BMC Nephrology最新文献

Background: Mechanistic pathways and biomarkers need to be explored to elucidate the pathogenesis of acute kidney injury (AKI). This study examined miR-107 expression in AKI and the molecular mechanisms underlying the regulation of ferroptosis-mediated AKI.

Methods: This study included 30 patients with AKI and 30 healthy individuals in the control group. The miR-107 serum expression levels were determined using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The HK-2 cells were subjected to ferroptosis in vitro, and a AKI mice model to study the effect of miR-107 in vivo. After RNA overexpression, malondialdehyde (MDA), lipid reactive oxygen species (ROS), and glutathione (GSH) levels were measured. Additionally, the regulatory relationship between miR-107 and its downstream pathway genes was analyzed.

Results: The down-regulated expression of miR-107 detected in the serum of patients with AKI suggested its utility as a potential diagnostic indicator for AKI. Moreover, miR-107 expression was down-regulated in both HK-2 cell models of AKI and HK-2 cell ferroptosis model. Upregulation of miR-107 decreased MDA expression and increased GSH expression in erastin (Era)-induced ferroptosis in HK-2 cells in vitro. Additional, AKI mice exhibited down-regulated expression levels of miR-107, and the ROS, MDA, and GSH expression changes in AKI mice were rescued after miR-107 overexpressed, which was consistent with the effect of Fer-1 treatment. Furthermore, the PI3K/Akt/mTOR pathway exhibited a correlation with miR-107 expression in Era-induced ferroptosis in HK-2 cells.

Conclusion: In summary, miR-107 is expressed at low levels in AKI and can inhibit ferroptosis in HK-2 cells, which may play a protective role against AKI.

Background: Immunoglobulin A nephropathy (IgAN), the most common glomerular disease, is characterized by immune complex deposition and abnormal complement system activation. Telitacicept targets B cells through multiple mechanisms, potentially offering therapeutic benefits in IgAN. This retrospective study aimed to evaluate the efficacy and safety of telitacicept.

Methods: Eleven patients with IgAN treated with telitacicept (160 mg, weekly) between August 2022 and December 2024 were included. The minimum follow-up period was 24 weeks, and the primary endpoint was renal remission rate at the final visit.

Results: Among the 11 patients, 6 (54.5%) achieved partial remission, including 3 (27.3%) with complete response. Following telitacicept treatment, 24-h proteinuria decreased from a baseline of 1.77 g/day (interquartile range [IQR]: 1.31-5.19 g/day) to 1.04 g/day (IQR: 0.27-1.41 g/day) at the last follow-up (P < 0.05), demonstrating a significant reduction in proteinuria. Urinary red blood cell counts decreased from 52.81 ± 110.95 to 9.62 ± 11.44 per high-power field. The main adverse reaction was an upper respiratory tract infection, with no serious events reported.

Conclusion: This study provided preliminary evidence that telitacicept may reduce proteinuria in patients with IgAN, with no serious safety concerns observed during this study. These preliminary real-world findings support the potential role of telitacicept in IgAN management and warrant confirmation in prospective multicenter studies.

Clinical trial number: Not applicable.

Background: Nephrotic syndrome (NS) is a clinical condition that results from the renal loss of protein exceeding the body's compensatory abilities. Dysproteinemia in the acute phase of the disease inevitably affects the nutritional status of children. It is unclear whether the situation will fully normalize in remission. The aim of the study was to assess the serum concentrations of retinol binding protein 4 (RBP4) and prealbumin (PA), as well as the body composition parameters in children with NS in remission in comparison to healthy counterparts.

Methods: Thirty nephrotic children at the age of 11.9 ± 4.6 years were enrolled and compared to healthy counterparts. RBP4 and PA serum concentrations together with selected basic biochemical parameters, were determined. Body composition parameters were determined based on the bioimpedance method using the Tanita MC-980MA device.

Results: In NS children the mean RBP4 concentration was 42.6 ± 11.6 mg/l, and mean PA concentration was 540.1 ± 442.1 µg/ml, and those values did not differ significantly from those in the control group (42.0 ± 10.9 mg/l and 372.8 ± 107.9 µg/ml, respectively). RBP4 concentration correlated positively with the age of the studied patients, while PA was not associated with age. Both studied markers did not show significant differences depending on the remission status - maintained with immunosuppressive therapy vs. without active treatment, as well as on the categorization according to the clinical course - steroid-sensitive NS vs. frequently relapsing or steroid-dependent NS. Based on bioimpedance measurements, the parameters characterizing body composition did not differ between NS group and controls.

Conclusions: RBP4 and PA, which can be considered as selected biochemical markers of nutritional status, as well as body composition measures based on the bioimpedance, do not indicate differences between children with remission of idiopathic NS and their healthy peers. Successful induction and maintenance of NS remission restores the assessed aspects of nutritional status of these children.

Background: Chronic kidney disease (CKD) has detrimental effects on health through multiple pathophysiological mechanisms, significantly reducing life expectancy and contributing to a substantial disease burden. Therefore, this study aims to explore the association of metabolic syndrome (MetS) and hyperuricemia (HUA) with all-cause and cardiovascular mortality in patients with chronic kidney disease (CKD).

Methods: Overall, 28,278 patients with CKD, defined by estimated glomerular filtration rate < 60 mL/min/1.73 m² or urine albumin creatinine ratio > 3 mg/mmol, MetS (≥ 3 of 5 criteria), and HUA (> 7.0 mg/dL in males, > 6.0 mg/dL in females) were assessed. The outcomes included all-cause and cardiovascular mortality. Associations were assessed using multivariate-adjusted Cox proportional hazards models and Kaplan-Meier survival analysis, supplemented by subgroup analyses and sensitivity tests.

Results: During a median follow-up of 13.21 years, 3564 all-cause deaths (17.28%) were recorded, including 1025 (4.97%) attributable to cardiovascular causes. After multiple adjustments, both HUA and MetS were strongly associated with all-cause and cardiovascular mortality. Patients with CKD and coexisting HUA or MetS exhibited a significantly higher risk of all-cause mortality (adjusted hazard ratio [aHR] = 1.45, 95% confidence interval [CI]: 1.30-1.62) and cardiovascular mortality (aHR = 2.09, 95% CI: 1.70-2.58) than those without HUA or MetS. Kaplan-Meier curves demonstrated that elevated uric acid levels and a high number of MetS components significantly reduced survival probability (P < 0.001), with an increasing trend as the uric acid levels and the number of MetS components increased. Subgroup and sensitivity analyses confirmed the robustness and consistency of our findings.

Conclusion: MetS and HUA significantly increased all-cause and cardiovascular mortality in patients with CKD, particularly in those with high uric acid levels and a high number of MetS components.

Clinical trial number: Not applicable.