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INTRODUCTION AND IMPORTANCE: Giant bladder stones, exceeding 100 g, are rare and typically affect males. This report describes an atypical case of a 35-year-old female with a 560-g bladder stone causing acute kidney injury without evidence of upper urinary tract stones. CASE PRESENTATION: A 35-year-old female presented with pelvic pain and urinary retention. Comprehensive imaging, including a KUB x-ray and subsequent ultrasound, revealed a giant bladder stone obstructing the ureters and causing bilateral hydronephrosis. Urinalysis showed a severe urinary tract infection. Given the stone's significant size and its firm attachment to the bladder wall, open cystolithotomy was performed. The patient recovered well and was subsequently discharged without postoperative complications. CLINICAL DISCUSSION: Giant bladder stones are rare in young females. This case highlights the uncommon presentation of a 560-g stone in a female, causing acute kidney injury while there were no upper tract stones detected. The role of urinary tract infection as a contributing factor is explored, although other etiological factors are also considered. CONCLUSION: Open cystolithotomy proved to be an effective treatment. Postoperative recommendations included dietary modifications to minimize the risk of recurrence. This case expands our knowledge of giant bladder stones in this population.
RESUMO
AIM: We investigate and compare the possible antitumor activity of clinically used angiotensin converting enzyme (ACE) inhibitors; captopril, perindopril and angiotensin II type 1 receptor (AT1R) blocker, losartan against hepatocarcinogenesis initiated by diethylnitrosoamines (DENA) and promoted by carbon tetrachloride (CCl(4)). MAIN METHODS: Diethylnitrosamine (DENA) (200mg/kgi.p.) initiated and carbon tetrachloride (CCl(4)) (2ml/kgi.p.) promoted hepatocarcinogenesis in male Wistar rats after 8weeks. RESULTS: Hepatocarcinogenesis was manifested biochemically by elevation of serum hepatic tumor markers tested; α-feto protein (AFP) and carcinoembryonic antigen (CEA). In addition, hepatic carcinogenesis was further confirmed by a significant increase in hepatic tissue growth factors; vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF). Moreover a marked increase in matrix metalloproteinase-2 and hydroxyproline content were also observed. Hepatocarcinogenesis was further confirmed by a significant decrease in hepatic endostatin and metallothonein level. KEY FINDINGS: Long-term administration of the selected drugs for 2weeks before and throughout the experimental period produced a significant protection against hepatic carcinogenesis. The present results claimed that different doses of the selected drugs succeeded in normalization of serum tumor markers. Furthermore, the drugs reduced the elevated level in the hepatic growth factors, matrix metalloproteinase-2 and hydroxyproline induced by the hepatocarcinogen. Moreover, the amelioration was also accompanied by augmentation of hepatic content of metallothionein and endostatin. Histopathological examination of liver tissues of rats treated with DENA-CCl(4) correlated with the biochemical observations. SIGNIFICANCE: These findings suggest a similar protective effect of ACE inhibitors; captopril; perindopril and AT1R blocker, losartan against premalignant stages of liver cancer in the DENA initiated and CCl(4) promoted hepatocarcinogenesis model in rats. Therefore, RAS especially angiotensin II (Ang II) and AT1R interaction plays a pivotal role hepatocarcinogenesis development.
