Main Pathological Changes of Benign Ureteral Strictures

Abstract

ObjectiveTo identify the pathological classification of benign ureteral strictures according to the histological features and explore the relationship between various pathological types and inflammatory cells, fibroblasts, and collagen.Patients and MethodsThirty one specimens from patients diagnosed with ureteral strictures between 2013 and 2021 were included and classified according to the histopathological characteristics. The number of fibroblasts and inflammatory cells was counted, and the proportion of type I and type III collagen in ureteral stricture tissues was detected by picrosirius red staining.ResultsWe identified three types of benign ureteral strictures in 31 specimens: inflammatory cell infiltration (n = 10, 32%), fibroplasia (n = 14, 45%), and hyalinization (n = 7, 23%), with significant differences in obstruction history and hydronephrosis grades among the three types. The number of inflammatory cells (lymphocytes, neutrophils and eosinophils) was significantly lower in hyalinization ureteral strictures than in the other two types (p < 0.05). The number of foreign-body giant cells associated with foreign-body reactions increased significantly in suture-induced ureteral strictures (p < 0.05). Fibroplasia type had the largest number of fibroblasts, whereas the other two types had smaller numbers. The results of type I and III collagen analysis showed that type I and III collagen were the most abundant in hyalinization among all ureteral stricture types (p < 0.05). Compared to ureteral strictures, the content of type I and III collagen in atresia increased significantly (p < 0.05).ConclusionCommon pathological types of benign ureteral strictures include inflammatory cell infiltration, fibroplasia, and hyalinization. Changes in type I and III collagen, inflammatory cells, and fibroblasts in different pathological types may be related to the progression of ureteral strictures.

The Degree of Hydronephrosis as an Indicator of the Necessity for Ureteric Dilatation during Ureteroscopic Lithotripsy

“…The identification of a lesser degree of HN as a risk factor for difficult ureter (DU) is thought to be related to the pathologic change in the ureter itself. In previous studies dealing with ureter pathology in difficult ureter [18,19], the pathology of ureter stricture has been reported to be related to inflammation, fibroplasia, hyalinization [18], polyp or granulation tissue growth secondary to stone, or other benign or neoplastic cause stricture [19]. In this study, a lesser degree of HN was identified as a risk factor for difficult ureter (DU), which is considered to be related to pathologic changes in the ureter itself, not to stone-related factors or clinical factors.…”

“…In this study, a lesser degree of HN was identified as a risk factor for difficult ureter (DU), which is considered to be related to pathologic changes in the ureter itself, not to stone-related factors or clinical factors. Although additional studies are needed, a low degree of HN can also be considered an indicator of ureter pathologic changes, as shown in the studies [18,19]. In addition, HN has been identified as a risk factor for DU, making surgery more difficult and resulting in worse outcomes.…”

“…In this study, only a rigid ureteroscope was used; however, in previous studies, a flexible scope and semirigid ureteroscope were used together. In this study, as in the study dealing with the pathophysiology of the ureter stricture itself [18,19], difficult ureter (DU) was thought to be related to the pathology of the ureter itself rather than a clinical, epidemiologic, or stone-related factor. This is why the results are different from previous studies dealing with difficult ureter (DU) [13][14][15].…”