Elderly patients with acute kidney injury (AKI) face a significantly increased mortality risk. Recent advances in machine learning technology have made it possible to predict the risk of death in patients at an early stage, which help to enable timely clinical intervention, optimize treatment strategies, and allocate hospital resources reasonably. We conducted a retrospective analysis of elderly patients admitted to the People’s Liberation Army General Hospital (PLAGH) between 2008 and 2018. This study included data on demographic characteristics, comorbidities, and laboratory test results. We employed five machine learning algorithms, including L2-regularized logistic regression (L2-logistic), Least Absolute Shrinkage and Selection Operator (LASSO), eXtreme Gradient Boosting (XGBoost), Random Forest (RF), and Multi-layer Perceptron (MLP). To address the class imbalance issue , we employed oversampling techniques. Model performance was primarily evaluated using the area under the receiver operating characteristic curve (AUC), and SHapley Additive exPlanations (SHAP) values were introduced to enhance the interpretability of the prediction models. A total of 1290 AKI patients were enrolled in the study, with a 28-day mortality rate of 25.43

Qiangguo Ao, Yabin Zhang, Yang Liu, Rui Zhu, Zhen Wu, Jiayu Guo, Jie Zhang, Ying Ding, Qingli ChengDepartment of Nephrology, The Second Medical Center of Chinese PLA General Hospital, National Clinical Research Centre for Geriatric Diseases, Beijing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Qingli Cheng; Ying Ding, Email qlcheng64@163.com; dingying@301hospital.com.cnPurpose: Acute kidney injury (AKI) carries a high burden in hospitalized older adults. While mean arterial pressure (MAP) is a key modifiable factor, the prognostic value of its dynamic, individualized assessment beyond static thresholds remains poorly defined in this population.Patients and Methods: In this retrospective cohort of 1248 hospitalized patients aged ≥ 65 years with AKI, we proposed and validated a three-dimensional hemodynamic assessment framework, evaluating: (1) the absolute MAP value at AKI onset (MAPonset); (2) the relative change from patient-specific baseline (MAP change rate); and (3) the time of recovery to baseline. We defined distinct hemodynamic phenotypes and assessed their association with major adverse kidney events within 90 days (MAKE-90) using Cox regression. The incremental predictive value was evaluated with random forest models.Results: Both MAPonset ≤ 65 mmHg (HR 1.33, 95% CI 1.05– 1.69) and a decline in MAP of ≥ 10% from baseline (HR 1.26, 95% CI 1.03– 1.54) independently predicted MAKE-90. Crucially, failure to recover within 72 hours was associated with a higher risk (HR 1.71, 95% CI 1.37– 2.15). The integrated phenotype of severe initial hypotension with delayed recovery identified patients with the poorest prognosis (HR 1.72, 95% CI 1.36– 2.17). Incorporating these dynamic parameters significantly improved the prediction of MAKE-90 (AUC increased from 0.71 to 0.76).Conclusion: This study suggests that a dynamic, individualized MAP assessment might refine risk stratification beyond static thresholds in hospitalized older adults with AKI. Internal evaluation of the integrated dynamic phenotype showed improved predictive performance for adverse outcomes. However, given the retrospective design and substantial potential for confounding, these findings are exploratory. They require rigorous external validation in prospective cohorts before any consideration for clinical application.Keywords: individualized assessment, mean arterial pressure, acute kidney injury, older patients, prognosis

Renal fibrosis, the common endpoint of chronic kidney disease, is exacerbated by renal ischemia. While human iPSC-derived MSCs (iMSCs) hold therapeutic promise, their role in modulating the ischemic renal microenvironment, particularly through macrophage-immune crosstalk, remains unclear. This study assesses whether iMSCs alleviate renal fibrosis by targeting macrophage-STING to restore capillaries. The protective effects of iMSC-conditioned medium (iMSC-CM) were assessed in H₂O₂‑induced HK‑2 and HUVEC models using CCK‑8, ROS staining, scratch assay, and tube formation assays. A mouse model of unilateral ischemia‑reperfusion (UIR) was established; mice received intravenous iMSCs or PBS. Kidneys were analyzed by histology, immunohistochemistry, qPCR, and Western blot. Transcriptomic sequencing revealed enrichment of immune-related pathways, including the STING pathway. To validate the role of STING, UIR mice were treated with the STING agonist DMXAA with or without iMSCs, and STING activation was assessed in LPS-stimulated macrophages in vitro. Macrophage polarization was evaluated by F4/80 co‑staining with CD86 (M1) or CD206 (M2). iMSC-CM mitigated H₂O₂-induced damage in HK-2 cells by promoting proliferation, reducing ROS levels, and suppressing fibrosis markers, and it promoted repair and angiogenesis in HUVECs. In vivo, iMSCs homed to injured kidneys, attenuated inflammation and fibrosis, notably reduced capillary rarefaction. Mechanistically, iMSC treatment profoundly inhibited STING activation in renal macrophages. This suppression disrupted a critical inflammatory axis: it reduced macrophage-derived IFN-β, leading to decreased infiltration of cytotoxic CD8⁺ T cells, which are detrimental to vascular endothelial cells. Consequently, the renal capillary network was preserved. Finally, STING agonist treatment abolished the anti-fibrotic benefits of iMSCs. Collectively, this work reveals that iMSCs ameliorate renal fibrosis via the macrophage STING/CD8+ T cell axis, thereby preserving renal capillaries and highlighting a novel mechanism for iMSC-based therapy.

Diabetic kidney disease (DKD) remains one of the most serious complications of type 2 diabetes, significantly impacting patients' morbidity and mortality. Microalbuminuria (mALB), a clinically validated biomarker, plays a key indicator for both early diagnosis and predicting the progression of DKD. However, existing point-of-care testing methods for albumin detection often suffer from limited sensitivity and operational complexity. To overcome these challenges, we developed and evaluated a fully printed, photonic crystal-integrated microarray-assisted point-of-care platform specifically designed for the rapid and precise detection of mALB. The system employs polymer latex microspheres, selected for their optical compatibility with detection fluorophores, as signal-enhancing carriers. By exploiting the photonic bandgap and photon localization effects inherent in photonic crystal structures, the platform significantly amplifies fluorescence signals in immunoassays, thereby substantially enhancing detection sensitivity and resolution. A detection method based on a double-antibody sandwich immunoassay was employed, enabling specific antigen-antibody binding and accurate quantification. Validation using clinical urine samples demonstrated the diagnostic efficiency of the platform. The full analysis can be executed in under 10 min, demonstrating a robust linear association between the fluorescence level and the mALB content.. The platform achieved a detection limit of 19.5 pg mL-1 and an accuracy of up to 92.9%. Further validation with 70 clinical urine samples confirmed that the platform exhibited a good diagnostic performance, demonstrating high sensitivity, specificity, and operational stability. In summary, this photonic crystal microarray-based point-of-care system offers a sensitive, accurate, and time-efficient solution for early DKD diagnosis and long-term disease monitoring. Its convenience and portability render it ideal for frequent assessments and long-term patient care, possibly enhancing results and decreasing medical expenses.

Introduction Limited research has focused on the prospective influence of insulin resistance (IR) on new-onset chronic kidney disease (CKD) in healthy screening populations. Therefore, we aimed to investigate how IR, assessed via the estimated glucose disposal rate (eGDR), and metabolism-related comorbidities influence new-onset CKD.Research design and methods This two-stage retrospective cohort study (cross-sectional and longitudinal analyses) used data from health check-up participants at the Chinese People’s Liberation Army General Hospital (2009–2021). The cross-sectional analysis included 83 346 participants with or without CKD; the longitudinal analyses included 13 738 participants without prior CKD who visited the hospital at least two times. The cross-sectional phase of this study analyzed the relationship between IR and CKD; the longitudinal phase analyzed the relationship between IR and new-onset CKD. The mediating role of metabolism-related comorbidities was also explored.Results In the cross-sectional analysis, 6.77% (n=5643) of patients had prior CKD. The eGDR was significantly higher in the non-CKD group than in the CKD group (9.16±2.11 vs 7.19±2.32, p<0.001). Higher eGDR was associated with lower CKD prevalence (OR: 0.91, 95% CI: 0.89 to 0.93, P for trend<0.001). In the cohort analysis, the average time to trigger endpoint events was 2.95±2.02 years, with 403 (2.93%) new-onset CKD cases reported. A linear correlation was observed between eGDR and new-onset CKD (p<0.001), with higher eGDR linked to reduced CKD risk (HR: 0.88, 95% CI: 0.82 to 0.96, P for trend=0.002). Mediation analysis revealed significant indirect effects of diabetes mellitus (17.1%), systolic blood pressure (22.0%), glycated hemoglobin (11.1%), and brachial–ankle pulse wave velocity (9.7%) (all p<0.05).Conclusions IR is independently linked to new-onset CKD, with blood glucose, blood pressure, and arterial stiffness mediating this relationship. These findings underscore the importance of managing IR and metabolic comorbidities to prevent CKD onset in at-risk populations.

Background:Diabetes significantly contributes to chronic kidney disease and end-stage kidney disease. With advancing haemodialysis (HD) technology and an ageing HD population, glycaemic control has become increasingly complex. Herein, we aimed to analyse the blood glucose fluctuations and hypoglycaemia risk factors in older adults with diabetes undergoing HD. Methods:This study included older adults with diabetes undergoing HD (April-July 2024). Continuous glucose monitoring assessed glycaemic profiles, comparing HD and non-HD days. Subgroup analyses examined all-day, dialysis-related, post-dialysis, and nocturnal hypoglycaemia. Results:Among 104 participants, 57 (54.8%) experienced hypoglycaemia on HD days versus 25 (24.0%) on non-HD days (P < .001). Two hours post-HD, 29 participants (27.88%) had hypoglycaemia compared with three (2.88%) (P < .001) on non-HD days. Mean blood glucose (MBG) was higher on HD days (7.59 vs. 7.45 mmol/l), with greater variability (coefficients of variation: 29.0% vs. 20.2%; standard deviation: 1.78 vs. 1.47 mmol/l; P < .001). Older age, morning dialysis, and lower MBG and BG at HD initiation increased hypoglycaemia risk during HD and within 2 h post-HD (all P < .05). Elevated MBG {odds ratio (OR) [95% confidence interval (CI)]: 0.20 (0.07, 0.58), P = .003} and BG ≥ 8.0 mmol/l at HD initiation (OR (95% CI): 0.04 (0.00, 0.34), P = .003) reduced hypoglycaemia risk during HD. Conclusion:Older adults with diabetes undergoing HD exhibited significant glycaemic fluctuations and hypoglycaemia prevalence on HD days, particularly during or post-dialysis. Maintaining higher MBG and pre-HD BG may reduce hypoglycaemia. These findings underscore the need for tailored glycaemic management.

This study examined the impact of inflammation on hypoxic renal tubular epithelial cell (RTEC) injury in a hyperglycemic environment, emphasizing the regulatory role of miR-125b and the mechanisms by which diabetes influences acute kidney injury. A hypoxia/reoxygenation (H/R) model was established in mouse RTECs. Mouse RAW264.7 macrophages were pre-treated under seven conditions: high glucose (HG), normal glucose (NG), HG + miR-125b inhibition (HG + miR-125b inhibitor), HG control (HG + vector), mannitol control (NG + mannitol), and M1/M2 macrophage positive controls. Each group was co-cultured with hypoxic/reoxygenated RTECs for 24 h. The optimal H/R model was achieved with 4 h of hypoxia followed by 24 h of reoxygenation. Macrophages pre-treated with HG and co-cultured with H/R RTECs showed significantly increased apoptosis, reactive oxygen species (ROS) fluorescence intensity, and epithelial injury/oxidative stress markers (lactate dehydrogenase [LDH] and malondialdehyde [MDA]), along with decreased antioxidant superoxide dismutase (SOD) levels. IL-1β levels significantly increased, while IL-10 levels decreased. All renal tubular injury markers increased significantly (P < 0.01 or P < 0.05). However, miR-125b inhibition reduced apoptosis, ROS, LDH, MDA, and renal injury marker levels while increasing SOD and IL-10 levels (P < 0.01 or P < 0.05). Thus, hyperglycemia-induced macrophage polarization toward the M1 phenotype exacerbates hypoxic RTEC damage, which can be partially mitigated by miR-125b inhibition.

Objective Because of the limited number of studies and small sample sizes, whether metabolic syndrome (MS) leads to the occurrence and progression of osteoporosis and the possible underlying mechanisms require further investigation. This study aimed to investigate the association between MS and osteoporosis, along with its influencing factors. Methods This observational cross-sectional study included 139,470 individuals aged ≥ 18 years who underwent health examinations from September 2014 to March 2022. Based on bone mineral density (BMD) screening results, the participants were categorized into a suspected osteoporosis or nonosteoporosis group (control). Participants were further divided into those who met 0 MS criteria, 1 MS criterion, 2 MS criteria, and ≥ 3 MS criteria (MS group). Participants who had undergone health examinations at least twice formed the follow-up cohort; a self-matched analysis was performed on those with follow-up periods ≥ 5 years and unchanged MS grouping. Results Several examination indicators in the suspected osteoporosis group showed statistically significant differences compared with the control group. The proportion of suspected osteoporosis in the MS group was significantly increased compared with that in the 0 MS criteria group (odds ratio [OR]: 1.215, Z = 29.11, P < 0.001, 95% confidence interval: 1.199–1.231). After adjusting for age, sex, smoking, and alcohol consumption, the 2 MS criteria group and MS group still had OR values > 1 (P < 0.001). In the follow-up cohort, the proportion of suspected osteoporosis increased gradually with an increase in the number of MS criteria met at baseline and during each follow-up visit (P < 0.05), with the highest proportion observed in the MS group. However, the proportion of suspected osteoporosis did not increase significantly over time in the different MS groups (P > 0.05). In the follow-up cohort, the proportion of individuals transitioning from normal BMD to suspected osteoporosis was higher in the MS group after ≥ 5 years of follow-up compared with the group meeting 0 MS criteria (0.08% versus 1.15%, χ2 = 10.76, P = 0.001). There was no significant difference in BMD values for the 0 MS criteria group after 5 years (P > 0.05), whereas the other three groups experienced a significant decrease in BMD values after 5 years (P < 0.05). Conclusion MS is an independent risk factor for osteoporosis, and the effect of risk factors related to MS on osteoporosis may exceed that of aging alone. The specific mechanisms warrant further investigation.

Objective:SOX11 is expressed in numerous malignancies, including hepatocellular carcinomas (HCC), but its oncogenic function has not been elucidated. Here, we performed a comprehensive bioinformatics analysis of the Liver Hepatocellular Carcinoma (LIHC) dataset to investigate the function of SOX11 in tumorgenesis. Methods:SOX11 expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were validated by immunohistochemistry (IHC). Co-expression, differential expression, and functional analyses utilized TCGA-LIHC, Timer 2.0, Metascape, GTEx, and LinkedOmics databases. Associations with immune infiltration, ferroptosis, and immune checkpoint genes were assessed. Genetic changes were explored via CBioPortal. Logistic regression, receiver operating characteristic curve (ROC), Kaplan-Meier analysis, and nomogram modeling evaluated associations with HCC clinicopathological features. SOX11's impact on proliferation and migration was studied in HepG2 and HuH7 cell lines. Results:SOX11 was significantly elevated in HCC tumors compared to controls. SOX11-associated genes exhibited differential expression in pathways involving extracellular membrane ion channels. Significant associations were found between SOX11 levels, immune infiltration, ferroptosis, and immune checkpoint genes in HCC tissue. SOX11 levels correlated with HCC stage, histologic grade, and tumor status, and independently predicted overall and disease-specific survival. SOX11 expression effectively distinguished between tumor and normal liver tissue. Spearman correlations highlighted a significant relationship between SOX11 and ferroptosis-associated genes. Decreased SOX11 levels in HepG2 and HuH7 cells resulted in reduced proliferation and migration. Conclusions:SOX11 was found to represent a promising biomarker within HCC diagnosis and prognosis together with being a possible drug-target.

To the Editor: Globally, acute kidney injury (AKI) is a common life-threatening condition. AKI is more prevalent in elderly patients, with increasing mortality rates. Compared with younger patients, older patients with AKI have a higher risk of persistent injury and poorer prognoses.[1] Older individuals often have comorbidities, increasing their susceptibility to AKI. Kidney Disease: Improving Global Outcomes (KDIGO) criteria define and stage AKI based on the higher stage of AKI defined by either serum creatinine (SCr) level or urine output (UO).[2] However, the record of UO is difficult to access in clinic, the data on the value of UO combined with SCr for AKI diagnosis or prognosis in elderly patients are lacking. Therefore, the objectives of this study were to investigate whether UO would influence the classification of AKI and improve the accuracy of prediction of the clinical prognosis in elderly patients. We performed a retrospective cohort study to assess the survival outcomes of AKI in older patients with different stages of AKI based on SCr alone or the combination criteria. The study included male patients aged >65 years who presented to the Second Medical Center (Geriatric Department) of the Chinese People's Liberation Army General Hospital with AKI between January 1, 2008, and December 31, 2018. Patients with either dialysis-dependent end-stage kidney failure or incomplete medical history were excluded from the study. Recruited patients were followed up for >90 days after the AKI occurence to determine the clinical outcome of mortality. This study was registered in ChiCTR (http://www.chictr.org.cn/, ChiCTR2200055518) and was approved by the Ethics Committee of Chinese People's Liberation Army General Hospital (No. S2022–342-01). The informed consent of the present study was waived owing to the retrospective nature. The SCr diagnostic criteria defined in the KDIGO AKI guidelines were adopted to recruit patients; the criteria were as follows: (1) increase in SCr >26.5 μmol/L within 48 h or (2) increase in SCr exceeding 1.5-fold above the baseline value within 7 days. The severity of AKI was classified by the KDIGO staging criteria using the SCr criteria alone or a combination of SCr or UO criteria. AKI was staged into three stages for severity. Categorical variables were presented as as a percentage (%) and were compared using the chi-squared test. The Kaplan-Meier method and log-rank test were used to compare the overall survival rates among patients with different stages of AKI based on different classification criteria. Data were obtained from hospital electronic health records. Age, comorbidities, and accompanying conditions (such as mechanical ventilation, proteinuria) at AKI onset were included in univariable logistic regression analysis. Variables with P < 0.05 in the univariable regression analysis were included in the multivariable binary logistic regression equation as covariates to estimate odds ratios (ORs) of AKI stages for mortality. Statistical analyses were performed using SPSS version 22.0, for Windows (SPSS Inc., Chicago, IL, USA). A total of 1509 eligible patients who experienced AKI were included in the final cohort. Based on SCr criteria alone, patients were categorized as follows: stage 1 AKI (n = 1314; 87.1%), stage 2 AKI (n = 151; 10.0%), and stage 3 AKI (n = 44; 2.9%). According to the KDIGO criteria, the distribution of AKI was as follows: stage 1, 1023 (67.8%); stage 2, 290 (19.2%); and stage 3, 196 (13.0%). Overall, 556 patients (36.8%) died within 90 days. Compared with survival group, non-survival group had higher proportion of severe AKI (stage 3), either defined by the SCr criteria alone or the KDIGO criteria (SCr criteria: 4.1% [23/556] vs. 2.2% [21/953], P < 0001; KDIGO criteria: 27.2% [151/556] vs. 4.7% [45/953], P < 0001). The 90-day survival rate decreased from 65.7% (863/1314) in those with stage 1 to 45.7% (69/151) and 47.7% (21/44) for those with stages 2 and 3 AKI, respectively, based on SCr criteria. Kaplan-Meier curves for 90-day cumulative survival showed a significantly lower survival rate in stage 2 or stage 3 compared to stage 1 when categorized by SCr criteria alone (stage 2 vs. stage 1, hazard ratio [HR] = 1.92, 95% CI [1.42–2.58], P < 0.001; stage 3 vs. stage 1, HR = 1.72, 95% CI [1.02–2.90], P = 0.009) [Figure 1A]. However, there was no significant difference between stage 2 and stage 3 (stage 2 vs. stage 3, HR = 0.90, 95% CI [0.50–1.62], P = 0.659). In comparison, 90-day cumulative survival rate decreased gradually with the severity of AKI based on the combination criteria (stage 2 vs. stage 1, HR=2.05, 95% CI [1.64–2.54], P < 0.001; stage 3 vs. stage 1, HR = 5.08, 95% CI [3.74–6.91], P < 0.001; stage 3 vs. stage 2, HR = 2.49, 95% CI [1.75–3.53], P < 0.001) [Figure 1B]. The 90-day cumulative survival rate decreased from 73.6% (753/1023) in those with stage 1 AKI to 53.64% (155/290) and 23.0% (45/196) in those with stages 2 and 3 AKI, respectively, based on the combination criteria.Figure 1: Associations between AKI stages and 90-day cumulative survival. (A) Kaplan-Meier survival curves for 90-day cumulative survival of older AKI patients based on SCr criteria only. (B) Kaplan-Meier survival curves for 90-day cumulative survival of older AKI patients based on the combination of SCr and UO. AKI: Acute kidney injury; CI: Confidence interval; KDIGO: Kidney Disease: Improving Global Outcomes; SCr: Serum creatinine; UO: Urine output.Logistic regression analysis was performed to further evaluate the ORs of AKI stages for mortality. Age, baseline estimated glomerular filtration rate, hypertension, hyperlipidemia, myocardial infarction, atrial fibrillation, chronic heart failure, chronic obstructive pulmonary disease, tumor, anemia, mechanical ventilation, and proteinuria were significant in the univariable logistic regression analysis and included in the multivariable binary logistic regression equation as covariates. According to the multivariable binary logistic regression, the mortality risk of patients with stage 3 AKI and stage 1 when defined by the SCr criteria alone was not statistically significant in the adjusted model (adjusted OR = 1.65, 95% CI [0.80–3.41], P = 0.179), while the adjusted mortality risk in patients with stage 3 AKI were significantky greater compared with those with stage 1 AKI when defined by the combination criteria (adjusted OR = 7.03, 95% CI [4.72–10.49], P < 0.001) [Supplementary Table 1, https://links.lww.com/CM9/B438]. Large studies have shown that even small increases in SCr levels are independently associated with increased mortality. Compared to patients without AKI, the odds of mortality were progressively higher for patients at higher AKI stages based on SCr alone.[3] However, in this study, older patients with stage 3 AKI defined by SCr alone did not exhibit worse survival than those with stage 2 AKI. In older individuals, SCr is not considered an ideal biomarker for AKI stage. Our findings support this claim and further indicate the limited usefulness of SCr for classification and prognosis prediction. The rise in SCr is often blunted in elder population due to reduced muscle mass.[4] Older patients with AKI may have a higher incidence of pre-renal, nephrotoxic, and obstructive issues.[5] Moreover, older patients are more prone to decreased renal perfusion due to heart failure, dehydration, or depletion of effective circulating volume. These risk factors can directly result in oliguria rather than increase SCr. The addition of UO criteria to SCr criteria leads to an earlier recognition of AKI in elderly patients. In this study, AKI stages based on the combination of UO and SCr criteria have a better discriminative ability of mortality than that based on SCr alone. These findings confirm the absolute necessity to diagnose and stage AKI using criteria combined with SCr and UO. This study has a few limitations. First, this was a single-center retrospective study, and so the results may not be generalizable to older patients with AKI in other locations. Second, our analysis is based on a male veteran cohort, which also limits the generalizability of our findings. Studies in older women with AKI may yield different results. Finally, the outcomes of AKI could be confounded by different causes, which were not individually discussed. In conclusion, survival outcomes did not significantly worsen with more advanced AKI stage when defined by SCr alone in older male patients. With the addition of UO to the SCr criteria, mortality increased gradually with severity of AKI across all stages. It is necessity to diagnose and stage AKI using criteria combined with SCr and UO in older male AKI patients. Funding This work was supported by a grant from the Special Scientific Research Project of Military Health Care (No. 21BJZ17) Conflicts of interest None.

BackgroundIn patients with acute heart failure (AHF) coexisting with oliguria, high doses of loop diuretics are often ineffective in increasing urine output and may adversely affect the patient's prognosis, especially in elderly patients. We investigated the efficacy of adding tolvaptan (TLV) on improving the prognosis in elderly patients with AHF coexisting with oliguria.MethodsAll data for this retrospective cohort study were extracted from the electronic medical record system of the Second Medical Center of Chinese PLA General Hospital from January 2018 to December 2020. Patients diagnosed with AHF coexisting with oliguria were enrolled in this study and were divided into TLV and non-TLV groups based on the use of TLV. The primary outcome was all-cause mortality at 7 and 90-day. The secondary outcomes were the remission of AHF within 7 and 30 days or continued progression of AHF, and new-onset chronic kidney disease (CKD) after 90 days. Cox proportional hazards regression was used to assess the relationships between all-cause mortality and diuretic regimens, demographics, laboratory parameters, comorbidities, and medications.ResultsA total of 308 patients met the study criteria for the final statistical analysis, and they had a median age of 91 years (88, 95). The results showed that the addition of TLV was associated with a decreased risk of the 7 and 90-day all-cause mortality in patients with AHF with oliguria [adjusted HR, 95% CI: 0.60 (0.37, 0.98), p = 0.042; 0.56 (0.41, 0.75), p < 0.001, respectively]. Adding TLV significantly increased urine output and decreased N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in 7 days, and alleviated the progression of AHF within 30 days. There were no statistically significant differences between the patients with or without TLV in terms of the occurrence of hypernatremia, the development of hepatic impairment within 30 days, and new-onset CKD after 90 days.ConclusionsThis study demonstrated that the addition of TLV was clinically effective in increasing urine output, and had favorable effects on alleviating AHF progression and may reduce the risk of all-cause mortality at 7 and 90-day in elderly patients with AHF with oliguria, and TLV had a good safety profile.Trial registrationhttp://www.chictr.org.cn/showprojen.aspx?proj=148046, identifier: ChiCTR2200055518.

绝大多数肾小球疾病是由免疫系统异常所介导的疾病，因此，免疫抑制剂在临床上肾小球疾病的治疗中常用。多数免疫抑制剂作用于T淋巴细胞和B淋巴细胞等免疫细胞，但近年来的研究表明，免疫抑制剂对肾小球足细胞也具有直接的作用。与单纯使用类固醇激素比较，免疫抑制治疗可以提高肾病综合征的缓解率、减少终末期肾病的发生率，但也有可能增加各种不良作用，给肾小球疾病患者带来危害。因此，临床上合理使用免疫抑制剂十分重要。首先，在开始进行免疫抑制剂治疗之前，应对患者进行传染病和各类感染性疾病的筛查、接种各类必要的疫苗，提前做好预防各类感染的措施。其次，要注意钙调蛋白抑制剂等免疫抑制剂本身所具有的肾毒性。第三，妊娠期和老年人对药物毒性的易感性明显增高，要特别注意这些特殊人群使用免疫抑制药物的安全性、慎重选择相关药物。第四，要注意免疫抑制剂的可能致癌作用，例如长期大量应用环磷酰胺可能会诱发膀胱癌等恶性病变。最后，临床上在使用免疫抑制剂时，需要根据不同药物的性质采取相关减毒措施以尽量减少药物的副作用，对于长期使用免疫抑制剂的患者应该定期进行癌症筛查以防患于未然。总之，在治疗肾小球疾病时使用免疫抑制剂需要临床医师对每一位患者进行缜密细心地诊治。近年来药物遗传学的发展也给免疫抑制剂在基因水平上的个体化用药带来了希望。

Urinary kidney injury molecule 1 (uKIM-1) serves as a reliable marker for the early diagnosis of acute kidney injury (AKI). The rapid and facile detection of changes in uKIM-1 is essential for early AKI diagnosis, ultimately improving the prognosis of patients. In this study, we developed a fully printed photonic crystal-integrated microarray with photonic crystal-enhanced fluorescence properties, which can detect uKIM-1 levels at the point-of-care. We confirmed its efficacy in the early diagnosis of AKI using clinical urine specimens. Direct quantitative detection of uKIM-1 was achieved within 10 min. The lowest limit of detection is 8.75 pg·mL −1 with an accuracy of 94.2%. The diagnostic efficacy was validated using 86 clinical urine samples, highlighting the high sensitivity and stability of the photonic crystal microarray. Consequently, a facile and reliable immunoassay was designed and prepared for the rapid quantitative detection of uKIM-1, which is crucial for the early identification and convenient detection of AKI in hospital or community settings. Rapid, convenient, cost-effective, and long-term monitoring of changes in uKIM-1 levels can assist clinicians in making timely adjustments to treatment regimens, preventing the transition from AKI to chronic kidney disease (CKD), improving the quality of life of patients with AKI, and reducing healthcare costs. It highlights the advantages of utilizing urine samples as a noninvasive and easily accessible medium for early detection and monitoring of kidney-related conditions.

Background Elderly patients exhibit a higher incidence of chronic heart failure (CHF). Patients with CHF can develop acute kidney injury (AKI) during follow-up, which can result in poor prognosis. This relationship between kidney dysfunction and levels of N-terminal pro-brain natriuretic peptides (NT-proBNP), with regard to prognosis, is complicated and has rarely been analyzed in elderly patients with CHF. Method We conducted a retrospective cohort study involving patients with a CHF history aged ≥ 65 years, who experienced an episode of AKI. Kaplan–Meier curves and Cox or logistic proportional hazards regression models were used to evaluate the association between serum NT-proBNP concentrations and mortality or renal recovery by day 90. Results A total of 1,160 eligible patients with AKI were available for the study. Of this sample, 41.5% of patients died within 90 days of the onset of AKI. Patients with a decreased change in NT-proBNP accompanying the episode of AKI had a lower risk (adjusted OR = 0.56, 95% CI = 0.34−0.91) of more severe AKI (stage 2 and 3 vs. stage 1). The more severe AKI were associated with higher mortality and non-recovery of renal function in elderly patients with CHF, independent of NT-proBNP levels. Elevated levels of baseline lnNT-proBNP (adjusted HR = 1.27, 95% CI = 1.17−1.38) predicted mortality in elderly patients with CHF within 90 days of AKI onset. Patients with a decrease in NT-proBNP accompanying AKI had a lower risk of mortality (adjusted HR = 0.62, 95% CI = 0.48−0.79). However, a decrease in NT-proBNP is a risk factor (adjusted OR = 1.59, 95% CI = 1.02−2.48) for the non-recovery of renal function following AKI–especially in elderly survivors with low baseline NT-proBNP levels. Conclusion A decreased change in NT-proBNP maybe protective for elderly patients with CHF by improving survival outcomes and preventing severe AKI. However, an excessive decrease in NT-proBNP is a risk factor for the non-recovery of renal function following AKI. Avoiding excessive changes in NT-proBNP may be protective for survival and renal injury prognosis.

ABSTRACT Several clinical studies have demonstrated that Jin Shui Bao capsules can attenuate the occurrence and progression of multiple types of kidney diseases. However, there is a lack of consensus regarding its therapeutic effects. Mounting evidence indicates that Jin Shui Bao capsules can effectively ameliorate kidney microcirculation and proteinuria, thereby improving kidney function and delaying disease progression. This review presents a discussion of the effects of Jin Shui Bao capsules on chronic glomerulonephritis, chronic kidney disease, diabetic kidney disease, and hemodialysis treatments. This paper may serve as a valuable reference for kidney disease treatments involving Chinese herbal medicines.

肺动脉高压(PH)是一组以肺循环高压为特征的慢性疾病,主要特征是肺动脉阻力进行性升高,最终导致患者因右心衰竭死亡.在老年慢性肾脏病(CKD)患者中,PH的存在与死亡、肾衰竭和住院的风险增加明显相关.一项对年龄67岁以上老年CKD患者的研究发现,在随访1～3年期间,发生PH者出现肾衰竭的风险较高,部分原因是急性肾损伤(AKI)事件和需要透析支持的AKI发生率较高,CKD合并PH不仅可以加速肾脏病的进展,而且明显增加CKD患者的病死率.

Induced pluripotent stem cells (iPSCs) have been the focus of cellular therapy studies. The use of iPSCs in regenerative medicine is limited by their tumorigenic potential. This study sought to determine whether iPSCs-derived podocytes attenuate acute kidney injury (AKI) and the molecular mechanism. Inoculation of iPSCs-podocytes significantly promoted the repair of kidney injury in AKI mice, reduced the levels of kidney injury factors Scr, BUN, and urinary NAG, and alleviated the inflammatory response. Histological analysis revealed a significant increase in the number of M2 macrophages and a significant decrease in M1 macrophages in the kidney tissues. Subsequently, the genes and signaling pathways that may be associated with kidney injury repair in mice were analyzed by RNA-seq and bioinformatics prediction. The polarization of M2 macrophages was promoted by MAF bZIP transcription factor B (Mafb)-mediated activation of C-C motif chemokine receptor 5 (Ccr5) and nicotinamide phosphoribosyltransferase (Nampt) signaling pathway. Taken together, these results show that iPSCs-podocytes depend on Mafb to activate the Nampt signaling pathway through transcriptional activation of Ccr5, thereby promoting the repair of AKI caused by ischemia-reperfusion.

急性肾损伤（AKI）具有发病率高、致死率高等特点，目前临床上缺乏有效的治疗方法。现应用的肾脏保护药物由于其生物利用度不高而难以有效治疗AKI。纳米药物载体（nanosized drug carriers，NDCs）的应用，可提高肾脏保护药物的生物利用度和靶向递送效率，以持续、受控的方式有效地将治疗剂靶向至所需组织，可延长肾脏保护剂的生物半衰期和血液循环时间，并减少其在健康组织中的脱靶毒性。本文综述了用于AKI治疗的肾脏纳米药物的研究现状，特别关注NDCs递送肾脏保护剂的肾组织靶向选择性机制、影响因素及其改善药物特性的作用，并对NDCs如何更好地治疗AKI 所面对的挑战及未来前景进行展望。