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Membranous nephropathy (MN), an autoimmune disease, can manifest at any age and is among the most common causes of nephrotic syndrome in adults. In 80% of cases, the specific etiology of MN remains unknown, while the remaining cases are linked to drug use or underlying conditions like systemic lupus erythematosus, hepatitis B virus, or malignancy. Although about one‐third of patients may achieve spontaneous complete or partial remission with conservative management, another third face an elevated risk of disease progression, potentially leading to end‐stage renal disease within 10 years. The identification of phospholipase A2 receptor as the primary target antigen in MN has brought about a significant shift in disease management and monitoring. This review explores recent advancements in the pathophysiology of MN, encompassing pathogenesis, clinical presentations, diagnostic criteria, treatment options, and prognosis, with a focus on emerging developments in pathogenesis and therapeutic strategies aimed at halting disease progression. By synthesizing the latest research findings and clinical insights, this review seeks to contribute to the ongoing efforts to enhance our understanding and management of this challenging autoimmune disorder. Membranous nephropathy, an autoimmune disease, can manifest at any age and is among the most common causes of nephrotic syndrome in adults. This review explores recent advancements in the pathophysiology of MN, encompassing pathogenesis, clinical presentations, diagnostic criteria, treatment options, and prognosis, with a focus on emerging developments in pathogenesis and therapeutic strategies aimed at halting disease progression .

Macrophages are highly plastic and heterogeneous innate immune cells that play pivotal roles in kidney development, kidney functions maintenance, immune surveillance, injury, repair, fibrosis and so on. Our understanding of embryonic derived and bone marrow–derived macrophages has evolved beyond the classical M1/M2 polarization paradigm, shifting toward a more nuanced investigation of macrophage subpopulations through the lens of functional specialization and tissue-specific adaptation. Recent advancements in single-cell and spatial transcriptomics have elucidated the diversity of kidney macrophages, revealing their critical contribution to kidney physiology and pathology. In acute kidney injury, macrophages orchestrate inflammatory cascades via cytokine secretion and inflammasome activation, whereas during the reparative phase, they promote tissue regeneration through anti-inflammatory pathways. However, persistent or dysregulated macrophage activation can lead to maladaptive repair and progression to chronic kidney disease characterized by kidney fibrosis. Therapeutically, targeting macrophage polarization, recruitment and macrophage-based adoptive cell therapy has emerged as a promising strategy for modulating kidney inflammation and fibrosis. This review delineates the multifaceted roles of diverse macrophage subsets in kidney physiology and pathology, while highlighting emerging therapeutic avenues and the translational challenges associated with macrophage-targeted interventions.

To explore the association between circulating mononuclear cell mitochondrial DNA copy number and the prognosis of sepsis patients based on the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3 definition). A total of 200 adult patients who had recently devoloped sepsis were prospectively recruited as the study cohort. Demographic and clinical data were recorded along with a 28-day outcome. Mononuclear cell mtDNA copy number was assessed by quantitative PCR. The 28-day outcome of sepsis patients was significantly associated with circulating mononuclear cell mtDNA copy number. The median mononuclear cell relative mtDNA copy number of survivors was significantly higher than that of nonsurvivors (406.68, range 196.65-625.35 vs. 320.57, range 175.98-437.33, p = 0.001). The Cox proportional hazard survival model analysis indicated that mononuclear cell relative mtDNA copy number was significantly negative associated with the 28-day outcome. For every additional unit of mononuclear cell mtDNA relative copy number, the risk of death falls by 0.1% (HR = 0.999, 95% CI = 0.998 to 1.000, p = 0.017). Our data indicate first that circulating mononuclear cellular mtDNA copy number might be helpful for outcome predictions in sepsis patients, and second that lower mtDNA copy number implied poor prognosis.

Background Diabetic myopathy is characterized by the loss of skeletal muscle mass and function. NOD‐like receptor family pyrin domain containing 3 (NLRP3)–mediated pyroptosis is a type of proinflammatory cell death, which can exacerbate significant muscle cell loss and adverse remodelling. The stimulator of interferon genes (STING) is an essential molecule involved in the regulation of inflammation and immune responses across various diseases. The regulatory mechanism by which STING affects muscle pyroptosis in diabetic myopathy remains unclear. Methods STING‐knockout and wild‐type (WT) mice underwent intraperitoneal injection of streptozotocin (STZ). STING small interfering RNA (siRNA) was transfected into fully differentiated C2C12 myotubes prior to glucose treatment. Muscle function tests, body composition analysis, transmission electron microscopy, scanning electron microscopy, western blotting, immunofluorescence, immunohistochemistry, histology, enzyme‐linked immunosorbent assay, and reverse transcription polymerase chain reaction were performed. Co‐immunoprecipitation assays were employed to investigate the interaction between STING and NLRP3. Results STING expression was elevated in the gastrocnemius muscle (GM) tissues of WT diabetic mice. STING‐deficient diabetic mice exhibited pronounced hyperglycaemia accompanied by hypoinsulinaemia, with no significant difference compared with WT diabetic mice. However, STING‐deficient diabetic mice demonstrated a significantly increased body weight and lean mass. A significant decrease in muscle weight, myofibrillar diameter and area, muscle function, and the expression of genes related to muscle atrophy (MuRF1, Atrogin1) were observed in WT diabetic mice, which was mitigated in STING‐deficient diabetic mice. STING deficiency reduced the number of GSDMD‐N formed pores and pyroptosis‐related components (NLRP3, caspase‐1, cle‐caspase‐1, GSDMD, and GSDMD‐N) in the GM tissues and was associated with a reduction in inflammatory chemokines. Similar changes were observed in vitro with glucose‐induced myotube atrophy and pyroptosis as seen in vivo. Activation of STING by the agonist diABZI exacerbated muscle atrophy and pyroptosis in C2C12 myotubes. Co‐localization of STING and NLRP3 was observed, and the interaction between STING and NLRP3 was enhanced in GM tissues from WT diabetic mice. We also found that STING could activate NLRP3 dependent on its channel activity, which can be attenuated by treated with C53 (an inhibitor of STING's ion‐channel function). Conclusions In conclusion, our results indicate that STING‐induced activation of the NLRP3 inflammasome leads to pyroptosis, resulting in muscle atrophy and dysfunction. These findings not only elucidate the mechanism of STING‐induced pyroptosis but also identify STING as a potential therapeutic target for diabetic myopathy.

Blood pressure variability (BPV) is significantly associated with cardiovascular diseases (CVD) and mortality in hemodialysis patients. However, the relationship between blood pressure and CVD in hemodialysis patients is complex and affected by many factors. The present study aimed to assess the association of long‐term predialysis BPV with all‐cause mortality and major adverse cardiovascular events (MACE). One thousand seven hundred twenty‐seven patients receiving maintenance hemodialysis were recruited in nine hemodialysis centers. Predialysis BPV was assessed over 1‐year intervals. Outcomes included all‐cause mortality and MACE during follow‐up periods. The mean age of the final cohort was 59 years, of which 57% were males. Greater predialysis systolic BPV was associated with an increased risk of all‐cause mortality (adjusted hazard ratio, 1.101; 95% confidence intervals 1.064–1.140) and MACE (adjusted hazard ratio, 1.091; 95% confidence intervals 1.059–1.125). Results were similar when systolic BPV was stratified by baseline systolic blood pressure. In conclusion, greater predialysis BPV among hemodialysis patients was associated with all‐cause mortality and MACE. Strategies to reduce blood pressure variability might be beneficial for hemodialysis patients.

ObjectiveThe aim of the present study was to determine whether the predialysis serum magnesium level was associated with morbidity of uraemic restless legs syndrome (RLS) in maintenance haemodialysis patients.DesignA retrospective observational study of morbidity of uraemic RLS was conducted.SettingPatients on maintenance haemodialysis three times a week.ParticipantsWe reviewed 578 patients receiving maintenance haemodialysis for >1 year as our cohort.Outcome measuresUraemic RLS was diagnosed according to International RLS Study Group criteria, and hypermagnesaemia was defined as serum magnesium level >1.02 mmol/L.ResultsThe prevalence of uraemic RLS was 14.4% in our study cohort. Univariate analysis indicated that patients with uraemic RLS differed significantly from non-RLS ones in certain demographic and clinical characteristics, including younger age, longer dialysis duration, higher serum parathyroid hormone level and higher prevalence of predialysis hyperphosphataemia and hypermagnesaemia. Binary logistic-regression model analysis indicated that predialysis hypermagnesaemia was independently associated with uraemic RLS and conferred an increase in morbidity of the syndrome (OR=2.024; 95% CI 1.160 to 3.532; p=0.013). Moreover, we found that dialysis duration and predialysis hyperphosphataemia were independently associated with morbidity of uraemic RLS.ConclusionsOur data indicated that the predialysis serum magnesium level was associated with morbidity of uraemic RLS in maintenance haemodialysis patients and that predialysis hypermagnesaemia might serve as an independent risk factor for the syndrome.

Background. In peritoneal dialysis (PD) patients, whether angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) could protect residual renal function is still controversial. To assess the effects of ACEIs and ARBs on the residual renal function and cardiovascular (CV) events in peritoneal dialysis patients, we performed a meta-analysis of randomized controlled trials. Materials and Methods. We searched PubMed, EMBASE, the Cochrane Library, the CNKI database, and the Wanfang database for relevant articles from database inception to November 30, 2019. Randomized controlled trials were included. The primary outcome was the decline in the residual renal function (RRF). Results. Thirteen trials with 625 participants were included in the meta-analysis. The average residual GFR declined by 1.79 ml/min per 1.73 m2 in the ACEI/ARB group versus 1.44 ml/min per 1.73 m2 in the placebo or active control group at 3 mo. The average residual GFR declined by 2.02 versus 2.06, 2.16 versus 2.72, and -0.04 versus 2.74 ml/min per 1.73 m2 in the placebo or active control group at 6 months (mo), 12 mo, and 24 mo, respectively. The decline in residual GFR showed a significant difference between the ACEI/ARB group and the placebo or active control group at 12 mo (MD=−0.64 ml/min per 1.73 m2; 95% CI: -0.97~-0.32; I2=44%; P<0.0001). No significant difference was observed in Kt/V, urinary protein excretion, weekly creatinine clearance, CV events, or serum potassium levels. Conclusions. In the present study, we found that the use of ACEIs and ARBs, especially long-term treatment, decreased the decline of RRF in patients on PD. ACEIs and ARBs do not cause an additional risk of side effects.

The balance between SUMOylation and deSUMOylation critically regulate cellular apoptosis, with SUMO-modified proteins implicated in ischemia/hypoxia injury. However, the specific contributions of SUMO-conjugated proteins in renal ischemia-reperfusion injury (IRI) remain poorly defined. SUMOylation in IRI was investigated Using proximal tubular-specific Senp3 conditional knockout (CKO) mice. While SENP3-deficiency did not induce tubular injury under basal conditions, its significantly attenuated renal damage following IRI. SUMOylation conferred protection against apoptosis in renal tubular epithelia cells during ischemia/hypoxia. Mass spectrometry revealed arginosuccinate synthase 1 (ASS1) as a key SUMO2/3 target (modified at K239 and K310) in IRI progression. Mechanistically, SENP3-mediated deSUMOylation promoted ASS1 nuclear accumulation in post-IRI tubular epithelial cells, subsequently activating the intrinsic apoptosis pathway via p53-dependent transcriptional upregulation. These findings nominate the SENP3-ASS1-p53 axis as a potential therapeutic target for renal IRI.

Methane-based membrane biofilm reactor (CH4-MBfR) is an emerging wastewater treatment technology based on gas-permeable membranes for oxidized pollutants (e.g., NO 3 - ) abatement. This paper reviews the operation principle of CH4-MBfR, the involved pathways in the aerobic/anaerobic methane oxidation coupled to denitrification (AMO/ANMO-D) process, as well as the recent key advances of CH4-MBfR for environmental applications.

Background. The aim of this study was to identify the blood potassium level beneficial to the postoperative recovery of gastrointestinal motility during continuous renal replacement therapy (CRRT) in patient undergoing open abdominal surgery. Materials and Methods. 538 critically ill patients after open abdominal surgery and receiving CRRT were retrospectively recruited as the study cohort. Demographic and clinical data were recorded along with an evaluation of the postoperative gastrointestinal motility. Results. Correlation analysis was used to assess the correlation coefficient, and then the variables with correlation coefficient value less than 0.5 were included in the binary logistic regression model. Binary logistic regression model indicated that the postoperative blood potassium level was independently associated with the recovery of gastrointestinal motility (OR=0.109, 95% CI= 0.063 to 0.190, p<0.001). Based on the normal range of blood potassium level, we selected the cut-off point of blood potassium level via Weight of Evidence analysis, which was 4.00 mmol/L. Compared with the patients with insufficient blood potassium levels (plasma potassium concentration < 4.00 mmol/L), those with sufficient blood potassium levels (plasma potassium concentration≥ 4.00 mmol/L) conferred an increase in the rate of 4-day postoperative recovery of gastrointestinal motility (OR= 4.425, 95% CI = 2.933 to 6.667, p<0.001). Conclusions. Maintaining the blood potassium concentrations at a relatively high level of the normal blood potassium range during CRRT would be beneficial to postoperative recovery of gastrointestinal motility.