Background: A high incidence of upper urinary tract urothelial carcinoma has been reported in the southwestern area of Taiwan, where arsenic water contamination was considered the main cause. However, there is no definite proof to show a correlation between arsenic water contamination and upper urinary tract urothelial carcinoma. To investigate the clinical and epidemiological features of patients with upper urinary tract urothelial carcinoma between arsenic water endemic and non-endemic areas, we analyzed patients in terms of characteristics, stratified overall survival, disease-free survival, and cancer-specific survival. Methods: The records of a total of 1194 patients diagnosed with upper urinary tract urothelial carcinoma were retrospectively reviewed. Clinical data and current medical status were collected from the medical records. Statistical analyses were performed to determine the clinical variables and stratified survival curves between endemic and non-endemic groups. Results: Female predominance was revealed in both endemic and non-endemic groups (male:female ratio = 1:1.2–1.4). No statistical differences were found in histological types, staging, and tumor size between the two groups. Nonetheless, patients with characteristics of aging and having end-stage renal disease were outnumbered in the non-endemic group, while a higher prevalence of previous bladder tumors and more ureteral tumors were found in the endemic group. Adjusted stratified cumulative survival curves suggested a poorer prognosis in endemic patients, especially in disease-free survival of early stage disease. Conclusions: A higher mortality rate with more previous bladder cancer history and ureteral tumors was seen in patients with upper urinary tract urothelial carcinoma residing in the arsenic water contamination area. This may be attributed to the long-term carcinogenic effect of arsenic underground water.

Urosepsis is a potentially life-threatening condition caused by urinary tract infections and is usually associated with urolithiasis-induced obstruction. No established guidelines exist regarding the optimal timing of antibiotic administration, appropriate duration of urinary drainage, or scheduling of definitive ureteroscopic lithotripsy (URSL) in patients with urolithiasis-induced obstructive acute pyelonephritis (APN). Therefore, this study aimed to investigate the key factors influencing the management of urosepsis secondary to upper ureteral stones, specifically focusing on the optimal duration of antibiotic therapy, risk factors for post-URSL fever, and timing of percutaneous nephrostomy (PCN) drainage to improve clinical outcomes. This retrospective study included 107 patients with urolithiasis-induced obstructive APN complicated by urosepsis who underwent treatment between 2013 and 2019. These patients underwent PCN drainage, followed by URSL. Data on patient demographics, comorbidities, laboratory results, microbiological cultures, and stone characteristics were obtained and analyzed. Among the 107 patients, 34 (32%) had post-URSL fever. The afebrile group received longer antibiotic therapy (7.1 vs. 5.7 days, p = 0.022) and had shorter postoperative hospital stays (3.1 vs. 5.3 days, p = 0.015). Logistic regression analysis showed that antibiotic duration and the interval from PCN to URSL were significant predictors of fever. Diabetes mellitus was a significant risk factor for post-URSL fever in patients treated with antibiotics for more than 7 days (odds ratio = 9.07, p = 0.03). Emergent PCN insertion was associated with earlier URSL and a shorter hospital stay. This study emphasizes the importance of determining the optimal duration of antibiotic therapy before URSL in patients with urosepsis complicated by upper ureteral stones. Post-URSL fever correlates with a shorter duration of antibiotic therapy, and emergent PCN insertion results in earlier URSL and a shorter hospital stay. Diabetes mellitus significantly predicted post-URSL fever.

Rationale: Xanthogranulomatous pyelonephritis (XGPN) is a form of chronic pyelonephritis caused by chronic calculus obstruction and bacterial infection, leading to the destruction of the renal parenchyma and calyces. Conservative treatment is usually not sufficient, and surgical intervention is still the main curative approach. XGPN with transdiaphragmatic extension and lung abscess formation is a rare condition. Patient concerns: We report a 64-year-old woman who presented with persistent productive cough. Diagnoses: Lung abscess secondary to XPGN. Both nephrostomy urine and sputum cultures showed Proteus mirabilis infection with the same antibiotic sensitivity spectrum, but blood culture was negative. Interventions: Laparoscopic radical nephrectomy and prolonged antibiotic treatment. Outcomes: The lung abscess and cough gradually resolved in 1 month after nephrectomy. Conclusion: Lung abscess secondary to transdiaphragmatic extension of XGPN is rare but should be considered in patients with lower lung infections that are unresponsive to treatment, especially infections due to unusual respiratory pathogens such as P mirabilis.

Rationale: Bladder calcification is a rare presentation that was first interpreted to be related to a urea-splitting bacterial infection. Aside from infection, other hypotheses such as schistosomiasis, tuberculosis, cancer, and cytokine-induced inflammatory processes have also been reported. Severe coronavirus disease 2019 (COVID-19) is known for its provoking cytokine storm and uninhibited systematic inflammation, and calcification over the coronary artery or lung has been reported as a long-term complication. Patient concerns: We presented a 68 years old man who had persistent lower urinary tract symptoms after recovery from severe COVID-19. No urea-splitting bacteria were identified from urine culture. Diagnosis: Cystoscopy examination revealed diffuse bladder mucosal and submucosa calcification. Interventions: Transurethral removal of the mucosal calcification with lithotripsy. Outcomes: The patient’s lower urinary tract symptoms improved, and stone analysis showed 98% calcium phosphate and 2% calcium oxalate. No newly formed calcifications were found at serial follow-up. Conclusion: Diffuse bladder calcification may be a urinary tract sequela of COVID-19 infection. Patients with de novo lower urinary tract symptoms after severe COVID-19 should be further investigated.