Mini-percutaneous nephrolithotomy versus retrograde intrarenal surgery for the treatment of 10-20-mm kidney stones in patients with ileal conduit: a comparative study.

BACKGROUND: Both mini-percutaneous nephrolithotomy (mPNL) and retrograde intrarenal surgery (RIRS) are two major strategies for the endourological management of kidney stones. In the current study, we aimed to compare the efficacy and safety of mPNL and RIRS for the treatment of 10-20 mm kidney stones in patients with ileal conduit. METHODS: Patients with a history of bladder cancer and ileal conduit who had undergone mPNL or RIRS for unilateral kidney stones 10-20 mm in size between January 2015 and June 2022 were retrospectively included. Baseline characteristics and perioperative outcomes were analyzed and compared between mPNL and RIRS. RESULTS: The failure rate of the initial surgery was 2.5% and 18.9% for mPNL and RIRS, respectively (P=0.025). In total, 39 and 30 patients were finally included in the mPNL and RIRS groups. One-session stone-free rate (SFR) was higher in the mPNL group than the RIRS group (97.4% vs. 66.7%, P=0.002). However, there was no statistically significant difference between the two groups with regard to operation time, postoperative hospitalization, complications according to Clavien-Dindo classification, as well as the change in hemoglobin, creatinine, procalcitonin, and pain Visual Analogue Scale Score before and after the surgery. Moreover, Results were consistent across subgroup analyses in patients stratified by years (2015-2018 and 2019-2022). CONCLUSIONS: Both mPNL and RIRS were feasible and safe for the treatment of 10-20 mm kidney stones in patients with ileal conduit. However, mPNL achieved superior SFR outcomes with a similar incidence of complications, and it might be a sensible alternative for selected patients.

Evaluating outcomes of patient-centered enhanced recovery after surgery (ERAS) in percutaneous nephrolithotomy for staghorn stones: An initial experience.

Objective: To evaluate the outcomes of patient-centered enhanced recovery after surgery (ERAS) in -percutaneous nephrolithotomy (PCNL) for staghorn stones. Patients and methods: A retrospective analysis of 106 patients with staghorn calculi who underwent PCNL treatment at the Third Xiangya Hospital from October 01, 2018 to September 30, 2021 was performed. The patients were divided into the ERAS group (n = 56) and traditional group (n = 50). The ERAS program focused on a patient-centered concept, with elaboration on aspects, such as patient education, nutritional support, analgesia, body warming, early mobilization, nephrostomy tube removal, and strict follow-up. Results: The total stone free rate and total complication rate were similar in both groups. The visual analogue scale (VAS) 6 h after surgery, ambulation off bed time, indwelling fistula time, indwelling catheter time, and postoperative hospital stays were lower in the ERAS group than in the traditional group (P < 0.05). The multiple session rate in the ERAS group (19, 28.57%) was lower than that in the traditional group (30, 60%) (P = 0.007). The 1-year stone recurrence rate in the ERAS group (7, 17.5%) was lower than that in the traditional group (14, 38.9%) (P = 0.037). Conclusion: The patient-centered ERAS in PCNL for staghorn stones accelerated rehabilitation by relieving postoperative pain, shortening hospitalization time, accelerating early ambulation, and reducing multiple session rate and 1-year stone recurrence rate, which have socioeconomic benefits.

Extrinsic apoptosis and senescence involved in growth kinetics of seminoma to cisplatin.

Seminoma is the most common type of testicular germ cell tumour and is highly sensitive to cisplatin therapy, which has not been fully elucidated. In this study, we comprehensively monitored dynamic changes of TCam-2 cells after cisplatin treatment. At an early stage, we found that both low and high concentrations of cisplatin induced the S-phase arrest in TCam-2 cells. By contrast, the G0G1 arrest was caused by cisplatin in teratoma NTERA-2 cells. Afterwards, high concentrations of cisplatin promoted the extrinsic apoptosis and high expressions of related genes (Fas/FasL-caspase-8/-3) in TCam-2 cells. However, when decreasing the cisplatin, the apoptotic cells were significantly reduced, and accompanied by cells showing senescence-like morphology, positive SA-ß-gal staining and up-regulation of senescence-related genes (p53, p21 and p16). Furthermore, the cell cycle analysis revealed that most of the senescent TCam-2 cells were irreversibly arrested in the G2M phase. G2M arrest was also observed in NTERA-2 cells treated with a low concentration of cisplatin, while no senescence-related phenotype was discovered. In addition, we detected the γ-H2AX, a DNA damage marker protein, and reactive oxygen species (ROS) and found both of which were elevated with the increase of cisplatin in TCam-2 cells. In conclusion, the extrinsic apoptosis and senescence are involved in the growth kinetics of TCam-2 cells to cisplatin, which provide some implications for studies on cisplatin and seminoma.

PGC1α plays a pivotal role in renal fibrosis via regulation of fatty acid metabolism in renal tissue. / PGC1αé€šè¿‡è°ƒæŽ§è‚¾ç»„ç»‡è„‚è‚ªé ¸ä»£è°¢åœ¨è‚¾çº¤ç»´åŒ–ä¸­å‘æŒ¥æž¢çº½ä½œç”¨.

Renal fibrosis is a common and irreversible pathological feature of end-stage renal disease caused by multiple etiologies. The role of inflammation in renal fibrosis tissue has been generally accepted. The latest view is that fatty acid metabolism disorder contributes to renal fibrosis. peroxisome proliferator activated receptor-gamma coactivator 1α (PGC1α) plays a key role in fatty acid metabolism, regulating fatty acid uptake and oxidized protein synthesis, preventing the accumulation of lipid in the cytoplasm, and maintaining a dynamic balanced state of intracellular lipid. In multiple animal models of renal fibrosis caused by acute or chronic kidney disease, or even age-related kidney disease, almost all of the kidney specimens show the down-regulation of PGC1α. Upregulation of PGC1α can reduce the degree of renal fibrosis in animal models, and PGC1α knockout animals exhibit severe renal fibrosis. Studies have demonstrated that AMP-activated protein kinase (AMPK), MAPK, Notch, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), epidermal growth factor receptor (EGFR), non-coding RNA (ncRNAs), liver kinase B1 (LKB1), hairy and enhancer of split 1 (Hes1), and other pathways regulate the expression of PGC1α and affect fatty acid metabolism. But some of these pathways interact with each other, and the effect of the integrated pathway on renal fibrosis is not clear.

Mechanism and influencing factors of crystal-cell interaction in the formation of calcium oxalate stones. / è‰é ¸é’™ç»“çŸ³å½¢æˆè¿‡ç¨‹ä¸­æ™¶ä½“-ç»†èƒžç›¸äº’ä½œç”¨çš„æœºåˆ¶åŠå½±å“å› ç´ .

Kidney stone is a disease with complex etiology and high incidence, and the most common chemical composition type of it is calcium oxalate stone. The formation of calcium oxalate stones includes crystal formation, crystal growth and aggregation, crystal interaction with renal tubular epithelial cells, and crystal invasion of renal interstitial extracellular matrix and so on. In these processes, crystal-cell interactions are essential for kidney crystal retention and kidney stone formation. Recently many studies have found that the interaction between crystal and renal tubular epithelial cells is closely related to various key binding molecules, endoplasmic reticulum stress of tubular cells, extracellular matrix proteins, and various lithotriptic drugs. Understanding the mechanism of crystal-cell interaction is of great significance for the prevention and early treatment of calcium oxalate stones.

Identification of Potential Predictor of Biochemical Recurrence in Prostate Cancer.

Background: Prostate cancer is a common malignancy in men. Radical prostatectomy is one of the primary treatment modalities for patients with prostate cancer. However, early identification of biochemical recurrence is a major challenge for post-radical prostatectomy surveillance. There is a lack of reliable predictors of biochemical recurrence. The purpose of this study was to explore potential biochemical recurrence indicators for prostate cancer. Materials and Methods: We analyzed transcriptomic data of cases with biochemical recurrence in The Cancer Genome Atlas (TCGA). Then, we performed integrative bioinformatics analyses to establish a biochemical recurrence predictor model of prostate cancer. Results: There were 146 differentially expressed genes (DEGs) between prostate cancer and normal prostate, including 12 upregulated and 134 downregulated genes. Comprehensive pathway enrichment analyses revealed that these DEGs were associated with multiple cellular metabolic pathways. Subsequently, according to the random assignment principle, 208 patients were assigned to the training cohort and 205 patients to the validation cohort. Univariate Cox regression analysis showed that 7 genes were significantly associated with the biochemical recurrence of prostate cancer. A model consisting of 5 genes was constructed using LASSO regression and multivariate Cox regression to predict biochemical recurrence of prostate cancer. Expression of PAH and AOC1 decreased with an increasing incidence of prostate cancer, whereas expression of DDC, LINC01436 and ORM1 increased with increasing incidence of prostate cancer. Kaplan-Meier curves and receiver operator characteristic (ROC) curves indicated that the 5-gene model had reliable utility in identifying the risk of biochemical recurrence of prostate cancer. Conclusion: This study provides a model for predicting prostate cancer recurrence after surgery, which may be an optional indicator for postoperative follow-up.

Sexual, physical, and overall adverse effects in patients treated with 5α-reductase inhibitors: a systematic review and meta-analysis.

Postfinasteride syndrome (PFS) is a term coined to characterize a constellation of reported undesirable sexual, physical, and neuropsychiatric side effects. In the present study, we conducted the meta-analysis to demonstrate whether the use of 5α-reductase inhibitors (5ARIs) increases the risk of PFS-like adverse effects. A search of studies published until May 10, 2020, was performed using PubMed, EMBASE, and the Cochrane Library. We included randomized controlled trials with at least one comparison between male patients receiving 5ARIs versus placebo for the treatment of benign prostatic hyperplasia (BPH) or androgenetic alopecia (AGA), and identified 34 studies from 28 articles that met our eligibility criteria. In the random-effects model, the overall use of 5ARIs exhibited a 1.87-fold risk of PFS-like adverse effects during the trial (95% confidence interval [CI]: 1.64-2.14). Regarding specific types of adverse effects, the use of 5ARIs had a 1.89-fold risk of sexual adverse effects (95% CI: 1.74-2.05) and was associated with an increased risk of physical adverse effects (relative risk [RR]: 1.31, 95% CI: 0.80-2.15), albeit without statistical significance. This meta-analysis helped to better define the adverse effects caused by 5ARIs. We concluded that the overall use of 5ARIs significantly increased the risk of PFS-like adverse effects in men with AGA or BPH during treatment. Enhanced awareness of and education on the PFS-like adverse effects are necessary for clinicians.

Knockdown of miR-423-5p simultaneously upgrades the eNOS and VEGFa pathways in ADSCs and improves erectile function in diabetic rats.

This study aimed to explore the possibility of miR-423-5p modified adipose-derived stem cell (ADSCs) therapy on streptozotocin (STZ)-induced diabetes mellitus erectile dysfunction (DMED) rats. MiR-423-5p was knocked down in ADSCs. ADSCs, NC-miR-ADSCs and miR-ADSCs were co-cultured with human umbilical vein endothelial cells (HUVECs). Normal and high glucose media were supplemented. The supernatant and HUVECs were collected for assessment of eNOS and VEGFa expression, cell proliferation, and apoptosis. HUVECs co-cultured with ADSCs or miR-ADSCs exhibited higher eNOS and VEGFa protein expression levels compared to DM groups. MiR-ADSCs enhanced HUVEC proliferation compared to the ADSCs and NC-miR-ADSCs. Lower apoptotic rates were observed when HUVECs were co-cultured with miR-ADSCs, compared to ADSCs and NC-miR-ADSCs. Fifteen male Sprague-Dawley (SD) rats aged 12 weeks were induced to develop diabetes mellitus by intraperitoneal injection with STZ, and five healthy SD rats were used as normal controls. Eight weeks after developing diabetes, the rats received ADSCs and miR-ADSCs via injection into the corpora cavernosa, whereas normal controls and DM controls were injected with saline. Erectile function and histological assessment of penile tissues were performed 8 weeks after injection. The ICP/MAP indicated that erectile function was impaired in the DM rats compared with the normal group. Injection of ADSCs and miR-ADSCs improved erectile function significantly and was associated with the overexpression of eNOS and VEGFa. MiR-423-5p knockdown in ADSCs ameliorated high glucose-mediated damage to HUVECs and improved erectile function in DM rats by inducing eNOS and VEGFa overexpression, indicating that miR-423-5p may be a potential target in the treatment of DMED.

The regulatory role of antisense lncRNAs in cancer.

Antisense long non-coding RNAs (antisense lncRNAs), transcribed from the opposite strand of genes with either protein coding or non-coding function, were reported recently to play a crucial role in the process of tumor onset and development. Functionally, antisense lncRNAs either promote or suppress cancer cell proliferation, migration, invasion, and chemoradiosensitivity. Mechanistically, they exert their regulatory functions through epigenetic, transcriptional, post-transcriptional, and translational modulations. Simultaneously, because of nucleotide sequence complementarity, antisense lncRNAs have a special role on its corresponding sense gene. We highlight the functions and molecular mechanisms of antisense lncRNAs in cancer tumorigenesis and progression. We also discuss the potential of antisense lncRNAs to become cancer diagnostic biomarkers and targets for tumor treatment.

Effect of autophagy on oxalate-induced toxicity of human proximal renal tubular epithelial cell. / è‡ªå™¬åœ¨è‰é ¸è¯±å¯¼äººè‚¾å°ç®¡ä¸Šçš®ç»†èƒžæŸä¼¤ä¸­çš„ä½œç”¨.

OBJECTIVES: To investigate the role of autophagy in oxalate-induced toxicity of human proximal renal tubular epithelial cell (HK-2). METHODS: HK-2 cells were exposed to oxalate (1 mmol/L) for 2 h and 3-methyladenine (3-MA) was used to inhibit autophagy. Then Western blotting was used to measure the expression of autophagy-related protein LC3II. Cell viability and cell apoptosis were measured by MTT assay and flow cytometry assay, respectively. RESULTS: Cytoplasmic vacuolization was observed in HK-2 cells after treating with oxalate for 2 h. However, 3-MA showed no effects on the formation of cytoplasmic vacuolization regardless of the dose at 1 or 5 mmol/L. The expression of LC3II protein was significantly increased in the HK-2 cells in the presence of oxalate (0.62±0.03 vs 0.35±0.02, P<0.05). The expression of LC3II protein in HK-2 cells was downregulated by 3-MA at both 1 and 5 mmol/L compared with the blank control (0.17±0.03 vs 0.35±0.02, 0.16±0.03 vs 0.35±0.02, both P<0.05). Oxalate-induced upregulation of LC3II was reversed by 3-MA only at the concentration of 5 mmol/L (0.47±0.04 vs 0.62±0.03, P<0.05) rather than 1 mmol/L (0.61±0.04 vs 0.62±0.03, P>0.05). Oxalate attenuated viability [(77.32±2.69)% vs 100%, P<0.05] and increased the apoptosis [(8.32±1.05)% vs (2.36±0.29)%, P<0.05] in HK-2 cells, and these effects were reversed by 3-MA only at the concentration of 5 mmol/L [(91.91±3.36)% vs (77.32±2.69)%, (3.45±0.21)% vs (8.32±1.05)%, respectively, both P<0.05] rather than 1 mmol/L [(80.48±3.41)% vs (77.32±2.69)%, (7.81±0.47)% vs (8.32±1.05)%, both P>0.05, respectively]. CONCLUSIONS: Autophagy of HK-2 cells is enhanced by oxalate at the concentration of 1 mmol/L. Inhibition of 3-MA-induced autophagy protects HK-2 cells from the oxalate-induced cytotoxicity.

Animal models of benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms are common clinical concerns that affect aging men all over the world. The underlying molecular and cellular mechanisms remain elusive. Over the past few years, a number of animal models of BPH, including spontaneous model, BPH-induction model, xenograft model, metabolic syndrome model, mechanical obstruction model, and transgenic model, have been established that may provide useful tools to fill these critical knowledge gaps. In this review, we therefore outlined the present status quo for animal models of BPH, comparing the pros and cons with respect to their ability to mimic the etiological, histological, and clinical hallmarks of BPH and discussed their applicability for future research.

Integrative Analysis of MicroRNA and Gene Interactions for Revealing Candidate Signatures in Prostate Cancer.

MicroRNA (miRNA)-gene interactions are well-recognized as involved in the progression of almost all cancer types including prostate cancer, which is one of the most common cancers in men. This study explored the significantly dysregulated genes and miRNAs and elucidated the potential miRNA-gene regulatory network in prostate cancer. Integrative analysis of prostate cancer and normal prostate transcriptomic data in The Cancer Genome Atlas dataset was conducted using both differential expression analysis and weighted correlation network analysis (WGCNA). Thirteen genes (RRM2, ORC6, CDC45, CDKN2A, E2F2, MYBL2, CCNB2, PLK1, FOXM1, CDC25C, PKMYT1, GTSE1, and CDC20) were potentially correlated with prostate cancer based on functional enrichment analyses. MiRNAs targeting these genes were predicted and eight miRNAs were intersections between those miRNAs and the hub miRNAs obtained from miRNA WGCNA analysis. Three genes (E2F2, RRM2, and PKMYT1) and four miRNAs (hsa-mir-17-5p, hsa-mir-20a-5p, hsa-mir-92a-3p, and hsa-mir-93-5p) were key factors according to the interaction network. RRM2 and PKMYT1 were significantly related to survival. These findings partially elucidated the dysregulation of gene expressions in prostate cancer. Efficient manipulations of the miRNA-gene interactions in prostate cancer may be exploited as promising therapeutics.

Toxicity assessment due to prenatal and lactational exposure to lead, cadmium and mercury mixtures.

The heavy metals lead (Pb), cadmium (Cd) and mercury (Hg) are common environmental pollutants that can be detected simultaneously in blood, serum, and urine samples from the general human population. However, there is limited information regarding toxicity of low-level exposure to Pb, Cd, and Hg mixtures. Our previous research showed the interaction of these three elements at low concentrations in vitro. In this study, we further evaluate early effects of low dose exposure to Pb, Cd, and Hg mixtures on the brain, heart, liver, kidney, and testicle in rats. Pregnant rats were exposed to various concentrations of heavy metal mixtures (MM) in drinking water, during gestation and lactation, and the impacts on offspring were measured at postnatal day 23. Our results showed that the concentrations of Pb, Cd, and Hg in the blood of rat pups were similar to those in the blood of the general human population. Additionally, the MM concentrations in their blood and brain significantly increased in a dose-dependent manner. MM exposure caused histopathological changes in the brain, liver, kidney and testicle. Statistically significant increases in liver CYP450 and PON1, kidney KIM1, and decrease in testicle SDH were observed. In the brain, significant increases were detected in oxidative stress, intracellular free calcium, and cell apoptosis. Further neurobehavioral testing revealed that MM exposure caused dose-dependent impairments in learning and memory as well as sensory perception. MM exposure also disrupted synapse remodeling, which may be associated with pathways involved in dendritic spine growth, maintenance, and elimination. These results suggested that exposure to Pb, Cd, and Hg mixtures, at human environmental exposure related levels, caused damage to multiple organs as well as impairments in neurobehavioral functions of rats. Our findings emphasize the need to control and regulate potential sources of heavy metal contamination.

Lead, cadmium, arsenic, and mercury combined exposure disrupted synaptic homeostasis through activating the Snk-SPAR pathway.

Lead (Pb), cadmium (Cd), arsenic (As), and mercury (Hg) are among the leading toxic agents detected in the environment, and they have also been detected simultaneously in blood, serum, and urine samples of the general population. Meanwhile early neurologic effects and multiple interactions of Pb, Cd, As, and Hg had been found in children from environmentally polluted area. However, the current studies of these four metals were mostly limited to the interactions between any two metals, whereas the interaction characteristics between any three and four metals were rarely studied. In our study, we firstly explored the characteristics of the neurotoxic interactions among these four elements in nerve cells with factorial designs. The results showed that Pb+Cd+As+Hg co-exposure had a synergistic neurotoxic effect that was more severe than that induced by any two or three metals, when their individual metals were at human environmental exposure (in the blood of U.S. population) relevant levels and below no observed adverse effect levels (NOAELs). Therefore, Pb+Cd+As+Hg co-exposure at human environmental exposure relevant levels were further selected to examine synaptic homeostasis as the cellular and molecular foundation of learning and memory. We reported for the first time that Pb+Cd+As+Hg co-exposure induced dose-dependent decreases of the dendritic lengths and branching, as well as spine density and mature phenotype in primary hippocampal neurons, and the stimulated neurite outgrowths in NGF-differentiated PC12 cells. And the above synaptic homeostasis disruption was associated with serum induced kinase (Snk)-spine associated Rap GTPase activating protein (SPAR) pathway. Our study suggests that human environmental Pb, Cd, As, and Hg co-exposure has the potential to evoke synergistic neurotoxicity even if their individual metals are below NOAELs, which reinforces the need to control and regulate potential sources of metal contamination.

Pb2+ modulates ryanodine receptors from the endoplasmic reticulum in rat brain.

Although the neurotoxic mechanism of lead (Pb2+) has been extensively studied, it is not well understood. The effects of Pb2+ on free cytosolic calcium (Ca2+) concentration and calcium-regulated events have been suggested to be major mechanisms in Pb2+ toxicity. Based on our previous findings that Pb2+ changes calcium release through ryanodine receptors (RyRs), the modulation of endoplasmic reticulum (ER) vesicular RyRs by Pb2+ was investigated further in the present study. The results of [3H]ryanodine binding assays showed that in the presence of a free Ca2+ concentration ([Ca2+]f) of 100µM, Pb2+ modulated the equilibrium of [3H]ryanodine binding to brain RyRs, with a U-type dose-response curve, where minimal binding was observed at a free Pb2+ concentration ([Pb2+]f) of 0.39µM. This modulation was also observed over a time course. Scatchard analysis indicated that both an increase in Kd and a possible decrease in Bmax were responsible for the decrease in binding induced by low [Pb2+]f. Moreover, the effects of Pb2+ on the function of ER RyRs in neurons might also be controlled by other RyR modulators. Whole-cell patch-clamp experiments revealed that dynamic calcium oscillations evoked by specific RyR agonists were depressed rapidly and reversibly by exposure to 10µM Pb2+. Our study indicates that RyRs are molecular targets of Pb2+, and this interaction disturbs Ca2+ signals and leads to neurotoxicity.

Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway.

Anacardic acid, which is commonly seen in plants of Anacardiaceae, is an important composition of cashew, ginkgo leaf and fruit, and it has been suggested in previous research to show antitumor activity. The main aim of the present study was to evaluate the anticancer effects of anacardic acid on cell apoptosis of prostatic cancer and molecular mechanisms of this phenomenon. In this study we found that anacardic acid inhibited cell proliferation, induced apoptosis and caspase-3/9 activities and Bax protein expression of prostatic cancer. Anacardic acid induced the ER stress inducing factors (BiP, CHOP, p-eIF2α), autophagy, LC3, Beclin-1, Atg 7 and DAPK3 protein expression, and suppressed p-Akt and p-mTOR protein expression of prostatic cancer. Si-CHOP was used to inhibit ER stress in prostatic cancer by anacardic acid, which showed that the cell proliferation was increased, apoptosis, and caspase-3/9 activities and Bax protein expression was suppressed, autophagy, LC3, Beclin-1, Atg 7 and DAPK3 protein expression was reduced, and p-Akt and p-mTOR protein expression was promoted. DAPK3 inhibited p-Akt and p-mTOR protein expression, enhanced the anticancer effects of anacardic acid on prostatic cancer through autophagy. For the first time, the present study showed that anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway.

Acute rejection after kidney transplantation promotes graft fibrosis with elevated adenosine level in rat.

AIMS: Chronic allograft nephropathy is a worldwide issue with the major feature of progressive allograft fibrosis, eventually ending with graft loss. Adenosine has been demonstrated to play an important role in process of fibrosis. Our study aimed to investigate the relationship between adenosine and fibrosis in renal allograft acute rejection in rat. MATERIALS AND METHODS: Wistar rats and SD rats were selected as experimental animals. Our study designed two groups. In the allograft transplantation group, kidneys of Wistar rats were orthotopically transplanted into SD rat recipients, the same species but not genetically identical, to induce acute rejection. Kidney transplantations of SD rats to SD rats which were genetically identical were served as the control. We established rat models and detected a series of indicators. All data were analyzed statistically. P<0.05 was considered statistically significant. RESULTS: Compared with the control group, levels of adenosine increased significantly in the allograft transplantation group, in which acute rejection was induced (P<0.05). Progressive allograft fibrosis as well as collagen deposition were observed. CONCLUSIONS: These findings suggested that level of adenosine was upregulated in acute rejection after kidney allograft transplantation in rat. Acute rejection may promote renal allograft fibrosis via the adenosine signaling pathways.

Villous Adenoma in Renal Pelvis With Manifestation of Percutaneous Fistula and Mucus Secretion.

A 70-year-old man, complaining of percutaneous fistula with jelly-like yellow mucus in the right kidney for a month, was admitted to our department. From computed tomography, stones and severe hydronephrosis but no suspicious mass was found in right kidney. Nephrectomy of right kidney was performed and pathological examination revealed a villous adenoma in the renal pelvis with moderate to severe atypical hyperplasia of glandular epithelium. Primary villous adenoma in renal pelvis is rare and believed to be related to chronic irritation of stone and inflammation. Mostly nephrectomy was performed before diagnosis was made.