Introduction: Ribosomal protein SA pseudogene 52 (RPSAP52) has been characterized as an oncogenic lncRNA in pituitary tumors. Analysis of TCGA dataset revealed the upregulation of RPSAP52 in glioblastoma (GBM). We, therefore, investigated the roles of RPSAP52 in GBM. Methods: A total of 50 GBM patients (33 males and 20 females; 54– 75 years; mean age: 61.8± 5.8 years) were selected from the 89 cases of GBM patients. Under the guidance of MRI, brain biopsy was performed to collect GBM tissues from each patient for the diagnosis of GBM. U-373 MG cells were employed and had transient transfections. qRNA, Western blot, and a series of experiments were performed to characterize their associations. Results: The results showed that RPSAP52 was upregulated in GBM patients, and its high expression levels predicted poor survival. In GBM tissues, expression levels of RPSAP52 were significantly and positively correlated with that of TGF-β 1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β 1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β 1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β 1 attenuated the effects of RPSAP52 siRNA silencing. Conclusion: Therefore, RPSAP52 upregulates TGF-β 1 to increase cancer cell stemness and predict postoperative survival in GBM.

Our study aimed to explore the intercorrelations of brachial‐ankle pulse wave velocity (baPWV), ankle‐brachial index (ABI), ambulatory arterial stiffness index (AASI), 24‐hour mean pulse pressure (24‐h PP), and augmentation index (AIx, AIx@75, the AIx standardized to a heart rate of 75) and compare the effectiveness of these markers for predicting renal outcomes. A total of 117 patients with chronic kidney disease (CKD) who received noninvasive arterial stiffness examinations were enrolled. We used correlation analysis and linear regression to explore the correlations between these five arterial stiffness markers and the Cox proportional hazards model and receiver operator characteristic (ROC) curve to assess the associations of markers with kidney disease outcomes. The median (interquartile range) of age and eGFR were 61 (49‐65) years and 50.5 (35.5‐84.1) ml/min/1.73 m², respectively. In Pearson correlation analysis, baPWV was significantly associated with 24‐h PP (r = .531, p < .001), AIx@75 (r = .306, p < .001). Additionally, 24‐h PP was associated with AASI (r = .507, p < .001) and AIx@75 (r = .217, p = .019). During follow‐up for a median of 25 months, 26.5% (n = 31) of patients had a composite outcome; of these, 10 initiated dialysis, 17 had 40% eGFR loss, and 4 died. Increased AASI, 24‐h PP, and baPWV were associated with poor renal outcomes in a univariate Cox analysis. After adjusting for age, sex, MAP, eGFR, and 24 hours proteinuria, 1‐SD increase in AASI and 24‐h PP was associated with renal outcomes. The ROC analysis yielded the largest area under the curve (AUC) of 0.727 (95% CI: 0.624 to 0.831; p < .001) for 24 ‐h PP. When the Youden's index was at its maximum, the 24‐h PP value was 52 mmHg. In conclusion, 24‐h PP, baPWV, and AIx@75 were linked well to one another. Arterial stiffness is a target for delaying the decline in kidney function. The use of 24‐h PP as an arterial stiffness marker should be valued in CKD clinical practice.

(1) Background: the epigenetic mechanisms underlying the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remain poorly understood; (2) Methods: to investigate this process, we conducted genome-wide DNA methylation sequencing to map the epigenetic changes during the AKI-CKD transition in a mouse model. By integrating DNA methylome and transcriptome analyses, we identified genes and signaling pathways regulated by DNA methylation throughout this progression; (3) Results: our analysis identified four candidate genes—Atp1a3, Ncf1, Lpl, and Slc27a2—that were regulated by DNA methylation and strongly correlated with kidney disease prognosis. Additionally, we found that the PPAR signaling pathways, among others, were implicated in this process. Treatment with DNA methyltransferase inhibitors mitigated fibrosis and improved lipid metabolism in the kidneys during AKI-CKD progression; (4) Conclusions: this study provides the first comprehensive epigenetic map of the AKI-CKD transition. Our findings offer new insights into the epigenetic regulation of kidney disease progression and highlight potential therapeutic targets to prevent the transition from AKI to CKD.

Background: Arterial stiffness influences the prognosis of patients with end-stage kidney disease; however, the factors that promote arterial stiffness in chronic kidney disease (CKD) patients remain unknown. We aimed to explore the clinical factors associated with arterial stiffness in CKD. Methods: Between September 2017 and September 2022, all CKD patients treated at the Department of Nephrology, General Hospital of the Chinese People’s Liberation Army, excluding dialysis patients, were screened and their medical records within the last month were collected. Arterial stiffness was measured by the augmentation index (AIx). The correlative clinical factors with arterial stiffness were explored in different linear regression models. Results: 559 patients were included in the study. AIx@75 increased as the deterioration of CKDG1–CKDG5, with values of 1 (−9, 11), 5.5 (−4, 13.25), 9 (0, 16), 12 (1.5, 23.5), and 22 (13, 28), respectively (Z = 63.03, p < 0.001). Multivariate linear regression analysis showed that AIx@75 was positively associated with female sex (β = 8.926, 95% confidence interval (CI) 6.291, 11.562, p < 0.001), age (β = 0. 485, 95% CI 0.39, 0.58, p < 0.001), mean arterial pressure (MAP) (β = 0.255, 95% CI 0.159, 0.35, p < 0.001), and was negatively associated with ACEI/ARB (β = −4.466, 95% CI −6.963, −1.969, p < 0.001) and glucocorticoid (β = −3.163, 95% CI −6.143, −0.183, p = 0.038). Smoking, eGFR, hemoglobin, and cause of disease were associated with AIx@75 in multivariate linear regression models when considering factors partly. Conclusions: Female, age, smoking, MAP, eGFR, cause of disease, ACEI/ARB, and glucocorticoid were found to be associated with atherosclerosis in CKD patients.

This study investigated the impact of 24-h urinary calcium excretion (UCaE) on renal function decline in hospitalized patients with and without chronic kidney disease (CKD). This study enrolled 3815 CKD patients in stages 1–4 and 1133 non-CKD patients admitted to the First Center of the Chinese PLA General Hospital between January 2014 and July 2022. The primary outcome for CKD patients was a composite of CKD progression, defined as a 40% decline in estimated glomerular filtration rate (eGFR) or end-stage kidney disease. Annual eGFR change was the secondary outcome. For non-CKD patients, the primary outcome was an eGFR decline of ≥20% or CKD incidence, while annual eGFR change was the secondary outcome. The association between UCaE and kidney function decline was assessed using Cox proportional hazards and generalized linear models. Primary outcomes were observed in 813 CKD patients and 109 non-CKD patients over a median follow-up of 3.0 and 4.1 years, respectively. For CKD patients, every 1-mmol/d increase in UCaE was associated with a 15% decreased risk of CKD progression. The hazard ratio (HR) was 0.85, with a 95% confidence interval (CI) of 0.77–0.93. For non-CKD patients, the risk of renal function decline decreased by 11%. The multivariate models indicated that there was an annual decrease in eGFR in both CKD and non-CKD patients, with a reduction of 0.122 mL/min/1.73 m²/year (p < 0.001) and 0.046 mL/min/1.73 m²/year (p = 0.004), respectively, for every 1-mmol/d increase in UCaE. CKD experiences a decrease in 24-h UCaE as early as stage 1, with a significant decline in stage 4. CKD and non-CKD patients with lower UCaE levels are at an increased risk of renal decline, regardless of other variables.

Objective: This study investigated the impact of 24-hour urinary calcium excretion (UCaE) on renal function decline in hospitalized patients with and without chronic kidney disease (CKD). Methods: This study enrolled 3,815 CKD patients with stages 1-4, and 1,133 Non-CKD patients admitted to the First Center of the Chinese PLA General Hospital between January 2014 and July 2022. The primary outcome for CKD was a composite of CKD progression defined as a 40% decline in estimated glomerular filtration rate (eGFR) and end-stage kidney disease and rapid kidney function decline [RKFD, defined as annual eGFR decline of ≥ 5 ml/min/1.73m ²/yr] as the secondary outcome. For Non-CKD patients, an eGFR decline of ≥ 20%, incidence of CKD, and a declining slope of ≥3 ml/min/1.73m ²/yr were the outcomes. The association between UCaE and kidney function decline was assessed using Cox proportional hazards and generalized linear models. Results: The primary outcome was observed in 813 CKD and 109 without CKD over a median follow-up of 3.0 and 4.1 years, respectively. For CKD patients, every 1-mmol/d increase in UCaE was associated with a 15% decreased risk of CKD progression. The hazard ratio (HR) was 0.85, with a 95% confidence interval (CI) of 0.77-0.93. And, for Non-CKD patients, the risk of renal function decline decreased by 11%. The multivariate models indicated that there was an annual decrease of eGFR in both CKD and Non-CKD, with a reduction of 0.122 ml/min/1.73m2/yr (P < 0.001) and 0.046 ml/min/1.73m2/yr (P = 0.004), respectively, for every 1-mmol/d increase of UCaE. Conclusions: CKD experiences a decrease in 24-hour UCaE as early as stage 1, with a significant decline in stage 4. CKD and Non-CKD patients with lower UCaE levels are at an increased risk of renal decline, regardless of other variables.