To our knowledge, no studies have defined and classified RUC as mimicking RCC. Aside from that, this study provided a new approach for diagnostic reference. The present predictive model could imply the presence of RUCs before surgery. The predictors from clinical data and CT findings assisted in distinguishing RUC from ccRCC.
This study illustrated that RUC was more likely to present infiltrative growth using renal parenchyma as the frame (bean shape) (Fig. 2c, d and Fig. 4). In contrast, the dominantly expanded tumor (ball shape) was more common in ccRCC (Fig. 5a-d). These results were consistent with previous reports [12, 18, 19]. The cyst-solid lesions were found uncommon in both RUC and ccRCC. Since multi-RUC with hydronephrosis displayed a cyst-solid lesion of the kidney, it was essential to distinguish it from the cystic-dominant ccRCC. The cyst-solid lesions of multi-RUCs were caused by multiple tumors, renal sinus walls, and hydronephrosis (Fig. 2e, f, and Fig. 4), which were also found by Prando et al. [8]. The cyst-solid ccRCC was composed of necrosis, cystic degeneration, and solid component, usually without hydronephrosis (Fig. 5). Most cyst-solid ccRCCs were exophytic and easy to be distinguished from RUCs (Fig. 5a, b). Endophytic cyst-solid ccRCCs having clear boundaries with heterogeneous solid components and noticeable enhancement were also easily distinguished from RUC (Fig. 5c, d). However, it was challenging to distinguish multi-RUCs with hydronephrosis from other endophytic cyst-solid ccRCCs (Fig. 2e, f and Fig. 5e, f).
In addition, due to infiltrative growth of RUC in the renal parenchyma, the renal contour, even for exophytic RUC, was maintained (Fig. 2c, d), whereas the ccRCC commonly deformed renal contour due to expansive growth (Fig. 5a, b). RUC was more prone to hydronephrosis due to the close relationship with the collecting system (Fig. 2, 4, and 6), which was consistent with findings from Prando et al. [8] and Chen et al. [15, 16]. In this study, the attenuation of RUC (Fig. 2, 4, 6) was lower than that of ccRCC (Fig. 5), with less heterogeneous enhancement as reported [12, 13]. This might attribute to the poor blood supply and limited possibilities of necrosis in RUC. Some scholars believed that necrosis and heterogeneous enhancement increased with larger ccRCC [30, 36, 37]. Additionally, the present study found that patients with RUC were more susceptible to hematuria due to its high possibility of urothelium invasion.
Although some features were excluded in the construction of the predictive model, such as age, CP, NP, and EP for the avoidance of overfitting; location and pseudo-capsular sign were excluded for predictor screening, they still represented positive function in differentiating RUC from ccRCC. In this study, patients with ccRCC were younger than those with RUC, similar to results from previous reports [12, 13, 15, 16]. Different from the report of Bata et al. (Only in CP and NP, the attenuation of ccRCC was significantly higher than RUCs’) [13], the attenuation of ccRCC (Fig. 5) was significantly higher than that of RUC (Fig. 2, 4, and 6) for each dynamic contrast-enhanced phase in our study. RUC was more likely to occur in the renal pelvis than in the calyces (Fig. 2a, b), and ccRCC were exophytic renal tumors for most cases (Fig. 5a, b), which were consistent with previous reports [12]. It is worth mentioning that pseudo-capsule signs were noted in 4 RUCs in this study (Fig. 6). Chen et al. reported a pseudo-sign in an RUC case with a kidney rupture [15]. Moreover, Chen et al. have also reported a pseudo-capsule sign in endophytic RUC [16]. The pseudo-capsule sign for the endophytic RUC case differed from that of RCC (Fig. 5a-d). However, this sign for the exophytic low-grade RUC might be similar to that of RCC (Fig. 6d, e). The former RUC cases were related to the compression of renal pelvis fat. The latter RUC cases might be ischemic necrosis led by the deposition of fibrous tissue after compression (Fig. 6a, b, c) [38].
Some characteristics of RUCs in our study were different from previous literature. The presence of nephrolith, hydronephrosis, flank pain, hematuria, and the cyst-solid lesion was not found in previous research articles [12, 18, 19], except Chen et al. [15, 16]. These consistencies might be attributed to different populations, lifestyles, and large lesions analyzed in this study. Besides, the incidence of CSI in ccRCC of ours seemed higher than those of reports. One reason may be that the previous reports are only about the incidence of CSI in RCC [14, 17]. RCC includes many histological types except ccRCC. Furthermore, the population in our study may be different from others.
This study had certain limitations. First, the sample size of RUC mimicking RCC remained small compared to that of ccRCC, which would be determined by the incidence of these two diseases. Second, it only demonstrated the clinical and CT characteristics of RUC and ccRCC without including other RCC subtypes in this study. Third, this study only focused on the diagnostic task of ccRCC and RUC without obtaining direct data for prognostic analysis.