Renal Failure最新文献

Background: Secondary hyperparathyroidism (SHPT) is a prevalent chronic complication in patients undergoing hemodialysis. Parathyroidectomy (PTX) is crucial for reducing mortality and improving the prognosis in the treatment of refractory hyperparathyroidism. However, it is often associated with a number of postoperative complications such as postoperative hypotension, hyperkalemia, and hungry bone syndrome. A previous study demonstrated that low blood pressure influences the patency of autogenous arteriovenous fistulas (AVF). Few studies have examined AVF dysfunction following PTX. This study aimed to identify and describe the risk variables associated with AVF dysfunction after PTX.

Methods: Cases of AVF dysfunction after PTX between 2015 and 2021 were studied. Four controls were identified for each patient and were matched for sex and age. Biochemical parameters and blood pressure of the patients before and after PTX were recorded. Risk factors for AVF dysfunction after PTX were identified using conditional logistic regression analysis.

Results: Sixteen patients and 64 controls were included in this study. Baseline demographic and laboratory data were compared. Patients in the AVF dysfunction group had lower levels of postoperative calcium than the controls. After surgery, calcium levels decreased more in patients with AVF dysfunction than in the control group. The decrease in systolic blood pressure (ΔSBP) after PTX was greater in the AVF dysfunction group than that in the control group. For each 1 mmHg increment in ΔSBP, the risk of AVF dysfunction after surgery increased by 11.6% (OR = 1.116, 95% CI, 1.005-1.239, p = .040). The likelihood of developing AVF dysfunction after surgery was twelvefold higher in diabetic patients than in non-diabetic patients (OR = 12.506, 95% CI, 1.113-140.492, p = .041). Among patients with ΔSBP > 5.8 mmHg after PTX, the AVF failure rate was significantly greater in patients with diabetes than in those without diabetes. Patients with a history of AVF failure had a nine-fold higher risk of developing AVF dysfunction (OR = 9.143, 95% CI, 1.151-72.627, p = .036). Serum albumin, hemoglobin, ΔiPTH, and age were not independent predictors of AVF dysfunction. The cutoff value for SBP was 5.8 mmHg, as determined by the Youden index of the receiver operating characteristic curve.

Conclusion: Decreased systolic blood pressure (ΔSBP) after PTX, diabetes, and AVF failure history were risk factors for AVF dysfunction following PTX in patients with SHPT. Diabetes patients with ΔSBP > 5.8 mmHg were more prone to AVF dysfunction after PTX.

Aim: This study explored the effect and mechanism of MAFF and HDAC6 on renal fibrosis and inflammation in lupus nephritis (LN).

Methods: IL-33 treated renal epithelial cells and MRL/lpr mice were respectively used for in vitro and in vivo experiments. The expressions of HDAC6, MAFF, and KLF5 were measured in cells and renal tissues. Before and after cell transfection, the morphological changes in renal tissues were observed using Hematoxylin and eosin (H&E) and Masson staining. The proteinuria, serum creatinine (SCr), blood urea nitrogen (BUN), and double-stranded DNA (dsDNA) levels were detected by biochemical analysis. The expressions of fibrosis and inflammation related proteins (including α-SMA, Vimentin, IL-1β, IL-6, and TNF-α), p65, and iNOS were also detected. The relationship among MAFF, HDAC6, and KLF5 was determined by chromatin immunoprecipitation and dual luciferase reporter gene assay.

Results: Renal tissues and cell models had elevated expressions of HDAC6 and KLF5, and decreased MAFF expression. HDAC6 suppression or MAFF overexpression led to suppression of proteinuria, SCr, BUN, and dsDNA levels, as well as attenuation of inflammatory infiltration and collagen deposition. HDAC6 can suppress MAFF expression via deacetylation to abolish its suppression of KLF5 expression, thus increasing KLF5 expression. In vivo and in vitro experiments showed the suppressive effect of HDAC6 suppression on renal fibrosis and inflammation can be abolished by KLF5 overexpression.

Conclusion: HDAC6 suppresses MAFF expression via deacetylation to elevate KLF5 expression, which consequently enhances fibrosis and inflammatory response in LN.

Objective: This study aimed to investigate the therapeutic effects of sulforaphane and the role of the Nrf2-Keap1/HO-1/ROS pathway in AngII-induced oxidative stress in podocyte injury.

Methods: Mouse mpc5 podocytes were divided into four groups: control (Con), AngII, AngII + sulforaphane (AngII + SFN), and control + sulforaphane (Con + SFN). Western blotting was used to detect protein expression of Nrf2-Keap1, antioxidant enzyme HO-1, and apoptosis-related proteins. ROS levels were measured using a ROS assay kit, and cell survival and viability were assayed using the CCK-8 kit. Molecular interactions between Nrf2 and sulforaphane were analyzed computationally.

Results: Compared with the Con group, podocytes treated with AngII alone exhibited inhibited proliferation, reduced cell viability, lower Bcl-2 expression, and higher cleaved caspase 3 expression. In the presence of sulforaphane, AngII group showed a mild inhibition on podocyte proliferation but did not induce the aforementioned changes in Bcl-2 and cleaved caspase 3 expression. Similarly, compared to the Con group, AngII treatment alone had lower Nrf2 expression and higher Keap1 expression in podocytes, accompanied by a significant decrease in ROS content. However, in the presence of sulforaphane, AngII failed to induce increases in Nrf2 and a decrease in Keap1 expression, as well as ROS levels. Furthermore, cells treated with sulforaphane exhibited higher HO-1 levels than control cells, and co-incubation with AngII did not alter HO-1 levels. Computational modeling revealed hydrophobic interactions between sulforaphane and the amino acid LYS-462 of Nrf2, as well as hydrogen bonding with amino acid HIS-465. The binding score between sulforaphane and Nrf2 was -4.7.

Conclusion: Sulforaphane alleviated AngII-induced podocyte oxidative stress injury via the Nrf2-Keap1/HO-1/ROS pathway, providing new insights into therapeutic compounds for mitigating chronic kidney disease.

The UK Deceased Donor Kidney Transplant Outcome Prediction (UK-DTOP) Tool, developed using advanced artificial intelligence (AI), significantly enhances the prediction of outcomes for deceased-donor kidney transplants in the UK. This study analyzed data from the UK Transplant Registry (UKTR), including 29,713 transplant cases between 2008 and 2022, to assess the predictive performance of three machine learning models: XGBoost, Random Survival Forest, and Optimal Decision Tree. Among these, XGBoost demonstrated exceptional performance with the highest concordance index of 0.74 and an area under the curve (AUC) consistently above 0.73, indicating robust discriminative ability and calibration. In comparison to the traditional Kidney Donor Risk Index (KDRI), which achieved a lower concordance index of 0.57, the UK-DTOP model marked a significant improvement, underscoring its superior predictive accuracy. The advanced capabilities of the XGBoost model were further highlighted through calibration assessments using the Integrated Brier Score (IBS), showing a score of 0.14, indicative of precise survival probability predictions. Additionally, unsupervised learning via k-means clustering was employed to identify five distinct clusters based on donor and transplant characteristics, uncovering nuanced insights into graft survival outcomes. These clusters were further analyzed using Bayesian Cox regression, which confirmed significant survival outcome variations across the clusters, thereby validating the model's effectiveness in enhancing risk stratification. The UK-DTOP tool offers a comprehensive decision-support system that significantly refines pre-transplant decision-making. The study's findings advocate for the adoption of AI-enhanced tools in healthcare systems to optimize organ matching and transplant success, potentially guiding future developments in global transplant practices.

Purpose: Increased myocardial T1 values on cardiovascular MRI (CMRI) have been shown to be a surrogate marker for myocardial fibrosis. The use of CMRI in patients on hemodialysis (HD) remains limited. This research aimed to explore the characteristics of native T1 values in HD patients and identify factors related to T1 values.

Methods: A total of thirty-two patients on HD and fourteen healthy controls were included in this study. All participants underwent CMRI. Using modified Look-Locker inversion recovery (MOLLI) sequence, native T1 mapping was achieved. Native CMRI T1 values were compared between the two groups. In order to analyze the relationship between T1 values and clinical parameters, correlation analysis was performed in patients on HD.

Results: Patients on HD exhibited elevated global native T1 values compared to control subjects. In the HD group, the global native T1 value correlated positively with intact parathyroid hormone (iPTH) (r = 0.418, p = 0.017) and negatively with triglycerides (r= -0.366, p = 0.039). Moreover, the global native T1 value exhibited a positive correlation with the left ventricular end-diastolic volume indexed to body surface area (BSA; r = 0.528, p = 0.014), left ventricular end-systolic volume indexed to BSA (r = 0.506, p = 0.019), and left ventricular mass indexed to BSA (r = 0.600, p = 0.005). A negative correlation was observed between the global native T1 value and ejection fraction (r = 0.-0.551, p = 0.010).

Conclusion: The global native T1 value was prolonged in HD patients compared with controls. In the HD group, the global T1 value correlated strongly with iPTH, triglycerides, and cardiac structural and functional parameters.

Background: The potential impact of elevated intra-abdominal pressure (IAP) on residual renal function (RRF) has not been determined. The objective of this study was to investigate the relationship between IAP and the rate of RRF decline in newly initiated peritoneal dialysis (PD) patients, and to identify the optimal IAP threshold value for delaying the deterioration of RRF.

Methods: A cohort of 62 newly initiated PD patients who completed both 6- and 12-month follow-up evaluations was obtained using the Durand method. A logistic regression model was used to identify variables associated with a rapid decline in RRF. Receiver operating characteristic (ROC) curves were generated to determine the optimal threshold value. Another retrospective cohort analysis was performed to validate the identified critical value.

Results: For each 1 cmH₂O increase in IAP, the risk of a rapid decline in the RRF increased by a factor of 1.679. Subsequent analysis revealed that patients in the high IAP group had more significant decreases in residual renal estimated glomerular filtration rate (eGFR) (Z = -3.694, p < 0.001) and urine volume (Z = -3.121, p < 0.001) than did those in the non-high IAP group. Furthermore, an IAP ≥15.65 cmH₂O was a robust discriminator for the prediction of the rate of RRF decline.

Conclusion: Patients in the high IAP group experienced a more rapid decline in RRF. Additionally, an optimal critical pressure of 15.65 cmH₂O was identified for predicting the rate of RRF decline. IAP, as one of the factors contributing to the rapid decline in RRF in the first year of PD, should be given due attention.

Background: The risk of cardiovascular events (CVEs) in peritoneal dialysis (PD) patients is high, but varies widely among individuals. Metabolic acidosis is prevalent in PD patients and may be involved in the development of CVEs. The aim of the study was to evaluate serum bicarbonate as a risk factor and derive a model of new CVE.

Methods: A predictive model was established by performing an observational study in 187 PD patients obtained from the First Affiliated Hospital of Anhui Medical University. The variables were extracted using least absolute shrinkage and selection operator (LASSO) regression, and the modeling was developed using multivariable Cox regression.

Results: Left ventricular hypertrophy (HR = 1.965, 95%CI 1.086-3.557) and history of CVEs (HR = 2.435, 95%CI 1.342-4.49) were risk parameters for a new CVE. Serum albumin (HR = 0.924, 95%CI 0.864-0.989) and bicarbonate levels (HR = 0.817, 95%CI 0.689-0.969) were protective parameters, in which the risk of CVEs was reduced by 7.6% and 18.3% for each 1-unit increase in serum albumin (g/L) and bicarbonate (mmol/L) levels, respectively. A nomogram based on the above predictive indicators was proposed with a C-statistic of 0.806, indicating good discrimination. Moreover, it successfully stratified patients into low-, intermediate-, and high-risk groups.

Conclusions: We performed a risk prediction model for the development of CVEs in patients with PD, which may help physicians to evaluate the risk of new CVEs and provide a scientific basis for further interventions. Further studies are needed to externally validate current risk models before clinical application.

Introduction: The prevalence of chronic kidney disease (CKD) is gradually increasing in the elderly population. At the same time, frailty has become one of the research hotspots in the field of geriatrics. Bibliometric analyses help to understand the direction of a field. Therefore, this study aimed to analyze the status and emerging trends of frailty in CKD patients.

Data and methods: The Web of Science Core Collection (WoSCC) database was screened for relevant literature published between 1 January 2000 and 31 December 2021. Next, publications were analyzed for information including authors, journals, cited references, citing journals, institutions, countries and regions, high-frequency keywords and co-citations using VOSviewer, Microsoft Excel, and R software.

Results: A total of 2223 articles were obtained, from which 613 relevant articles were selected based on title and abstract screening. There was an upward trend in the number of annual publications and Johansen KL was considered the most contributing author in the field. The Clinical Journal of the American Society of Nephrology was the most productive research journal. Johns Hopkins University is the most published organization. The United States is the global leader in the field and contributes the most to research. Research hotspots focus on epidemiological studies of frailty and frailty intervention.

Conclusions: This study presents a comprehensive bibliometric analysis of CKD and frailty research. Key findings highlight the current focus on early screening and assessment of frailty in CKD patients, as well as physical function interventions in frail patients.

Background: Inflammation plays a crucial role in occurrence of kidney injury, and specific dietary patterns can influence systemic inflammation levels. However, the relationship between dietary inflammatory potential and early-stage kidney damage remains unclear.

Method: 2,108 participants was recruited from 2001-2002 National Health and Nutrition Examination Survey (NHANES). Dietary Inflammatory Index (DII) is utilized to assess dietary inflammatory potential, calculated through a 24-h dietary recall questionnaire. Early renal injury was evaluated using urinary albumin to creatinine (UACR), cystatin C (CysC), β-2 microglobulin (β2M), and estimated glomerular filtration rate (eGFR) based on serum creatinine (eGFRs), cystatin C (eGFRc), and both Scr and CysC (eGFRs&c). Participant characteristics were analyzed, and association between DII, hypertension, and early renal injury markers was explored using multiple linear and logistic regression models.

Results: The average age of participants was 53.9 years. DII exhibited a positive correlation with UACR (β = -0.048[0.017,0.078]), β2M (β = 0.019[0.010,0.027]), CysC (β = 0.012 [0.004,0.021]). Conversely, a negative correlation was observed between DII and eGFRc (β = -1.126[-1.554, -0.699]), eGFRs&c (β=-1.101[-1.653, -0.549]). A significant association was observed between hypertension and abnormality of early kidney damage markers. Subgroup analysis reveals that the positive correlation between DII and the occurrence of abnormal markers of early kidney damage is only observed in individuals with hypertension. Furthermore, an interaction between DII and hypertension was detected in eGFRs&c (OR:1.250[1.042, 1.499], p for interaction = 0.03).

Conclusion: Higher levels of DII may be associated with occurrence of early kidney damage. For individuals with hypertension, avoiding excessive consumption of pro-inflammatory foods may reduce the risk of renal injury.