cutoff ≥ 2.7 mm; sensitivity 96.6%, specificity 99.1%), followed by PFS grade (AUC 0.963; cutoff ≥ 2; sensitivity 100%, specificity 89.3%) and procalcitonin (AUC 0.957; cutoff ≥ 0.2 ng/mL). On Firth's penalized multivariate analysis, the primary two-variable Firth model identified UWT (OR 62.20 per mm; p < 0.001) and upper ureteral location (OR 14.27; p = 0.040) as independently associated with failed access (apparent AUC 0.986; 5-fold cross-validated AUC 0.967). The combined model achieved an AUC of 0.997 as an exploratory model with adequate calibration (Hosmer-Lemeshow test, p = 0.936). Exploratory DCA suggested potential net benefit across clinically relevant threshold probabilities. UWT ≥ 2.7 mm and PFS grade ≥ 2 on preoperative NCCT may be useful predictors of FA during unstented ureteroscopy, although these findings require external validation before clinical application. Incorporating these readily measurable CT parameters into a proposed preoperative risk-stratification algorithm may optimise surgical planning and patient counselling.

Individuals with disabilities who are unable to maintain oral intake are at high risk of inadequate oral hygiene because of reduced masticatory stimulation and impaired self-cleansing, leading to excessive dental calculus accumulation. However, the effects of this on tooth eruption are poorly understood. Herein, we report the case of an 18-year-old boy with CHARGE syndrome managed with gastrostomy feeding since childhood. Following prolonged inadequate oral care, severe dental calculus accumulated throughout the dentition. Thick calculi encased the mandibular right first and second deciduous molars, physically obstructing eruption of the permanent premolars. Because safe delivery of care could not be ensured under local anesthesia, treatment was performed under general anesthesia. Full-mouth scaling, mobile deciduous tooth extraction, and restorative procedures were performed. No periodontal pockets were observed, and radiographic assessment showed no alveolar bone resorption. After calculus removal, the impacted premolar erupted spontaneously within 2 months and had achieved complete eruption 8 months later. This case demonstrates that severe dental calculus accumulation can cause reversible eruption disturbances in children who do not receive oral intake. Early dental intervention, continuous oral hygiene management, and multidisciplinary care are essential for preventing oral and systemic complications in children with disabilities.

A man in his early 40s presented with urinary symptoms and was diagnosed with a right ureteric calculus, hydronephrosis and urinary tract infection. A non-contrast CT scan of the kidneys, ureters and bladder revealed an incidental pelvic mass in the rectovesical pouch, initially suspected as a gastrointestinal stromal tumour/fibroma. Multidisciplinary management prioritised cystoscopy-guided double-J stenting for obstruction and infection. In a second admission, ureteroscopic lithotripsy with stenting and a laparoscopic low anterior resection were planned simultaneously. Following ureteroscopic lithotripsy, diagnostic laparoscopy identified a large peritoneal loose body (PLB), which was retrieved laparoscopically, avoiding resection. Peritoneal loose bodies are extremely rare, benign entities prone to misdiagnosis as malignancy on imaging, leading to unnecessary major surgery and psychological distress. This case highlights the pathogenesis, clinical features, differential diagnoses and characteristic imaging findings of PLB, emphasising the value of preoperative recognition and diagnostic laparoscopy to prevent unnecessary major surgery.

Inguinal herniation of the bladder is a rare urologic occurrence, with intrascrotal bladder herniation containing calculi an exceptionally uncommon presentation. We report a 79-year-old African American man with chronic urinary retention and prior irradiation for prostate cancer who presented with a right inguinal hernia containing the majority of the bladder with intraluminal calculi. Intraoperatively, the bladder was found to be incarcerated despite a preoperative description as reducible. Despite proper anatomic restoration of the bladder, the patient failed a voiding trial at 2 months and suffered 3 hospitalizations over the follow-up period, highlighting the longer-term urologic sequelae of chronic bladder dysfunction.

Pancreatic neuroendocrine tumours (PNETs) are malignant processes and are identified as being the rarest of all pancreatic cancers. Here we present the case of a 62-year-old male with a background of chronic lymphocytic leukaemia (CLL) who was investigated over 18 months for progressive hepatic cystic lesions with no known aetiology. Imaging revealed main pancreatic duct dilatation without an identifiable intrinsic or extrinsic cause, coupled with enlarged mesenteric lymph nodes. Endoscopic ultrasound identified multiple cystic liver lesions of different sizes, some reflecting the presence of septations. The calibre of the main pancreatic duct was noted to be dilated in the absence of calculi, raising suspicion for a focal inflammatory process or chronic pancreatitis. Fine needle aspiration was performed from the pancreas, liver and lymph nodes; samples were sent for cytological analysis. This revealed the presence of a well-differentiated neuroendocrine tumour, WHO grade 2, across all three sites. The neuroendocrine multidisciplinary team (MDT) classified the tumor as stage T1N1M1a and recommended treatment with somatostatin analogue with palliative intent. This case reflects the diagnostic challenges of atypical PNET presentations and emphasises the crucial role of endoscopic ultrasound with tissue sampling in establishing a definitive diagnosis.

Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of metastatic non-small-cell lung cancer (NSCLC) but can cause a broad spectrum of immune-related adverse events (irAEs) affecting multiple organ systems. Although common irAEs are well characterized, immune-related cystitis is rare and may pose a significant diagnostic challenge, particularly when urine cytology demonstrates atypical urothelial cells that mimic high-grade urothelial carcinoma. We present the case of a 55-year-old man with metastatic squamous cell carcinoma of the lung who developed hematuria and non-bacterial cystitis during pembrolizumab therapy in the setting of multiple other irAEs, including hypophysitis resulting in secondary adrenal insufficiency and hypothyroidism. Following the onset of hematuria, computed tomography (CT) of the abdomen and pelvis demonstrated an acute cystitis picture. Importantly, there was no evidence of urinary calculi or progression of pelvic metastatic disease to otherwise explain his symptoms. Urine cytology subsequently showed marked urothelial atypia concerning for high-grade urothelial carcinoma, creating a significant diagnostic dilemma. Cystoscopic evaluation, however, revealed a normal bladder mucosa without erythema, lesions, or findings suggestive of carcinoma in situ; no biopsy was performed. The absence of an identifiable urothelial malignancy or bacterial infection, together with the temporal association with pembrolizumab and the patient's concurrent multisystem irAEs, supported an immune-related etiology. This case highlights the potential for ICI-associated cystitis to produce cytologic atypia that closely mimics high-grade urothelial carcinoma and underscores the importance of integrating cytomorphologic findings with clinical history, radiologic and cystoscopic findings, microbiologic studies, and treatment history to avoid misdiagnosis. Recognition of this rare irAE is essential for appropriate management and prevention of unnecessary interventions.

Excess adiposity and altered body fat distribution are increasingly recognized as important contributors to metabolic disorders, including kidney stone disease (KSD). However, how to best assess obesity-related KSD risk and the temporal relationship remain unclear. This 10-year retrospective longitudinal cohort study included participants undergoing annual health examinations. Data on demographics, KSD, and six anthropometric indices were collected. Cox regression stratified by sex was used. Model 1 examined the associations of baseline indices with 10-year incident KSD, while Model 2 examined the associations of the 5-year mean indices with incident KSD during years 6-10. Kaplan-Meier survival curves compared event-free probability. Restricted cubic spline regression assessed non-linear relationships. Sex-stratified 10-wave cross-lagged panel models examined overall adjacent-wave temporal associations between anthropometric indices and KSD across the ten annual assessments. A total of 24,418 participants were included. In Model 1, high baseline body mass index (BMI) was significantly associated with a higher 10-year risk of KSD among females (HR, 1.35; 95% CI, 1.03-1.78), while waist circumference (WC), waist-to-hip ratio (WHR), BMI, weight-adjusted-waist index (WWI) and body roundness index (BRI) were significantly associated with incident KSD in male participants (all HRs, 1.06-1.11; P<0.001). Survival analysis showed higher event-free probability in females with lower WHR and BMI (all P<0.05), and in males with lower BMI, WHR, WC, WWI, and BRI (all P<0.001). In Model 2, all indices except a body shape index (ABSI) were significantly associated with subsequent 5-year KSD risk in males (all P<0.001), whereas no significant associations in females. Cross-lagged panel analyses suggested significant temporal associations of WC, BMI, WWI, WHR, and BRI with subsequent KSD in males, whereas no such associations were observed in females. Sex-specific anthropometric patterns were observed in relation to KSD. Multiple indices of overall and central adiposity were consistently associated with KSD in males, whereas the associations were less consistent in females. Anthropometric indices alone may therefore be insufficient to characterize KSD risk in females, highlighting the potential contribution of additional metabolic, hormonal, and other sex-specific factors.

Randall's plaque (RP) consists of subepithelial hydroxyapatite (HAP) deposits within renal papillae and provides a well‑established attachment substrate for a subset of idiopathic calcium oxalate (CaOx) kidney stones. However, RP has traditionally been viewed as a passive mineral surface onto which crystals accrete, with comparatively less focus on the cellular and molecular events that build the plaque itself. The renal papillary interstitium has been indicated as a dynamic microenvironment that undergoes molecular remodeling during plaque‑associated mineralization. The present review aimed to organize the current evidence regarding interconnected processes that may overlap in vivo rather than occur in a fixed sequence. Physicochemical conditions in the inner medullary interstitium favor HAP nucleation and provide the foundation for plaque formation. Epithelial injury responses, regulated cell death, osteogenic‑like fibroblasts and immune remodeling may contribute to the development of a pro‑calcific microenvironment; however, the spatial relationship, temporal order and plaque specificity of these processes remain incompletely defined. Macrophage polarization may influence whether local crystal‑associated inflammation and mineralization are amplified or reduced. As interstitial HAP deposits enlarge and become exposed through focal disruption of the renal papillary epithelium, these deposits can interact with pelvic urine and support CaOx nucleation and overgrowth. Systemic metabolic abnormalities and urinary or gut microbiome alterations are associated with stone disease and may modify the papillary microenvironment; however, direct evidence that they alter human RP burden is lacking to date. Of note, available animal and cell models demonstrate selected aspects of mineralization or crystal injury but do not reproduce the chronic, progressive interstitial HAP plaque observed in humans. In conclusion, considering RP as an interstitial microenvironmental disorder may help identify potential biomarkers of early papillary remodeling and generate potential therapeutic strategies for stone prevention in the future.

BACKGROUND Thyrotoxicosis is associated with well-recognized and clinically significant complications, including congestive heart failure and cardiac arrhythmias. The relationship between hyperthyroidism and hepatic dysfunction is complex, with several proposed pathophysiological mechanisms; however, direct cholestatic injury is frequently overlooked. Although mild liver enzyme elevation is common in hyperthyroidism, clinically overt jaundice is rare. Nevertheless, increasing evidence from case reports and case series suggests that thyrotoxicosis, especially Graves disease, can result in cholestatic-pattern jaundice. This temporal association is supported by substantial improvements in jaundice and liver biochemistry after antithyroid therapy. CASE REPORT A 62-year-old woman presented with a 1-month history of right upper quadrant abdominal pain, unintentional weight loss, and jaundice. Laboratory evaluation demonstrated cholestatic-pattern liver injury, and abdominal ultrasound revealed a solitary gallstone without evidence of acute or chronic cholecystitis. Abdominal computed tomography demonstrated right-sided heart failure with pericardial and bilateral pleural effusions and congestive hepatopathy. Endoscopic retrograde cholangiopancreatography showed no filling defects, excluding biliary obstruction. Because the patient had persistent sinus tachycardia, thyroid function tests were performed. The findings were consistent with primary hyperthyroidism and elevated thyroid-stimulating hormone receptor antibodies); thyroid ultrasound and scintigraphy results supported toxic multinodular goiter. Treatment with methimazole led to dramatic improvement of the jaundice. Given the possibility of competing etiologies, thyrotoxicosis was considered the most likely contributing factor to cholestatic jaundice onset. CONCLUSIONS This case highlights the importance of considering hyperthyroidism in the differential diagnosis of jaundice, particularly in diagnostically challenging cases.