Objective To investigate the correlation between statins and contrast-induced acute kidney injury (CI?AKI) and provide a reference basis for clinical practice. Methods It was a retrospective cohort study. The adult patients were admitted to Peking University First Hospital from January 1, 2018, to December 31, 2020, and received at least one intravascular iodinated contrast administration during hospitalization. The clinical data of the patients were collected. The enrolled patients were divided into statin group and non-statin group according to statin exposure. The exposure of statins was defined as use of any type of statins within 48 hours before iodinated contrast administration. The primary outcome was in-hospital AKI defined as AKI developed after contrast administration and before discharge, with 30 days as the endpoint observation time, and the secondary outcome was post-contrast AKI (PC?AKI) defined as AKI onset within 72 hours after contrast administration. Cox regression model was applied to investigate the correlation between statin prescription prior to contrast administration and clinical outcomes. Pre-specified interaction analysis was conducted to examine modification effect of age, gender, baseline estimated glomerular filtration rate (eGFR), diabetes and the injection method of contrast. Results Among 10 321 enrolled patients, the age was 63 (54, 71) years old, and 6 274 (60.8%) patients were males. There were 2 372 (23.0%) patients taking statins before the use of iodinated contrast agents, and the person-time incidence rate of in-hospital AKI was 2.5 per 1 000 person-days. The person-time incidence rate of statin users and statin non-users was 3.2 and 2.4 per 1 000 person-days, respectively. Compared with the non-statin group, age, serum creatinine and the proportions of males, admitted to the intensive care unit, lipid metabolism disorder, hypertension, diabetes, cerebrovascular diseases, cardiovascular diseases, using renin-angiotensin- aldosterone inhibitors, using diuretics, using non-steroidal anti-inflammatory drugs, using proton pump inhibitors, iodinated contrast administration via artery, eGFR<60 ml·min^-1·(1.73 m²)^-1 were higher, while the proportions of general anesthesia surgery, severe liver diseases and tumors, and eGFR were lower in the statin group (all P<0.05). Among 10 321 patients, 5 867 patients had serum creatinine measurement within 72 hours after iodinated contrast administration, among which 70 patients (4.0 per 1 000 person-days) developed PC?AKI. Multivariate Cox regression analysis showed that statin use was an independent protective factor for in-hospital AKI (HR=0.65, 95% CI 0.45?0.93, P=0.017) and PC?AKI (HR=0.44, 95% CI 0.22?0.88, P=0.020). Subgroup analysis showed the significant interaction between diabetes and statin use (P for interaction=0.039), and the protective effect of statins against in-hospital AKI was only observed in non-diabetic group (HR=0.45, 95% CI 0.26?0.77). There were no significant differences in subgroups stratified by age, sex, baseline eGFR and the injection method of contrast (all P for interaction>0.05). Conclusions Statin use prior to iodinated contrast administration is correlated with reduced risks of in-hospital AKI and PC-AKI in hospitalized patients, and the correlation between statin use and in-hospital AKI is more significant in non-diabetic patients. It is suggested that statin use before the application of iodinated contrast agents in hospitalized patients may prevent the occurrence of AKI.

Objective To evaluate the expression of tertiary lymphoid structures (TLS) in renal tissues, and the relationship between TLS and clinicopathological changes and prognosis in idiopathic membranous nephropathy (IMN) patients. Methods It was a single center retrospective study. The patients with IMN diagnosed by renal biopsy at Shengjing Hospital Affiliated to China Medical University from January 2018 to December 2020 were enrolled, and their clinicopathological data were collected. Immunohistochemistry was used to evaluate the expression of TLS in renal tissues. According to whether TLS expression in renal tissues was positive or not, the patients were divided into TLS-positive group and TLS-negative group, and the baseline differences in clinicopathological data between the two groups were compared. The clinical remission included complete remission and partial remission. Logistic regression analysis was used to analyze the correlation between serum phospholipase A2 receptor (PLA2R) antibody titer and positive TLS expression in renal tissues. Kaplan-Meier survival curve and log-rank test were performed to analyze the differences of proteinuria remission rates between TLS-positive and TLS-negative groups. Cox regression analysis was employed to identify the related factors of proteinuria remission. The receiver operating characteristic (ROC) curve was used to evaluate the value of TLS in predicting proteinuria remission. Results A total of 120 IMN patients were included in this study, with age of 50.00 (40.00, 57.75) years and 78 (65.00%) males. The 24-hour urinary protein was (7.54±4.14) g, 89 (74.17%) patients were positive for serum PLA2R antibody, and the serum PLA2R antibody titer was 90.49 (48.88, 155.33) RU/ml. Immunohistochemical results showed that TLS was mainly distributed in the renal cortex glomeruli or around renal blood vessels in renal tissues. There were 43 patients in the TLS-positive group and 77 patients in the TLS-negative group. The positive rate of serum PLA2R antibody in the TLS-positive group was 83.72% (36/43). Compared with the TLS-negative group, the TLS-positive group had lower serum albumin (t=-3.474, P<0.001) and estimated glomerular filtration rate (Z=-2.076, P=0.045), while serum creatinine (t=2.006, P=0.028), 24-hour urinary protein (t=4.140, P<0.001), serum PLA2R antibody titer (Z=4.628, P=0.001), glomerulosclerosis degree (Z=2.403, P=0.019), and proportions of hypertension (χ2=6.511, P=0.011), renal interstitial fibrosis (χ2=4.088, P=0.043), renal interstitial inflammatory cell infiltration (χ2=9.261, P=0.002), tubular atrophy (χ2=4.936, P=0.026) and extremely high-risk of kidney disease progression (χ2=9.352, P=0.002) were higher. Multivariate logistic regression analysis showed that serum PLA2R antibody titer was an independent factor correlated with positive TLS expression in renal tissues (OR=1.014, 95% CI 1.007-1.021). The median follow-up time was 18.00 (95% CI 16.07-19.93) months. Kaplan-Meier survival curve showed that the proteinuria remission rate in the TLS-positive group was lower than that in the TLS-negative group (Log-rank χ2=9.339, P=0.002). Cox regression analysis showed that positive TLS expression was an independent factor correlated with proteinuria remission (HR=0.228, 95% CI 0.177-0.297). ROC curve showed that TLS had a certain clinical predictive value for proteinuria remission (AUC=0.703, 95% CI 0.608-0.798). Conclusions IMN patients with positive TLS expression in renal tissues have a lower proteinuria remission rate, more severe pathological damage, and a higher risk of disease progression. TLS is expected to become a pathological marker for predicting the severity and prognosis of IMN.

Objective To evaluate the efficacy and safety of rituximab (RTX) in the treatment of idiopathic membranous nephropathy (IMN), explore the influencing factors of the therapeutic effect and construct a nomogram model for predicting the therapeutic effect. Methods A single retrospective study was conducted in IMN patients in the First Affiliated Hospital of Zhejiang University School of Medicine from January 2017 to December 2022. All patients received monotherapy with RTX and were followed up for at least 12 months. RTX regimen adopted a B-cell guided regimen to achieve 0 cells/μl of peripheral blood CD19+ B cells through multiple administrations, followed by monitoring every 2?3 months and adding doses as needed to maintain this state. The complete response rate, partial response rate, and composite response rate at 6 months, 12 months and the end of follow up were analyzed. Logistic stepwise regression and R language were applied to construct a nomogram model for efficacy prediction. The receiver operating characteristic (ROC) curve, calibration curve and Hosmer-Lemeshow test were used to internally validate the nomogram model. Results A total of 147 IMN patients were included in the study, with age of 56 (47, 65) years, 99 (67.4%) males. There were 69 (46.9%) newly treated patients, 78 (53.1%) retreatment patients. The follow-up time was 14.4 (12.0, 15.0) months. The total RTX dose was 1 800 (1 200, 2 400) mg. The composite response rates at 6 months, 12 months and the end of the follow-up were 36.7% (54/147), 59.9% (88/147) and 63.3% (93/147), respectively. The complete remission rates at 6 months, 12 months and the end of the follow-up were 6.1% (9/147), 13.6% (20/147) and 19.7% (29/147), respectively. Logistic stepwise regression analysis showed that age ≥ 65 years (OR=0.335, 95% CI 0.135?0.833), retreatment (OR=0.333, 95% CI 0.144?0.771), high cholesterol (OR=0.716, 95% CI 0.577?0.888), high serum creatinine (OR=0.978, 95% CI 0.963?0.993) and B-cell reconstruction within 6 months (OR=0.273, 95% CI 0.115?0.645) were independent correlated factors affecting composite remission. Based on these factors, a nomogram model for predicting the therapeutic effect of RTX in IMN patients was constructed. The ROC curve indicated that the accuracy of this model in predicting composite remission was good (AUC=0.814, 95% CI 0.744-0.883). The calibration curve showed that the predicted composite response rate had a good fit with the actual response rate (Hosmer-Lemeshow test χ²=11.917, P=0.155). Conclusions RTX has good efficacy and safety as a monotherapy for IMN patients. The constructed nomogram prediction model has high discrimination and accuracy to predict the efficacy of RTX treatment for IMN.

Objective To investigate the effects and mechanisms of cyclic adenosine monophosphate (cAMP) on cisplatin-induced acute kidney injury (AKI). Methods GSE227970 dataset derived from human renal tubular epithelial cells (HK-2 cells) in the GEO database was downloaded, and Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analysis were performed in normal and cisplatin-damaged cells. Eighteen 8-week-old male C57BL/6J mice with body weight of (22±2) g were randomly divided into normal group, cisplatin group and cAMP group according to random number table method, with 6 mice in each group. cAMP group was intraperitoneally injected with 30 mg/kg glumine cyclic adenosine monophosphate, while normal group and cisplatin group were intraperitoneally injected with the same volume of 0.9% sodium chloride solution for 10 consecutive days. The cisplatin and cAMP groups were intraperitoneally injected with 20 mg/kg cisplatin once on the 8th day. The body weight and kidney weight of mice were weighed, and kidney weight to body weight ratio was calculated. The blood urea nitrogen (BUN) and serum creatinine (Scr) in mice were detected. HE staining was used to evaluate the degree of renal injury. Western blotting was used to detect the protein expression of AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling pathway in renal tissues. In vitro experiments, HK-2 cells were set up in normal group, cisplatin group, cAMP group and cAMP+AMPK inhibitor group. Immunofluorescence was used to detect the protein expression of phosphorylated (p)-AMPK in HK-2 cells. Adenosine triphosphate content and ratio of NAD⁺ to NADH in cells were detected. Flow cytometry was used to detect cell apoptosis. Results Biological signal analysis showed that axon guidance, Ras-related protein 1 signaling pathway and cAMP signaling pathway were significantly changed in cisplatin group. The body weight, kidney weight and kidney weight/body weight ratio in cisplatin group were significantly lower than those in normal group (all P<0.05). However, after cAMP treatment, kidney weight was significantly higher compared with cisplatin group (P<0.05), and body weight and kidney weight/body weight ratio also increased, but the differences were not statistically significant (both P>0.05). BUN, Scr and renal tubular injury score in cisplatin group were significantly higher than those in normal group (all P<0.05). After cAMP treatment, BUN, Scr and renal tubular injury score were significantly lower than those in cisplatin group (all P<0.05). Western blotting results showed that cAMP treatment could significantly increase the decreased AMPK/ACC signaling pathway protein in the renal tissues of cisplatin-induced mice (all P<0.05). In vitro experiments, immunofluorescence detection showed that the expression of p-AMPK protein in cisplatin-induced HK-2 cells decreased, and the addition of cAMP increased the expression of p-AMPK protein in cisplatin-induced HK-2 cells (all P<0.05). cAMP treatment could alleviate cisplatin-induced injury in HK-2 cells, restore the reduction of adenosine triphosphate content and NAD⁺/NADH ratio, and reduce the apoptosis induced by cisplatin (all P<0.05), while AMPK inhibitor could eliminate the protective effect of cAMP on cisplatin-induced injury in HK-2 cells. Conclusion cAMP can play a protective role in renal injury caused by cisplatin, and its mechanism may be related to activation of AMPK/ACC signaling pathway.

The paper reports a case of Fabry disease in a child with non-singular nocturnal enuresis as the first symptom. The boy developed unexplained nocturnal enuresis with frequent daytime urination since the age of 6. Fabry disease was detected and diagnosed by chance through high-risk screening. The activity of α-galactosidase A by dry blood spot was 1.97 μmol·L^-1·h^-1 , and there was c.640-801G>A mutation in GLA gene. Urine routine, urinary microprotein and renal function were normal. However, there were mulberry bodies found in urine deposition microscopy, suggesting the presence of kidney injury. This case suggests that enuresis can be the first symptom of Fabry disease, and mulberry bodies can be seen in the urine at the early stage of the disease.

The paper reports a case of endocapillary proliferative glomerulonephritis without immune complex deposition, presenting with acute kidney injury and proteinuria. Renal pathology was characterized by predominant T cells and CD68⁺ macrophages infiltration in glomerular capillaries without immunocomplex deposits. After glucocorticoid therapy, the patient's condition has improved and reached complete remission. This type of renal pathology is extremely rare. Through literature review, it is considered that they may be caused by abnormal immune cells such as T cells and/or macrophages-mediated immune responses. It should be taken seriously in clinical practice, and its underlying causes and pathogenesis need further research.

Akkermansia muciniphila, a probiotic is discovered years earlier, colonizes the human intestinal mucosa. In recent years, researchers have found the correlation between Akkermansia muciniphila and progression of kidney diseases based on the theory of the gut-kidney axis. The abundance of Akkermansia muciniphila in the gut changes during the onset, regression and treatment of renal diseases such as congenital nephrology, chronic kidney disease, complications after renal transplantation. The research on the correlation between Akkermansia muciniphila and renal diseases is still in the initial stage. The review introduces the research progress on the role of Akkermansia muciniphila in renal diseases from three aspects: the biological characteristics of Akkermansia muciniphila, the abundance change in the progression of renal diseases, and their biological effects to provide references for the following research on the mechanisms of Akkermansia muciniphila in renal diseases and the application of clinical renal disease treatment.

Chronic kidney disease (CKD) is a major disease that severely harms the public health. As the disease progresses, patients may experience systemic complications involving multiple organs and finally develop end-stage kidney disease (ESKD), which severely threatens the lives of patients. And they have to rely on renal replacement therapies such as hemodialysis, peritoneal dialysis, or kidney transplantation to survive, imposing a heavy burden on families and society. Delaying the progression of CKD to reduce the incidence of ESKD and the risk of various severe complications is the primary goal of CKD treatment. Based on the latest evidence-based data and integrating the clinical practice experience of experts, this guideline has focused on formulating the comprehensive strategies including risk assessment for disease progression, strategies for delaying the disease progression, and management of complications in CKD. It is the aim to provide clinical practitioners with guidance on CKD management practices based on the latest evidence and suitable national conditions.