The bioactive components of Astragalus membranaceus and Salvia miltiorrhiza improved cardiac and renal function in chronic heart failure (CHF) and chronic kidney disease (CKD), respectively. However, the common regulating molecular mechanisms remain unclear. The aim of this study was to investigate these mechanisms using bioinformatics, network topology, and molecular dynamics simulation techniques. The active components and target sites of A. membranaceus and S. miltiorrhiza were obtained from the Traditional Chinese Medicine Systems Pharmacology database. The targets of CKD and CHF were obtained from various databases for a protein-protein interaction analysis. The Gene Ontology (GO) function and Kyotoencyclopedia of genes and genomes (KEGG) pathway enrichment of intersection targets were analyzed by using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database. Molecular docking and dynamic simulations were conducted on the core ingredients and targets. The diagnostic efficiency of the key targets was evaluated by using receiver-operating characteristic (ROC) curves. A total of 70 active ingredients and 158 common targets were found. The top five core targets were AKT1, STAT3, TP53, MAPK1, and RELA. The GO enrichment analysis included apoptosis and oxidative stress. The KEGG pathway enrichment results indicated that the drug pair regulated the AGE-receptor for AGE signaling pathway, fluid shear stress and atherosclerosis, and the IL-17 signaling pathway. Molecular docking and dynamic simulations confirmed that the core ingredients had good affinity and stability with the key targets. The ROC curves confirmed the accuracy of every key target for identifying CKD and CHF and demonstrated that combining them improves diagnosis. The combination of A. membranaceus and S. miltiorrhiza proved effective for the treatment of CKD and CHF through various components, targets, and mechanisms. Moreover, it may predict the diagnostic value of key targets, providing a reference for clinical diagnostic applications.

Th is study was conducted to explore the role of OIP5-AS1 in a fibrosis cell model through its interaction with miR-181a-5p. An in-vitro fibrosis model was established by inducing human renal tubular epithelial cells (HK2) with TGF-β1. The expression levels of OIP5-AS1 and miR-181a-5p in the control (Normal) and model (TGF-β1) groups were measured using Quantitative Real-time Polymerase Chain Reaction (qPCR).. qPCR and Western Blot (WB) were used to detect the expression of genes and proteins related to fibrosis and EMT in the two groups of cells. Subsequently, The effect of OIP5-AS1 on TGF-β1-induced fibrosis in HK2 cells was investigated by assessing cell proliferation using the CCK-8 assay and analyzing the expression of fibrosis- and EMT-related proteins through WB.. The targeting relationship between OIP5-AS1 and miR-181a-5p, as well as the influence of OIP5-AS1 on miR-181a-5p expression, was investigated using a dual-luciferase reporter assay. Subsequently, the impact of miR-181a-5p upregulation on the proliferation of TGF-β1-induced HK2 cells was examined through a CCK-8 assay. The study found that TGF-β1 treatment upregulated OIP5-AS1, α-SMA, Col-IV, and FN in HK2 cells while downregulating miR-181a-5p and E-cadherin. OIP5-AS1 downregulation promoted cell proliferation and inhibited fibrosis-related proteins. MiR-181a-5p was identified as a direct target of OIP5-AS1, and its upregulation enhanced cell proliferation. Conclusion . The suppression of OIP5-AS1 attenuates TGF-β1-induced fibrosis in HK2 cells through the regulation of miR-181a-5p.

Diabetic nephropathy (DN) is a chronic microvascular complication of diabetes mellitus, leading to end-stage kidney disease and increased mortality. Early detection and treatment are essential to prevent DN. This study aims to develop a diagnostic prediction model for early DN. Methods. This retrospective analysis study was conducted on 205 patients with type 2 diabetes mellitus (T2DM) treated between September 2019 and September 2022. Patients with stage A1 albumin-to-creatinine ratio (ACR) (< 30 mg/g) were categorized as the simple diabetes mellitus group (n = 134), and those with ACR 30-300 mg/g at stage A2 were classified as the early diabetic nephropathy group (n = 71). Relevant ultrasound parameters and hematological indices were selected through univariate and multivariate screenings. A nomogram model was constructed based on the results of multi-factor screening. Internal validation was performed by using Bootstrap methods with 1000 repetitions, receiver operating characteristic (ROC) curve analysis evaluated model differentiation, calibration curves verified model consistency, and decision curve analysis assessed clinical utility. Results. Multivariate logistic regression identified renal artery resistance index (RI), renal cortex shear wave velocity (SWV), Cystatin C (CysC), Retinol-binding protein (RBP), and Glycated Hemoglobin (HbA1C) as significant factors for early DN (all P < .05). The nomogram model showed good differentiation and consistency and has high clinical value and practicality in predicting DN. The prediction model for early DN, based on conventional ultrasound parameters and hematological indices, demonstrates good prediction efficiency and clinical practicability.

Autosomal dominant polycystic kidney disease (ADPKD), as a widespread inherited cystic kidney disease has a prevalence of ~1/1000 live births. However, there are rare reports of the association of ADPKD with nephrotic range proteinuria such as lupus nephritis (LN). In this study, we report a patient with ADPKD who manifested a sudden increase of urinary protein excretion with positive anti-double stranded DNA and antinuclear antibody tests. Finally, based on percutaneous ultrasound-guided renal biopsy LN was proved. This report advises clinicians to evaluate ADPKD patients periodically and perform complementary clinical and laboratory investigations in cases with unusual presentations such as nephrotic syndrome.

This study was conducted to evaluate the predictive power of the Surgical Apgar Score (SAS) based on surgical blood loss, the lowest intraoperative heart rate and mean arterial pressure in foreseeing short- and long-term effects of radical nephrectomy (RN) on renal function. A prospective investigation was conducted on 111 patients who underwent RN for kidney tumors at a tertiary hospital between 2016 and 2019. The SAS and age-adjusted Charlson Comorbidity Index (CCI) scores were calculated in relation to glomerular filtration rates (GFR) changes on postoperative 1st day, 3rd and 12th months. Patients in higher risk groups, stratified on the basis of SAS, had longer operation times, extended hospital stays, increased bleeding, and higher blood transfusion rates (P < .001).No significant difference existed between preoperative and early postoperative GFR values in SAS-stratified risk groups (P = .802, P = .342, respectively). However, a significant GFR decrease occurred in the high-risk group compared to the moderate and low risk groups at postoperative 3rd (60.79 ± 16.86, 76.22 ± 24.20, 69.80 ± 18.92,respectively) and 12th months (53.57 ± 12.74, 71.61 ± 17.52, 71.86 ± 19.33, respectively)(P = .034, P < .001). CCI scores predicted preoperative GFR in low, moderate, and high-risk groups (111.58 ± 30.91 ml/min, 94.81 ± 22.55 ml/min, and 85.43 ± 32.69 ml/min, respectively)(P = .001), but GFR changes between CCI-defined risk groups were not significant at postoperative 3rd and 12th months (P = .546, P = .481). A significant correlation was found between SAS estimated during the RN procedure and GFR changes at three and twelve months after surgery. Based on SAS, early kidney-preserving therapies like diet, and avoidance of nephrotoxic agents may be recommended for high-risk patients to prevent prolonged GFR alterations.

To investigate the effect of continuous renal replacement therapy (CRRT) in patients with severe acute kidney injury (AKI) by using Nafamostat Mesilate (NM). Eighty patients with AKI who underwent CRRT from March 2022 to January 2022 were divided into control group (n = 40, treated with unfractionated heparin) and Observation group (n = 40, treated with NM). The duration of the first filter use, the number of filters used 72 hours after treatment, coagulation and renal functions, adverse reactions, bleeding events, length of stay in intensive care unit (ICU) and survival status at 28 days were compared between the two groups. The observation group used the first filter for a longer period of time than the control group, and after 72 hours of treatment, the number of filters used was less than that of the control group (P < .05); Compared with before treatment, the levels of fibrinogen (FIB) and platelet count (PLT) in the observation group and control group decreased after 48 hours of treatment, while the levels of activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), and international normalized ratio (INR) increased. However, the levels of FIB and PLT in the former group were higher, while the levels of APTT, PT, TT, and INR were lower (P < .05); Compared with before treatment, the levels of creatinine (Scr), urea nitrogen (BUN), and serum cystatin C (CysC) in the observation group and control group decreased after 48 hours of treatment, and the former was even lower (P < .05); the incidence of bleeding events in the observation group was lower than that in the control group, the length of stay in ICU was shorter than that in the control group, and finally the 28-day survival rate was higher than that in the control group (P < .05). The adverse reactions of the two groups were similar (P > .05). NM can improve the coagulation function and renal function in patients with severe AKI undergoing CRRT, prolong the duration of the filter use, reduce the number of filters used, shorten the length of ICU stay, reduce the incidence of bleeding events, and improve the prognosis.

Activation of the complement system following transplantation may result in allograft rejection. Our study aimed to evaluate the potential relationship between factors affecting kidney transplant success and complement 5 (C5) using bioinformatic tools. GenCards and Genemania were used to provide the genetic functional information belonging to the C5 gene, and genomic browsers of STRING, UCSC, KEGG were used to reveal interactions with other genes and various pathways. MiRDB was used to specify the miRNAs that were associated with the C5 gene. The UniProt database was used to determine the tissues that expressed the C5 gene using protein-protein interactions. In the bioinformatic analyses performed, high levels of C5 gene expression were found in the naiive kidney. Twenty-five genes were found to be strongly associated with C5. Fifty-four miRNAs targeting the C5 gene were specified. The C5 gene was found to be involved in biologic processes such as complement activation (FDR = 6.46e-22), complement binding (FDR = 2.20e-06), cytolysis (FDR = 4.82e-14), regulation of complement activation (FDR = 4.08e-24), positive regulation of vascular endothelial growth factor production (FDR = 0.0430), regulation of macrophage chemotaxis (FDR = 0.0447), activation of the immune response (FDR = 1.26e-13), leukocyte-mediated immunity (FDR = 1.41e-09), innate immune response (FDR = 3.05e-09), allograft rejection (FDR = 2.40e-12), oxidative injury response (FDR = 0.00016), and trigerring of the beginning of the complement cascade (FDR = 0.0244). The data obtained in this study will be used to guide future experimental investigations in the field of transplantation, and these data will give physicians with insight into allograft status following transplantation.

Acute kidney injury (AKI) is commonly precipitated by sepsis. Continuous veno-venous hemofiltration (CVVHD) is a critical intervention for managing AKI, but further exploration is needed to understand its effects on novel renal injury markers and patient outcomes. The aim of this study is to evaluate the impact of CVVHD on novel renal injury markers and its prognostic significance in individuals suffering from sepsis-related AKI. Retrospective analysis was carried out on the medical data of 84 patients with sepsis-induced AKI treated at Baoji High-Tech Hospital from February 2022 to August 2023. We assessed changes in serum biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and liver fatty acid-binding protein (L-FABP) pre- and post-CVVHDF treatment, and correlated these changes with the Acute Physiology and Chronic Health Evaluation II (APACHE II) score. Cox regression was utilized to identify independent prognostic factors influencing 28-day survival, from which Kaplan-Meier curves and a prognostic nomogram were derived. A significant reduction in the serum concentrations of s-NGAL, L-FABP, and KIM-1 was observed following treatment (all P < .001). A positive correlation between these serum biomarkers and APACHE II scores was observed both before and after CVVHDF treatment (all P < .001). According to multivariate Cox regression analysis, coronary heart disease (P = .016), the stage of renal injury (P = .014), APACHE II score (P < .001), and s-NGAL (P < .001) were independent predictors of prognosis for 28-day survival. CVVHD effectively decreases KIM-1, L-FABP, and NGAL levels, thereby enhancing kidney function in individuals suffering from sepsis-related AKI. Key prognostic indicators for 28-day survival include the presence of coronary artery disease, advanced kidney injury stage, APACHE II score ≥ 26, and NGAL levels ≥ 5.49.

Autosomal Dominant Polycystic kidney disease (ADPKD) is defined as one of the most common genetic disorders and the cause of kidney failure or end-stage kidney disease (ESKD). Several studies have shown that renin-angiotensin system has an important role in pathogenesis of ADPKD. The aim of this study was to examine the association between the angiotensin converting enzyme (ACE) gene Deletion/Deletion (D/D) polymorphism and risk of ADPKD among Iranian patients from west Azerbaijan province of Iran. This case-control study was conducted on 40 patients and 72 controls. Genetic polymorphism of the ACE gene was determined using polymerase chain reaction (PCR) and electrophoresis. The frequency (frequency%) of ACE gene I/I, I/D, D/D genotypes were 5 (12.5%), 12 (30%), 23 (57.5%) in cases and 16 (22.22%), 30 (41.67%), 26 (36.11%) in controls, respectively. The frequency (frequency%) of ACE gene I and D alleles were 22 (27.5%) and 58 (72.5%) in cases and, 62 (43.06%) and 82 (56.94%) in controls, respectively. Statistical analysis indicated that there were significant differences among the cases and controls regarding ACE gene D/D genotypes (P = .028). The ACE gene D/D genotype was associated with increased ADPKD susceptibility with an OR of 2.39, (95%) CI = (1.09-5.28), and P = .028. But in the case of ACE gene, I/I and I/D genotypes, there were no statistically significant differences between cases and controls (P > .05). Considering allelic comparison, the ACE gene D allele was associated with ADPKD susceptibility with an OR of 1.99, (95%) CI = (1.1-3.6), and P = .021. Our findings suggest that ACE gene D/D genotype was associated with ADPKD.

Uremic pruritus (UP) is a disturbing symptom in a quite large proportion of hemodialysis (HD) patients. Recent studies have indicated a potential role of interleukin-31 (IL-31) in the pathophysiology of pruritus, and it is becoming a promising therapeutic target for UP. Hemoperfusion (HP) is an extracorporeal technique that has been shown to be effective in absorbing molecules which may be responsible for inducing pruritus. In this study, we conducted this study to explore whether additional HP could enhance the removal of IL-31 in UP patients. The study was conducted in two parts. In Part A, the prevalence and intensity of UP were recorded and the basal serum IL-31 level was determined three times a week in HD patients. Patients with detectable serum IL-31 levels in part A were included in Part B. Each patient had two 4-h test sessions: conventional HD or HD plus HP (HDHP). The reduction ratio (RR) of IL-31 from HD and HDHP was compared. Forty patients completed part A and 40% of them were suffering from UP. Serum IL-31 was detected at significantly higher percentages in UP patients than in non-UP patients (50% vs 4.2%). Serum levels of IL-31 in UP patients were significantly higher than that in non-UP patients (median: 8.35pg/ml vs 7.8pg/ml). Serum IL-31 levels were significantly correlated with pruritus intensity in patients with UP(r = 0.55, P < .05). Eight patients were enrolled and completed part B. The use of combined HD and HP treatment produced a better RR for IL-31 than HD alone (34.26 ± 1.43% vs 15.28 ± 2.11%, P < .01). IL-31 may play an important role in the pathophysiology of uremic pruritus. The addition of hemoperfusion to conventional hemodialysis provides enhanced removal of IL-31.