The purpose of this meta-analysis was to systematically assess the influence of three-dimensional (3D) printing technology in laparoscopic partial nephrectomy (LPN) of complex renal tumors. Methods: A systematic literature review was performed in June 2020 using the Web of Science, PubMed, Embase, the Cochrane library, the China National Knowledge Infrastructure (CNKI), and the Wanfang Databases to identify relevant studies. The data relative to operation time, warm ischemic time, intraoperative blood loss, positive surgical margin, reduction in estimated glomerular filtration rate (eGFR), and complications (including artery embolization, hematoma, urinary fistula, transfusion, hematuria, intraoperative bleeding, and fever) were extracted. Two reviewers independently assessed the quality of all included studies, and the eligible studies were included and analyzed using the Stata 12.1 software. A subgroup analysis was performed stratifying patients according to the complexity of the tumor and surgery type or to the nephrometry score. Results: One randomized controlled trial (RCT), two prospective controlled studies (PCS), and seven retrospective comparative studies (RCS) were analyzed, involving a total of 647 patients. Our meta-analysis showed that there were significant differences in operation time, warm ischemic time, intraoperative blood loss, reduction in eGFR, and complications between the LPN with 3D-preoperative assessment (LPN-3DPA) vs. LPN with conventional 2D preoperative assessment (LPN-C2DPA) groups. Positive surgical margin did not differ significantly. Conclusion: The LPN-3DPA group showed shorter operation time and warm ischemic time, as well as less intraoperative blood loss, reduction in eGFR, fewer complications for Jiang et al. 3D Printing and LPN patients with complex renal tumor. Therefore, LPN assisted by three-dimensional printing technology should be a preferable treatment of complex renal tumor when compared with conventional LPN. However, further large-scale RCTs are needed in the future to confirm these findings.

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Aim: To clarify the mechanism of NEAT1, an aberrantly upregulated lncRNA in Randall's plaques (RP) similar to biomineralization, in mediating osteogenic differentiation of human renal interstitial fibroblasts. Materials & methods: A comprehensive strategy of bioinformatic analysis and experimental verification was performed. Results: BMP2 silence abolished the osteogenic differentiation of human renal interstitial fibroblasts promoted by NEAT1. Mechanically, NEAT1 not only induced the nucleolar translocation of EGR1 binding to BMP2 promotor, but also functioned as a sponge of miR-129-5p in the cytoplasm to promote BMP2 expression. Moreover, there was a positive correlation between NEAT1 and BMP2 expression in RP instead of normal renal papilla. Conclusion: NEAT1 acted as a key mediator of BMP2 to promote human renal interstitial fibroblast osteogenic differentiation, through which NEAT1 might be involved in RP formation.

Background Randall’s plaques (RP) are identified as anchored sites for kidney calcium oxalate stones, but the mechanism remains unclear. Given the importance of osteogenic-like cells in RP formation and OCT4 in reprogramming differentiated cells to osteoblasts, the current study explored the potential role of OCT4 in RP formation. Methods OCT4 and biomineralization were evaluated in RP, and immunofluorescence co-staining was performed to identify these cells with alteration of OCT4 and osteogenic markers. Based on the analysis of tissue, we further investigated the mechanism of OCT4 in regulating osteogenic-like differentiation of primary human renal interstitial fibroblasts (hRIFs) in vitro and vivo. Results We identified the upregulated OCT4 in RP, with a positive correlation to osteogenic markers. Interestingly, fibroblast marker Vimentin was partially co-localized with upregulated OCT4 and osteogenic markers in RP. Further investigations revealed that OCT4 significantly enhanced the osteogenic-like phenotype of hRIFs in vitro and in vivo. Mechanically, OCT4 directly bound to BMP2 promoter and facilitated its CpG island demethylation to transcriptionally promote BMP2 expression. Furthermore, combination of RIP and RNA profiling uncovered that lncRNA OLMALINC physically interacted with OCT4 to promote its stabilization via disrupting the ubiquitination. Additionally, OLMALINC was upregulated in fibroblasts in RP visualized by FISH, and a positive correlation was revealed between OLMALINC and OCT4 in RP. Conclusions The upregulation of OCT4 in hRIFs was a pathological feature of RP formation, and OLMALINC/OCT4/BMP2 axis facilitated hRIFs to acquire osteogenic-like phenotype under osteogenic conditions, through which the pathway might participate in RP formation. Our findings opened up a new avenue to better understand RP formation in which osteogenic-like process was partially triggered by lncRNAs and pluripotency maintenance related genes.