Renal cell carcinoma (RCC) is one of the most prevalent tumors in the urinary system, and the incidence of RCC is on the rise, resulting in 13,920 estimated deaths in the United States in 2022 [1]. About 75% of RCC cases are clear cell renal cell carcinoma (ccRCC), which leads to most RCC-related deaths [2]. Up to 13.3% of RCC patients would develop venous tumor thrombosis, which is one of the most challenging diseases in urology [3]. Surgical resection was the preferred treatment for locally advanced RCC complicated with tumor thrombus [4]. Even after curative resection, 57% of patients with RCC and tumor thrombus would develop tumor recurrence and metastasis, resulting in a 5-year over-survival (OS) rate of 39% [5]. Therefore, it is urgently needed to identify patients with poor prognoses who may benefit from early systemic treatment.

Biomarkers could help identify patients with poor prognoses and help determine who will benefit from systematic treatment and who may avoid unnecessary treatment to spare side effects and high economic burden [6]. Multiple molecular biomarkers could help evaluate the progression and prognosis of RCC, in which Ki-67 is one of the most popular biomarkers [7,8]. Ki67 is a well-known proliferation marker for the evaluation of cell proliferation and plays a critical role in mitosis throughout the cell cycle [7]. Ki67 continues to degrade during G0 and G1 and continues to produce from phase S until mitotic exit [7]. Ki-67 was considered to be a reliable biomarker and has been used in routine clinical practice [6,9]. In recent years, Ki-67 has received increasing attention as an attractive prognostic marker and potential therapeutic target in malignant tumors [10,11]. Ki-67 index was reported to be positively correlated with advanced tumor stage in renal cell carcinoma [12]. Furthermore, new treatment strategies based on the therapy targeting proliferative nuclear marker (Ki-67) hold promise for providing priority/personalized treatment options for improving the survival and prognosis of RCC [13]. However, the cut-off values of Ki-67 differed among the studies [12,[14], [15], [16], [17], [18]], and there was no well-defined threshold to distinguish patients’ survival. In addition, no study has focused on the prognostic value of Ki-67 in ccRCC and tumor thrombus.

Therefore, we conducted this study to determine the optimal cut-off value to stratify the prognosis of patients with ccRCC and tumor thrombus. Furthermore, we explored the relationship between Ki-67 expression and pathological characteristics of ccRCC and tumor thrombus.