Thromboembolism (TE) is a common and serious complication of nephrotic syndrome (NS). NS is associated with hypercoagulability, which may be induced by changes in coagulation, anticoagulant, and fibrinolytic factors. Moreover, accumulating evidence supports the hypothesis that the complex interactions between genetic and acquired risk factors in TE should be considered and that genetic susceptibility should not be ignored. Extracellular vesicles (EVs) also play unique roles. Further research on EVs may provide new insights into the discovery and treatment of TE associated with NS. The occurrence of NS accompanied by TE may be associated with various risk factors. Preventive anticoagulant therapy can not only reduce the risk of TE in patients but also aggravate the risk of bleeding. Heparin and vitamin K antagonists (VKAs), traditional anticoagulant drugs, have been extensively applied in the prevention and treatment of thromboembolic diseases, and emerging direct oral anticoagulants (DOACs) also provide an alternative choice. Owing to the particularity of NS, the safe application of DOACs still needs to be addressed. This review aimed to comprehensively describe the pathophysiology of TE in NS, as well as analyze the associated risk factors, the opportunity for preventive anticoagulation, and current anticoagulant information.

Objective Hypocalcemia after parathyroidectomy (PTX) results in tetany, diarrhea, cardiac arrhythmia, and even sudden death. However, a meta-analysis or systematic evaluation of risk factors with the occurrence and development of hypocalcemia in patients with secondary hyperparathyroidism (SHPT) after PTX has never been performed. Methods A thorough search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and EMBASE, was performed to retrieve relevant studies from database inception to June 2021. Quality of the included studies was assessed by two independent reviewers using the Newcastle-Ottawa Scale. Review Manager 5.3 and Stata 16.0 were used for meta-analysis. The random-effects model was adopted to calculate the 95% CIs (I (2)> 50% or p < 0.05) of the combined effect size and the corresponding homogeneous data. Otherwise, a fixed-effects model was used. Results Thirteen studies including 2990 participants who met the inclusion criteria were enrolled in the present meta-analysis. The overall quality of the enrolled studies had a score of >7 points. Risk factors significantly related to hypocalcemia in patients with SHPT after PTX were preoperative serum calcium (OR 0.19, 95%CI 0.11-0.31), preoperative alkaline phosphatase (ALP) (OR 1.01, 95% CI 1.01-1.02), and preoperative intact parathyroid hormone (iPTH) (OR 1.38, 95%CI 1.20-1.58). Meanwhile, age (OR 0.97, 95%CI 0.87-1.10) was not significantly correlated with hypocalcemia after PTX. Conclusions Based on the current evidence, preoperative serum calcium, preoperative ALP, and preoperative iPTH were significant predictors of hypocalcemia in patients with SHPT after PTX. More attention should be given to patients with these risk factors for the prevention of postoperative hypocalcemia.

The present study aimed to detect the levels of microRNA (miR)-33a-5p in the renal tissue, serum and urine of patients with primary IgA nephropathy (IgAN), thereby preliminarily exploring the association between the levels of miR-33a-5p and the condition of primary IgAN to provide evidence for the expression of miR-33a-5p in the serum and urine of IgAN patients as a clinical marker. Reverse-transcription quantitative PCR was performed to evaluate the level of miR-33a-5p in IgAN patients according to severity and pathological classification. The results suggested that the levels of miR-33a-5p in the serum, urine and kidney tissues of patients with IgAN were lower than those of the control tissues obtained from cancer patients (0.28±0.25 vs. 1.00±0.45, P<0.05; 0.34±0.28 vs. 1.00±0.53, P<0.05; 0.47±0.27 vs. 1.00±0.38, P<0.05, respectively). Receiver operating characteristic curve analysis suggested that the serum and urine levels of miR-33a-5p may be used as a marker to differentiate renal injury in IgAN patients from healthy individuals. At the same time, according to the estimated glomerular filtration rate (eGFR) and Lee classification of nephropathy, it was determined that with the progression of renal failure and the increase of the pathological grade of kidney tissue, the relative level of miR-33a-5p in kidney tissue also decreased (eGFR <50 ml/min vs. eGFR ≥50 ml/min/1.73 m2 group: 0.38±0.27 vs. 1.00±0.34, P<0.001; Lee grade ≤3 group vs. Lee grade >3: 1.00±0.48 vs. 0.38±0.45, P<0.05). This result suggested that the levels of miR-33a-5p in serum, urine and kidney tissues decreased with the severity of renal injury and the progression of renal failure in patients with IgAN. Hence, miR-33a-5p detected in the serum and urine may be used as a non-invasive biomarker to reflect the progression of renal injury and renal failure in patients with IgAN.

Podocytes are the key cells involved in protein filtration in the glomerulus. Once proteins appear in the urine when podocytes fail, patients will end with renal failure due to the progression of glomerular damage if no proper treatment is applied. The injury and loss of podocytes can be attributed to diverse factors, such as genetic, immunologic, toxic, or metabolic disorders. Recently, autophagy has emerged as a key mechanism to eliminate the unwanted cytoplasmic materials and to prolong the lifespan of podocytes by alleviating cell damage and stress. Typically, the fundamental function of extracellular vesicles (EVs) is to mediate the intercellular communication. Recent studies have suggested that, EVs, especially exosomes, play a certain role in information transfer by communicating proteins, mRNAs, and microRNAs with recipient cells. Under physiological and pathological conditions, EVs assist in the bioinformation interchange between kidneys and other organs. It is suggested that EVs are related to the pathogenesis of acute kidney injury and chronic kidney disease, including glomerular disease, diabetic nephropathy, renal fibrosis and end-stage renal disease. However, the role of EVs in podocyte autophagy remains unclear so far. Here, this study integrated the existing information about the relevancy, diagnostic value and therapeutic potential of EVs in a variety of podocytes-related diseases. The accumulating evidence highlighted that autophagy played a critical role in the homeostasis of podocytes in glomerular disease.

Nephrotic syndrome, a rare complication of secondary syphilis and syphilitic minimal change disease, has only been fully documented in one case thus far. The current study describes two cases of nephrotic syndrome with minimal change disease due to syphilis infection. One case was of a 15-year-old boy while the other was a 47-year-old male. Both patients showed renal pathologic characteristics of minimal change disease and both were positive for the rapid plasma reagin (RPR). Prolonged antibiotic therapy with penicillin or ceftezole resulted in full remission in the two cases. In conclusion, it is important to recognize that syphilis is a reversible cause of nephrotic syndrome with minimal change disease. Antibiotic therapy can result in complete remission.

Cases of aggressive fibromatosis of the abdominal wall after peritoneal dialysis catheterization are relatively rare in clinical practice. A case of aggressive fibromatosis of the abdominal wall (AF) was retrospectively analyzed for clinical, imaging, pathological, diagnostic and treatment, and literature review was combined. The male patient, 27 years old, underwent peritoneal dialysis catheterization for 2 years due to peritoneal dialysis. This time, he was admitted for treatment due to the re-occurrence of peritoneal infection. The CT showed circular low-density shadow in the shape area of the abdominal wall catheter, which was wrapped around the drainage tube. The patient underwent surgical resection of the tumor and was diagnosed as aggressive fibromatosis by postoperative HE staining and immunohistochemistry.

乙型病毒性肝炎（HBV）是一种由乙型肝炎病毒引起,以肝脏病变为主的传染性疾病,对人类健康造成巨大威胁。据报道,全球有超过3.5亿人口携带乙肝病毒,每年约有60万人死于HBV相关疾病[1]。乙肝相关性肾炎（HBV-GN）作为HBV感染的肝外表现之一,是亚洲最常见的继发性慢性肾小球肾炎[2]。我国HBV-GN的发病率也高于世界其他地区[3]。HBV-GN病理类型多种多样,几乎所有的肾脏病理改变都可以出现在此种疾病中,目前常

Type 2 diabetes (T2D) accounts for about 90% of all diabetes patients and incurs a heavy global public health burden. Up to 50% of T2D patients will eventually develop neuropathy as T2D progresses. Diabetic peripheral neuropathy (DPN) is a common diabetic complication and one of the main causes of increased morbidity and mortality of T2D patients. Obstructive sleep apnea (OSA) affects over 15% of the general population and is associated with a higher prevalence of T2D. Growing evidence also indicates that OSA is highly prevalent in T2D patients probably due to diabetic peripheral neuropathy. However, the interrelations among diabetic peripheral neuropathy, OSA, and T2D hitherto have not been clearly elucidated. Numerous molecular mechanisms have been documented that underlie diabetic peripheral neuropathy and OSA, including oxidative stress, inflammation, endothelin-1, vascular endothelial growth factor (VEGF), accumulation of advanced glycation end products, protein kinase C (PKC) signaling, poly ADP ribose polymerase (PARP), nitrosative stress, plasminogen activator inhibitor-1, and vitamin D deficiency. In this review, we seek to illuminate the relationships among T2D, diabetic peripheral neuropathy, and OSA and how they interact with one another. In addition, we summarize and explain the shared molecular mechanisms involved in diabetic peripheral neuropathy and OSA for further mechanistic investigations and novel therapeutic strategies for attenuating and preventing the development and progression of diabetic peripheral neuropathy and OSA in T2D.

布氏杆菌病（Brucellosis）简称布病,是一种严重的人畜共患疾病,对世界多个地区及国家造成严重的健康及经济负担 [1] 。有研究表明,全世界每年约有50万人感染布病,发病人群主要分布于牧业发达地区及乡村,在我国该病主要分布于内蒙古自治区、吉林省、黑龙江、新疆和陕北等牧区[2,3]。多数感染布病的患者,都有明确的既往史,如接触患畜或其

One of the commonest causes of end-stage renal disease is diabetic kidney disease (DKD). Renal fibrosis, characterized by the accumulation of extracellular matrix (ECM) proteins in glomerular basement membranes and the tubulointerstitium, is the final manifestation of DKD. The TGF-β pathway triggers epithelial-to-mesenchymal transition (EMT), which plays a key role in the accumulation of ECM proteins in DKD. DCCT/EDIC studies have shown that DKD often persists and progresses despite glycemic control in diabetes once DKD sets in due to prior exposure to hyperglycemia called "metabolic memory." These imply that epigenetic factors modulate kidney gene expression. There is evidence to suggest that in diabetes and hyperglycemia, epigenetic histone modifications have a significant effect in modulating renal fibrotic and ECM gene expression induced by TGF-β1, as well as its downstream profibrotic genes. Histone modifications are also implicated in renal fibrosis through its ability to regulate the EMT process triggered by TGF-β signaling. In view of this, efforts are being made to develop HAT, HDAC, and HMT inhibitors to delay, stop, or even reverse DKD. In this review, we outline the latest advances that are being made to regulate histone modifications involved in DKD.

糖尿病肾病（DN）是糖尿病（DM）常见微血管并发症,它是引起的终末期肾病（ESRD）的主要原因,在发展中国家其发病率亦正逐步增加[1]。蛋白尿是DN常见的临床表现,DM患者随着病程延长,逐渐发展至DN,继而出现蛋白尿、肌酐升高等指标异常,但并非所有DM患者肾脏损害均由DN所致,由于DN与糖尿病肾病合并非糖尿病肾病(DN+

Hepatitis C virus (HCV) is a major cause of liver-associated morbidity and has an increasing prevalence worldwide. Hepatitis C virus infection may lead to chronic hepatitis, cirrhosis and liver failure. However, it is also associated with a wide range of extra-hepatic complications, such as cryoglobulinemia, an immune complex disease associated with cryoglobulin leading to multiple organ damage and, while the major symptom is vasculitis. The present study reported on a-58-year-old woman who was diagnosed with HCV-associated cryoglobulinemia with skin, kidney and blood system damage and biopsy-proven cryoglobulinemia membrano-proliferative glomerulonephritis. HCV RNA clearance occurred within a few weeks of interferon treatment and the patient was then treated by prednisolone and sustained interferon. While the therapeutic effect was obvious at first, the disease reappeared in combination with refractory infection and multiple organ failure, and the patient finally died. HCV-associated cryoglobulinemia is uncommon in developing countries such as China, while treatment guidelines remain to be established, particularly if complex complications are present.

目的 探讨老年2型糖尿病(T2DM)伴单纯糖尿病肾病(DN)、非糖尿病肾病(NDRD)和DN合并NDRD的临床及病理特点.方法 回顾性分析住院行肾活检的70例老年T2DM患者的临床及病理资料,详细比较DN、NDRD、DN+NDRD三组的临床及病理特点,并与同期203例非老年T2DM患者的临床及病理资料进行对比.结果 按病理分型的3个亚组:DN亚组占25.27%[(14+55)/273],NDRD亚组占63.74%[(44+130)/273],DN+NDRD亚组占10.99%[(12+18)/273].其中,DN亚组老年患者占5.13%,非老年患者占20.15%;NDRD亚组老年患者占16.12%,非老年患者占47.62%;DN+NDRD亚组老年患者占4.39%,非老年患者占6.59%.总体上老年组的DM病史、肾衰竭发生率明显高于非老年组,而老年组体重指数(BMI)、肾小球滤过率(eGFR)、血清白蛋白水平明显低于非老年组(P<0.05).老年组DN亚组的肾衰竭发生率明显高于非老年组,而BMI、24 h尿蛋白定量(UP)明显低于非老年组;老年组的NDRD亚组肾衰竭发生率明显高于非老年组,而BMI、eGFR明显低于非老年组(P<0.05);老年组DN+NDRD亚组的肾病综合征发病率和24 h-UP明显高于非老年组.老年组内DN亚组的24 h-UP、BMI明显低于DN+NDRD亚组;NDRD亚组DM病史、24 h-UP明显低于DN+NDRD亚组.非老年组内DN亚组的DM病史、24 h-UP明显高于NDRD亚组,而BMI、eGFR低于NDRD亚组;非老年组内DN亚组的24 h-UP明显高于DN+NDRD亚组,而血清白蛋白明显低于DN+NDRD亚组;非老年组内NDRD亚组的24 h-UP、血清白蛋白低于DN+NDRD亚组.病理诊断方面,老年组、非老年组及两组的NDRD亚组中,膜性肾病占的比例都是最大,IgA肾病次之.在老年组和非老年组的DN+NDRD亚组中,高血压肾小动脉硬化是最常见的病理类型.结论 老年T2DM中NDRD并不少见,DN、NDRD及DN+NDRD的临床表现难以鉴别,只有通过肾活检才能最终明确DN、NDRD和DN+NDRD的诊断.为提高老年T2DM患者肾脏疾病的缓解率和存活率,还需要大型、多中心、随机的前瞻性研究明确老年T2DM患者的肾脏病变特点.

Transforming growth factor beta1- (TGF-β1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-β1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-β1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-β1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-β1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-β1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.

Catheter malfunction caused by migration of the catheter tip is an ongoing challenge in patients on continuous ambulatory peritoneal dialysis. Reimplantation of a new catheter by open operation exposes the patient to additional hazards and costs. Non-operative treatment such as manual reduction, appropriate exercises and purgative enema tend to have a poor success rate. In this study, we report our experience with six patients on continuous ambulatory peritoneal dialysis in whom the migrated catheter tip was restored to the pelvic cavity with use of a processed gastroscopic brush.

Diabetic nephropathy (DN) remains a leading cause of mortality worldwide despite advances in its prevention and management. A comprehensive understanding of factors contributing to DN is required to develop more effective therapeutic options. It is becoming more evident that histone acetylation (HAc), as one of the epigenetic mechanisms, is thought to be associated with the etiology of diabetic vascular complications such as diabetic retinopathy (DR), diabetic cardiomyopathy (DCM), and DN. Histone acetylases (HATs) and histone deacetylases (HDACs) are the well-known regulators of reversible acetylation in the amino-terminal domains of histone and nonhistone proteins. In DN, however, the roles of histone acetylation (HAc) and these enzymes are still controversial. Some new evidence has revealed that HATs and HDACs inhibitors are renoprotective in cellular and animal models of DN, while, on the other hand, upregulation of HAc has been implicated in the pathogenesis of DN. In this review, we focus on the recent advances on the roles of HAc and their covalent enzymes in the development and progression of DN in certain cellular processes including fibrosis, inflammation, hypertrophy, and oxidative stress and discuss how targeting these enzymes and their inhibitors can ultimately lead to the therapeutic approaches for treating DN.

To investigate the clinical and histopathological features of non-diabetic renal disease (NDRD) superimposed on diabetic nephropathy (DN) in northeastern Chinese patients with type 2 diabetes mellitus (T2D), and compare the changes with those of pure DN and isolated NDRD.

Diabetic nephropathy (DN), a common complication associated with type 1 and type 2 diabetes mellitus (DM), characterized by glomerular mesangial expansion, inflammation, accumulation of extracellular matrix (ECM) protein, and hypertrophy, is the major cause of end-stage renal disease (ESRD). Increasing evidence suggested that p21-dependent glomerular and mesangial cell (MC) hypertrophy play key roles in the pathogenesis of DN. Recently, posttranscriptional modifications (PTMs) have uncovered novel molecular mechanisms involved in DN. However, precise regulatory mechanism of histone lysine methylation (HKme) mediating p21 related hypertrophy associated with DN is not clear. We evaluated the roles of HKme and histone methyltransferase (HMT) SET7/9 in p21 gene expression in glomeruli of diabetic rats and in high glucose- (HG-) treated rat mesangial cells (RMCs). p21 gene expression was upregulated in diabetic rats glomeruli; chromatin immunoprecipitation (ChIP) assays showed decreased histone H3-lysine9-dimethylation (H3K9me2) accompanied with enhanced histone H3-lysine4-methylation (H3K4me1/3) and SET7/9 occupancies at the p21 promoter. HG-treated RMCs exhibited increased p21 mRNA, H3K4me level, SET7/9 recruitment, and inverse H3K9me, which were reversed by TGF-β1 antibody. These data uncovered key roles of H3Kme and SET7/9 responsible for p21 gene expression in vivo and in vitro under diabetic conditions and confirmed preventive effect of TGF-β1 antibody on DN.

Diabetic nephropathy (DN) is the most serious chronic complications of diabetes; 20-40% of diabetic patients develop into end stage renal disease (ESRD). However, exact pathogenesis of DN is not fully clear and we have great difficulties in curing DN; poor treatment of DN led to high chances of mortality worldwide. A lot of western medicines such as ACEI and ARB have been demonstrated to protect renal function of DN but are not enough to delay or retard the progression of DN; therefore, exploring exact and feasible drug is current research hotspot in medicine. Traditional Chinese medicine (TCM) has been widely used to treat and control diabetes and its complications such as DN in a lot of scientific researches, which will give insights into the mechanism of DN, but they are not enough to reveal all the details. In this paper, we summarize the applications of herbal TCM preparations, single herbal TCM, and/or monomers from herbal TCM in the treatment of DN in the recent 10 years, depicting the renal protective effects and the corresponding mechanism, through which we shed light on the renal protective roles of TCM in DN with a particular focus on the molecular basis of the effect and provide a beneficial supplement to the drug therapy for DN.

International Entrepreneurship, is not what happens, China also actively solve business problems of college students. For this problem, college students should clear business purpose, andgive full play to their own advantages, strive to solve the problem in the process of entrepreneurship. Make a contribution to innovation and entrepreneurship education in China.