Objective To determine whether argon-beam-coagulation (ABC) suture-free technique results in more favorable renal function than conventional suture technique after laparoscopic partial nephrectomy. Methods This study was a single-center, open-label randomized controlled study. A total of 32 patients with T1a renal tumor and R.E.N.A.L score ≤7 were recruited. The primary endpoint of the study was the absolute variation of the ipsilateral split renal function (SRF) at 12 months. The following secondary endpoints were addressed: the 1, 3, 6, and 12-months variation of eGFR; the 1, 3, 6-months variation of SRF; perioperative outcomes (including operative time, warm ischemia time, time to hemostasis, blood loss). Results The suture-free group had a significantly shorter operative time (90.4 ± 22.0 minutes vs. 117.8 ± 23.5 minutes, p = 0.003) and warm ischemia time (9.6 ± 4.7 minutes vs. 21.3 ± 8.3 minutes, p < 0.001) than the suture group. At the last follow-up, the change of ipsilateral SRF was 7.5 ± 5.1 ml/min for the suture-free group and 13.1 ± 6.7 ml/min for the suture group (p = 0.014). The change of eGFR demonstrated a similar trend (5.5 ± 4.4 ml/min vs. 12.6 ± 6.0 ml/min, p=0.001). Multivariate linear analysis confirmed that suture-free technique was associated with a less decrease of renal function. Conclusions Suture-free partial nephrectomy is a feasible technique for T1a renal masses and benefits long-term SRF and eGFR compared to conventional procedure.

OBJECTIVE:This study aimed to analyze the clinical efficacy of the Jianpi Shengxue tablet for treating renal anemia. METHODS:A total of 200 patients with renal anemia from December 2020 to December 2022 were enrolled and randomly divided into two groups. Patients in the control group were treated with polysaccharide-iron complex, and those in the experimental group were administered Jianpi Shengxue tablet. After 8 weeks of continuous treatment, the therapeutic outcomes regarding anemia were compared between the two groups. RESULTS:After treatment, the red blood cell (RBC) count, hematocrit (HCT), reticulocyte percentage (RET), ferritin (SF), serum iron (SI), transferrin saturation (TSAT), and serum albumin (ALB) all increased (P<0.01), and the clinical symptom score and total iron binding capacity decreased (P<0.01) in the experimental group. Moreover, the improvements in RBC, HCT, RET, SF, SI, TAST, ALB, and clinical symptoms (fatigue, anorexia, dull skin complexion, numbness of hands and feet) in the experimental group were significantly greater than those in the control group (P<0.05). The total effective rate for treating renal anemia was significantly higher in the experimental group than in the control group (P<0.01). CONCLUSION:The Jianpi Shengxue tablet demonstrates efficacy in treating renal anemia, leading to significant improvements in the laboratory examination results and clinical symptoms of patients with renal anemia.

Aims: Endothelial inflammation is crucial in the initiation and progression of atherosclerosis, whereas cholesterol crystals (CCs) play a key role in atherogenesis. However, the effects and origination of CCs on endothelial inflammation are not well understood.Results: In the present study, we found that CCs appeared in the subendothelial space of the partially ligated carotid artery only 1 week after Western diet feeding, which was before immune cell infiltration. In vitro, CCs were generated by human aortic endothelial cells (HAECs) upon low-density lipoprotein treatment. These endothelial cell (EC)-derived CCs increased the expression of intercellular cell adhesion molecule-1 (ICAM1) and vascular cell adhesion molecule-1 (VCAM1). Mechanistic studies demonstrated that CC-induced pyroptosis was critical for endothelial inflammation. Knockdown of gasdermin D (GSDMD) inhibited CC-induced endothelial inflammation, attenuated plaque progression, and decreased macrophage content. Accordingly, the inhibition of GSDMD reduced the CC-induced increase of VCAM1 and ICAM1 in HAECs. Furthermore, CC-mediated pyroptosis was found to be caspase-1 (CASP1)-dependent. Inhibition of CASP1 also reduced endothelial inflammation and attenuated plaque progression. The expression of GSDMD was increased in human atherosclerotic plaques. These findings identify that EC-derived CCs may be an important driving force in the pathogenesis of atherosclerosis.Innovation: This study uncovered a new understanding that CC-induced pyroptosis contributes to endothelial inflammation in early atherogenesis.Conclusion: Targeting endothelial GSDMD or CASP1 contributes to the repression of vascular inflammation and atherogenesis.

Disturbed flow (DF) plays a critical role in the development and progression of cardiovascular disease (CVD). Hydrogen sulfide (H2S) is involved in physiological processes within the cardiovascular system. However, its specific contribution to DF-induced vascular remodeling remains unclear. Here, we showed that the H2S donor, NaHS suppressed DF-induced vascular remodeling in mice. Further experiments demonstrated that NaHS inhibited the proliferation and migration of vascular smooth muscle cells (VSMCs) induced by platelet-derived growth factor-BB (PDGF), as well as the autophagy triggered by DF and PDGF. Mechanistically, RNA-Seq results revealed that NaHS counteracted the PDGF-induced upregulation of lactate dehydrogenase B (LDHB). Overexpression of LDHB abolished the protective effect of NaHS on DF-induced vascular remodeling. Furthermore, LDHB interacted with vacuolar-type proton ATPase catalytic subunit A (ATP6V1A), leading to lysosomal acidification, a process that was attenuated by NaHS treatment. The residues of leucine (Leu) 57 in ATP6V1A and serine (Ser) 269 in LDHB are critical for their interaction. Notably, the expression of LDHB was found to be elevated in vascular tissues from patients with abdominal aortic aneurysms (AAA) and thoracic aortic aneurysms (TAA). These data identify a molecular mechanism by which H2S attenuates DF-induced vascular remodeling by inhibiting LDHB and disrupting the interaction between LDHB and ATP6V1A, thereby impeding the autophagy process. Our findings provide insight that H2S or targeting LDHB has therapeutic potential for preventing and treating vascular remodeling.

Abstract Cystoscopy is the current gold standard for diagnosing bladder cancer (Bca), but its invasive nature often results in patient discomfort. This study aims to debise a new strategy to enhance BCa detection. We collected data from 30 BCa patients between January and June 2022. We obtained spontaneously voided urine specimens from these patients before and after administering extracorporeal bladder vibration. These specimens underwent routine cytologic examination and fluorescence in situ hybridization (FISH). Furthermore, we conducted a follow‐up 3 months postoperation. We recollected urine specimens before and after extracorporeal bladder vibration, repeating the cytologic examination and FISH. Our findings indicated an increase in the number of exfoliated cells in patients' urine postvibration compared to previbration. The liquid‐based cell staining results showed an increased detection rate of abnormal cells in the urinary sediment of patients with both low and high‐grade urothelial carcinoma postvibration. Similarly, the FISH results revealed an increased detection rate of CEP3 and CEP7 positive cells postvibration. Additionally, 3 months postoperation, we found abnormal cells in the urine of one patient previbration and in three patients postvibration. Further cystoscopic biopsy confirmed that these three patients had developed tumor recurrence. Our study substantiates that the extracorporeal bladder vibration assay significantly enhances BCa detection and the prediction of tumor recurrence. This method is simple, quick, and cost‐effective, making it a promising approach worthy of widespread clinical application.

Dear Editor,Although the incidence of prostate cancer（PCa） has decreased in recent decades in Western countries, it has gradually increased in China due to the increasingly longer life expectancy and more popular westernized diet [1] .

Over the last decade, more than 10 independent SNPs have been discovered to be associated with the risk of renal cell carcinoma among different populations. However, the biological functions of them remain poorly understood. In this study, we performed eQTL analysis, ChIP-PCR, luciferase reporter assay, and Cox regression analysis to identify the functional role and underlying mechanism of rs67311347 in RCC. The ENCORI database, which contains the lncRNA–miRNA–mRNA interactions, was used to explore the possible target miRNA of ENTPD3-AS1. The results showed that the G > A mutation of rs67311347 created a binding motif of ZNF8 and subsequently upregulated ENTPD3-AS1 expression by acting as an enhancer. The TCGA-KIRC and our cohorts both confirmed the downregulation of ENTPD3-AS1 in RCC tissues and demonstrated that increased ENTPD3-AS1 expression was associated with good OS and PFS. Furthermore, ENTPD3-AS1 interacted with miR-155-5p and activated the expression of HIF-1α, which was an important tumor suppressor gene in the development of RCC. The functional experiments revealed that overexpression of ENTPD3-AS1 inhibited cell proliferation in RCC cell lines and the effect could be rescued by knocking down HIF-1α. Our findings reveal that SNP-mediated lncRNA-ENTPD3-AS1 upregulation suppresses renal cell carcinoma via miR-155/HIF-1α signaling.

Acute immune rejection is one of the most serious complications of heart transplantation, and its mechanism has always been a hot spot. Th17 cells and cytokine interleukin-17 (IL-17) have been proved to be involved in acute immune rejection, and the signaling pathway mechanism has attracted our interest. It has been confirmed that the Janus kinase 2-signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway is involved in the differentiation of CD4(+) T cells, so we focus on whether the JAK2/STAT3 signaling pathway is involved in the occurrence of acute immune rejection by regulating the Th17/IL-17 axis. In this study, we used Bagg's Albino c mice and C57BL/6 mice to construct heterotopic heart transplantation models, which were divided into the acute rejection group and AG490-treated group (n = 5), and donor tissue and serum were collected in 3 experimental days from the recipient mice for H&E staining analysis of paraffin sections and ELISA, Western blot, flow cytometry, and real time-polymerase chain reaction. The results showed that the acute rejection rating of the heart decreased, and the expression of related factors decreased significantly after using the inhibitor AG490, suggesting that the JAK2/STAT3 signaling pathway regulates expression of the Th17/IL-17 axis in cardiac allograft rejection.

Renal ischemia-reperfusion injury (IRI) after renal transplantation often leads to the loss of kidney graft function. However, there is still a lack of efficient regimens to prevent or alleviate renal IRI. Our study focused on the renoprotective effect of 3-Deazaneplanocin A (DZNep), which is a histone methylation inhibitor. We found that DZNep significantly alleviated renal IRI by suppressing nuclear factor kappa-B (NF-κB), thus inhibiting the expression of inflammatory factors in renal tubular epithelial cells in vivo or in vitro. After treatment with DZNep, T cell activation was impaired in the spleen and kidney, which correlated with the downregulated expression of T-cell immunoglobulin mucin (TIM)-1 on T cells and TIM-4 in macrophages. In addition, pretreatment with DZNep was not sufficient to protect the kidney, while administration of DZNep from before to after surgery significantly ameliorated IRI. Our findings suggest that DZNep can be a novel strategy for preventing renal IRI following kidney transplantation.

BACKGROUND:Long non-coding RNAs (lncRNAs) can affect tumorigenesis. Data from The Cancer Genome Atlas (TCAG) suggest that LINC02783 is highly expressed in renal cell carcinoma (RCC) and is expected to be a potential biological target. We conducted this study to verify this.PATIENTS AND METHODS:We conducted this study to verify the opinion that "LINC02783 is highly expressed in renal cell carcinoma (RCC) and is expected to be a potential biological target". We employed quantitative real-time polymerase chain reaction (qRT-PCR) to test LINC02783 expression in RCC tissues, CKK-8 assay and transwell assay to assess the viability and invasion of RCC cells, Western blot to quantify Sox-4 expression, dual-luciferase reporter (DLR) assay and RNA immunoprecipitation (RIP) assay to analyze the interaction between LINC02783 and miR-20b, in vivo experiments to test tumor formation.RESULTS:We detected high LINC02783 expression in RCC patients. Patients with higher LINC02783 levels had a markedly poorer prognosis. In vitro and in vivo, the down-regulation of LINC02783 suppressed the viability and invasion of RCC cells. The DLR assay results revealed that LINC02783 enhanced Sox-4 expression by regulating miR-20b. LINC02783 can act as a sponge for miR-20b to inhibit Sox-4 expression.CONCLUSION:LINC02783 is highly expressed in RCC patients and indicates a poor prognosis. LINC02783 can affect the occurrence and progression of RCC through the miR-20b/Sox-4 axis, making it a promising target for the treatment of RCC.

Our previously study shown that Lysophosphatidylcholine Acyltransferase1 (LPCAT1) is overexpressed in castration resistant prostate cancer (CRPC) relative to primary prostate cancer (PCa), and androgen controls its expression via the Wnt signaling pathway. While highly expressed in CRPC, the role of LPCAT1 remains unclear. In vitro cell experiments referred to cell transfection, mutagenesis, proliferation, migration, invasion, cell cycle progression and apoptosis, Western blotting, Pulse-chase RNA labeling. BALB/c nude mice were used for in vivo experiments. We found that LPCAT1 overexpression enhanced the proliferation, migration, and invasion of CRPC cells both in vitro and in vivo. Silencing of LPCAT1 reduced the proliferation and the invasive capabilities of CRPC cells. Providing exogenous PAF to LPCAT1 knockdown cells increased their invasive capabilities; however platelet activating factor acetylhydrolase (PAF-AH) and the PAFR antagonist ABT-491 both reversed this phenotype; proliferation of CRPC cells was not affected in either model. LPCAT1 was found to mediate CRPC growth via nuclear re-localization and Histone H4 palmitoylation in an androgen-dependent fashion, increasing mRNA synthesis rates. We also found that LPCAT1 overexpression led to CRPC cell resistance to treatment with paclitaxel. LPCAT1 overexpression in CRPC cells drives tumor progression via increased mRNA synthesis and PAF production. Our results highlight LPCAT1 as a viable therapeutic target in the context of CRPC.

This study aimed to investigate the underlying mechanism of mesenchymal stem cells (MSCs) on protection of renal ischemia reperfusion injury (IRI). Exosomes originated from MSCs (MSC-ex) were extracted according to the instructions of Total Exosome Isolation Reagent. Rats were divided into five groups: sham-operated, IRI, MSC, MSC-ex, and MSC-ex + RNAase group. MSCs or MSC-ex were injected via carotid artery. The renal function test and pathological detection were applied to determine the renoprotection of MSC-ex on IRI. Western blotting and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were conducted to examine the levels of apoptosis-related proteins and inflammatory cytokines. Our results revealed that MSC-derived exosomes attenuated renal dysfunction, histologic damage, and decreased apoptosis. The expression levels of inflammatory cytokines, such as interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), and interferon gamma (IFN-γ), were decreased by the MSC-ex treatment. The expression levels of caspase-9, cleaved caspase-3, Bax, and Bcl-2 caused by IR were also inhibited by MSC-ex. MSC-ex + RNAase group shared the similar pattern of changes with IRI group, likely due to the ability of RNA hydrolase to eliminate the function of exosomes. Our results demonstrated that exosomes originating from MSCs have protective effects on IRI via inhibiting cell apoptosis and inflammatory responses. Out findings may provide a new insight into therapeutic mechanism of MSCs on renal IRI.

AIMS:To investigate the protective effects of downregulating ETaR expression on renal ischemia reperfusion injury (IRI).MAIN METHODS:The renal IRI model was generated by clamping the left renal artery for 60 min followed by nephrectomy of the right kidney. ETaR siRNA were perfused through the renal artery during ischemia. HE staining was performed to assess histological injury. PCR was performed to determine the expression of NF-κb, TNF-α, IFN-γ, IL-6 and TGF-β. ELISA was used to determine the levels of ET-1, TGF-β and eNOS. The level of nitric oxide (NO) was tested by the NO detection kit. The expression of PI3K, Akt, sGC and PKG were evaluated by western blot.KEY FINDINGS:ETaR siRNA treatment reduced the levels of serum creatinine and urea nitrogen, decreased the number of apoptotic cells, and ameliorated histological damage after IRI. PCR results demonstrated that IRI increased mRNA levels of inflammatory factors, which were inhibited by ETaR siRNA treatment. ELISA result showed that ETaR siRNA decreased the levels of ET-1, TGF-β and eNOS in the renal tissues after IRI. Western blot results demonstrated that ETaR siRNA activated the PI3K/Akt and sGC/PKG signaling pathway. Conversely, the NOS inhibitor, L-NAME, reversed the effects of ETaR siRNA treatment.SIGNIFICANCE:ETaR siRNA treatment inhibited inflammatory response and improved renal function after renal IRI. The underlying mechanisms of ETaR siRNA treatment may be through increasing eNOS activity through PI3K/Akt signaling, which subsequently increased NO production. The increased NO reduces the expression of ET-1 by inhibiting transcription of ET-1-associated genes via the sGC/PKG signaling pathway.

Objective To explore the protective effect of ETaR siRNA on renal ischemia reperfusion injury (IRI) by changing the immuno-microenvironment in rats .Methods A total of 40 male Sprague-Dawley (SD) rats were randomized into four groups of sham ,IR ,negative siRNA and ETaR siRNA .A renal IRI model was generated by clamping left renal artery .ETaR siRNA was delivered into kidney through renal vein by a retrograde 'hydrodynamic' injection .Blood samples were collected for detecting renal function and kidney tissue harvested for Hematoxylin & Eosin (HE) staining , TdT-mediated dUTP Nick-End Labeling (TUNEL) staining ,polymerase chain reaction (PCR) and Western blot at 48 h post-reperfusion .Results Serum creatinine ,blood urea nitrogen and renal apoptotic cells increased and renal tissue was injured after IR . The changes were inhibited by ETaR siRNA . PCR showed that ETaR siRNA treatment significantly down-regulated the expressions of inflammatory factors TNF-α , IFN-γ and IL-6 and transcription factor NF-κB induced by IR .Conclusions ETaR siRNA can effectively improve the immunomicroenvironment and thereby alleviate renal ischemia reperfusion injury .

Background: Ischemia-reperfusion injury (IRI) is one of the major causes of postoperative renal allograft dysfunction, which is mainly the result of proinflammatory reactions including inflammatory responses, oxidative stress, and metabolic disorders. Resveratrol (RSV) plays an important role in protecting various organs in IRI because it reduces oxidative stress, lessens the inflammatory response, and exerts anti-apoptotic effects. The aim of this study was to demonstrate the renoprotective effect of RSV in inhibiting inflammatory responses, reducing oxidative stress, and decreasing cell apoptosis in vivo and in vitro. Methods: RSV was administered before renal ischemia and H2O2 induction. Serum and kidneys were harvested 24 h after reperfusion and NRK-52E cells were collected 4 h after H2O2 stimulation. Serum creatinine and blood urea nitrogen were used to assess renal function. Hematoxylin and eosin staining was performed to assess histological injury. Quantitative real-time PCR and enzyme-linked immunosorbent assay were used to assess proinflammatory cytokine expression. Oxidative stress–related proteins, such as Nrf2 and TLR4, were evaluated by western blot. Terminal deoxynucleotidyl transferase–mediated dUTP-biotin nick end labeling assay was used to detect apoptotic cells in tissues, and western blot was used to evaluate the expression of caspase-3, -8, and -9 in this study. Results: RSV inhibited inflammatory responses and improved renal function after renal IRI. Additionally, RSV decreased oxidative stress and reduced cell apoptosis by upregulating Nrf2 expression, downregulating the TLR4/NF-κB signaling pathway, and by decreasing caspase-3 activity and caspase cascades. Conclusion: Our study demonstrated the mechanisms underlying RSV renoprotection. We found that RSV exerts its greatest effects by blocking inflammatory responses, lowering oxidative stress, and reducing apoptosis via the Nrf2/TLR4/NF-κB pathway.

This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected to renal I/R injury were treated with HSYA at 0.5 h prior to I/R injury. Renal function, histopathological analysis, and cells apoptosis were measured in vivo. In vitro, proximal renal tubular cells (HK-2) were subjected to hypoxia/reoxygenation (H/R). Apoptotic cell death and inflammatory cytokines, Toll-like receptor 4 (TLR4), and nuclear factor (NF)-κB expression were determined. Treatment of I/R rats with HSYA markedly reduced the levels of serum creatinine and blood urea nitrogen, attenuated renal cell apoptosis, alleviated changes in renal tissue morphology, and reduced IL-1β, TNF-α, and caspase-3 release. In vitro, HSYA effectively decreased NF-κB p65 and inflammatory cytokines, such as IL-1β, TNF-α, and IL-6. Thus, HSYA can protect renal function from I/R injury by ameliorating acute kidney injury and partly by promoting tubular cell survival via the TLR4/NF-κB pathway. These results suggest that HSYA can be used to prevent I/R-induced acute kidney injury.

Complement activation is involved in the pathogenesis of ischemia reperfusion injury (IRI), which is an inevitable process during kidney transplantation. Therefore, complement-targeted therapeutics hold great potential in protecting the allografts from IRI. We observed universal deposition of C3d and membrane attack complex in human renal allografts with delayed graft function or biopsy-proved rejection, which confirmed the involvement of complement in IRI. Using FB-, C3-, C4-, C5-, C5aR1-, C5aR2-, and C6-deficient mice, we found that all components, except C5aR2 deficiency, significantly alleviated renal IRI to varying degrees. These gene deficiencies reduced local (deposition of C3d and membrane attack complex) and systemic (serum levels of C3a and C5a) complement activation, attenuated pathological damage, suppressed apoptosis, and restored the levels of multiple local cytokines (e.g., reduced IL-1β, IL-9, and IL-12p40 and increased IL-4, IL-5, IL-10, and IL-13) in various gene-deficient mice, which resulted in the eventual recovery of renal function. In addition, we demonstrated that CRIg/FH, which is a targeted complement inhibitor for the classical and primarily alternative pathways, exerted a robust renoprotective effect that was comparable to gene deficiency using similar mechanisms. Further, we revealed that PI3K/AKT activation, predominantly in glomeruli that was remarkably inhibited by IRI, played an essential role in the CRIg/FH renoprotective effect. The specific PI3K antagonist duvelisib almost completely abrogated AKT phosphorylation, thus abolishing the renoprotective role of CRIg/FH. Our findings suggested that complement activation at multiple stages induced renal IRI, and CRIg/FH and/or PI3K/AKT agonists may hold the potential in ameliorating renal IRI.

BACKGROUND/AIMS:Previous studies imply that telocytes may have a protective effect on fibrosis in various organs, including the liver, colon, and heart. The effect of telocytes on renal fibrosis remains unknown. Herein, this study was designed to investigate the effect of telocytes on renal fibrosis and the potential mechanisms involved.METHODS:In a unilateral ureteral obstruction (UUO)-induced renal fibrosis model, telocytes were injected via the tail vein every other day for 10 days. The degree of renal damage and fibrosis was determined using histological assessment. The expression of collagen I, fibronectin, epithelial-mesenchymal transition markers, and Smad2/3 phosphorylation was examined by western blot analyses. Real-time PCR and enzyme-linked immunosorbent assay were performed in vivo to detect the levels of transforming growth factor (TGF)-β1 and various growth factors.RESULTS:Telocytes attenuated renal fibrosis, as evidenced by reduced interstitial collagen accumulation, decreased expression of fibronectin and collagen I, upregulation of E-cadherin, and downregulation of α-smooth muscle actin. Furthermore, telocytes decreased serum TGF-β1 levels, suppressed Smad2/3 phosphorylation, and increased the expression of hepatocyte growth factor (HGF) in rat kidney tissue following UUO. Blockage of HGF counteracted the protective effect of telocytes on UUO-treated kidneys. Through the detection of HGF mRNA levels in vitro, we found that telocytes had no effect on HGF expression compared with renal fibroblasts.CONCLUSION:Telocytes attenuated UUO-induced renal fibrosis in rats, likely through enhancing the expression of HGF in an indirect manner.

Immunosuppressant drugs for renal transplant mycophenolate mofetil (MMF) and enteric-coated mycophenolate sodium (EC-MPS) cause gastrointestinal (GI) disorders. The specific site of GI tract targeted by MMF and EC-MPS remains unclear.

Abstract Background: Unilateral renal tumor cryoablation and contralateral radical nephrectomy of bilateral renal tumors were performed by transumbilical three-dimensional (3D) multichannel laparoendoscopic single-site (LESS) surgery, in an attempt to verify the feasibility and safety of the procedure, sum up the operational experience, and evaluate the surgical outcome. Case Presentation: This was a 47-year-old female patient with a body mass index of 27.34 kg/m2 without backache, low back pain, hematuria, urinary urgency, frequent urination, dysuria, and other symptoms. Contrast-enhanced CT scan of the kidney on admission showed four masses in the left kidney and two masses in the right kidney. Preoperative serum creatinine (SCr) was 87 μmol/L. Operation was performed under general anesthesia by first laying the patient in a left lateral position. A 2-cm longitudinal transumbilical skin incision was made to expose the right kidney for complete dissection of the two tumors. First, puncture biopsy was performed, and then two freeze–thaw cryoablation cycles for the two tumors were performed. At last, the patient was laid in a right lateral position for radical nephrectomy of the left kidney. The operative duration, cryoablation time, and estimated blood loss were 200 minutes, 40 minutes, and 100 mL, respectively. Postoperative pathological examination revealed clear-cell renal cell carcinoma. The right glomerular filtration rate tested was 42.36 mL/minute and SCr was 131 μmol/L at day 5 after surgery. There was no evidence of contrast enhancement at the cryoablative region as shown by renal contrasted CT scan performed 4 days after surgery and renal contrasted MRI scan performed 6 weeks after surgery, indicating that there was no tumor remnant or recurrence. Conclusion: Our preliminary experience shows that the treatment of bilateral renal tumors with unilateral renal tumor cryoablation and contralateral radical nephrectomy by transumbilical 3D LESS is safe, feasible, and effective. It may prove to be a viable option for patients with significant comorbidities and an insensitive treatment intention.