Acute kidney injury (AKI) usually requires renal replacement therapy (RRT). Common RRT modes include peritoneal dialysis, continuous renal replacement therapy, intermittent hemodialysis and continuous low-efficiency hemodialysis. In clinical practice, there is still controversy over how to select the appropriate RRT mode for AKI patients and when initiating RRT is more beneficial for AKI patients. This article summarizes previous studies on the impact of RRT mode and initiation timing on the prognosis of AKI patients, with the aim of providing assistance for clinical decision-making.

Acute Kidney Injury (AKI) is a common and severe complication after cardiac surgery. The pathogenesis of cardiac surgery-associated AKI (CSA-AKI) is complex, and it is associated with increased patient mortality and poor renal prognosis. To identify high-risk patients as early as possible, numerous clinical studies have explored perioperative risk factors and developed a variety of biomarkers with good diagnostic capabilities. Currently, multiple prediction models for AKI after cardiac surgery have been developed internationally; however, there is no effective treatment for CSA-AKI. Therefore, implementing reasonable and comprehensive preventive strategies is crucial. In addition, the clinical application of some interventions is controversial, which means more research and exploration are needed to make more informed decisions regarding the prevention and treatment of CSA-AKI.

Intervertebral disc degeneration (IDD) is largely attributed to impaired endogenous repair. Nucleus pulposus-derived stem cells (NPSCs) senescence leads to endogenous repair failure. Small extracellular vesicles/exosomes derived from mesenchymal stem cells (mExo) have shown great therapeutic potential in IDD, while whether mExo could alleviate NPSCs senescence and its mechanisms remained unknown. We established a compression-induced NPSCs senescence model and rat IDD models to evaluate the therapeutic efficiency of mExo and investigate the mechanisms. We found that mExo significantly alleviated NPSCs senescence and promoted disc regeneration while knocking down thioredoxin (TXN) impaired the protective effects of mExo. TXN was bound to various endosomal sorting complex required for transport (ESCRT) proteins. Autocrine motility factor receptor (AMFR) mediated TXN K63 ubiquitination to promote the binding of TXN on ESCRT proteins and sorting of TXN into mExo. Knocking down exosomal TXN inhibited the transcriptional activity of nuclear factor erythroid 2-related factor 2 (NRF2) and activator protein 1 (AP-1). NRF2 and AP-1 inhibition reduced endogenous TXN production that was promoted by exosomal TXN. Inhibition of NRF2 in vivo diminished the anti-senescence and regenerative effects of mExo. Conclusively, AMFR-mediated TXN ubiquitination promoted the sorting of TXN into mExo, allowing exosomal TXN to promote endogenous TXN production in NPSCs via TXN/NRF2/AP-1 feed-forward circuit to alleviate NPSCs senescence and disc degeneration.

Acute kidney injury (AKI) usually requires renal replacement therapy (RRT). Common RRT modes include peritoneal dialysis, continuous renal replacement therapy, intermittent hemodialysis and continuous low-efficiency hemodialysis. In clinical practice, there is still controversy over how to select the appropriate RRT mode for AKI patients and when initiating RRT is more beneficial for AKI patients. This article summarizes previous studies on the impact of RRT mode and initiation timing on the prognosis of AKI patients, with the aim of providing assistance for clinical decision-making.

Acute Kidney Injury (AKI) is a common and severe complication after cardiac surgery. The pathogenesis of cardiac surgery-associated AKI (CSA-AKI) is complex, and it is associated with increased patient mortality and poor renal prognosis. To identify high-risk patients as early as possible, numerous clinical studies have explored perioperative risk factors and developed a variety of biomarkers with good diagnostic capabilities. Currently, multiple prediction models for AKI after cardiac surgery have been developed internationally; however, there is no effective treatment for CSA-AKI. Therefore, implementing reasonable and comprehensive preventive strategies is crucial. In addition, the clinical application of some interventions is controversial, which means more research and exploration are needed to make more informed decisions regarding the prevention and treatment of CSA-AKI.

OBJECTIVES: Long-term elevated blood pressure may lead to kidney damage, yet the pathogenesis of hypertensive kidney damage is still unclear. This study aims to explore the role and significance of leucine-rich alpha-2-glycoprotein-1 (LRG-1) in hypertensive renal damage through detecting the levels of LRG-1 in the serum and kidney of mice with hypertensive renal damage and its relationship with related indexes. METHODS: C57BL/6 mice were used in this study and randomly divided into a control group, an angiotensin II (Ang II) group, and an Ang II+irbesartan group. The control group was gavaged with physiological saline. The Ang II group was pumped subcutaneously at a rate of 1.5 mg/(kg·d) for 28 days to establish the hypertensive renal damage model in mice, and then gavaged with equivalent physiological saline. The Ang II+irbesartan group used the same method to establish the hypertensive renal damage model, and then was gavaged with irbesartan. Immunohistochemistry and Western blotting were used to detect the expression of LRG-1 and fibrosis-related indicators (collagen I and fibronectin) in renal tissues. ELISA was used to evaluate the level of serum LRG-1 and inflammatory cytokines in mice. The urinary protein-creatinine ratio and renal function were determined, and correlation analysis was conducted. RESULTS: Compared with the control group, the levels of serum LRG-1, the expression of LRG-1 protein, collagen I, and fibronectin in kidney in the Ang II group were increased (all P<0.01). After treating with irbesartan, renal damage of hypertensive mice was alleviated, while the levels of LRG-1 in serum and kidney were decreased, and the expression of collagen I and fibronectin was down-regulated (all P<0.01). Correlation analysis showed that the level of serum LRG-1 was positively correlated with urinary protein-creatinine ratio, blood urea nitrogen, and blood creatinine level in hypertensive kidney damage mice. Serum level of LRG-1 was also positively correlated with serum inflammatory factors including TNF-α, IL-1β, and IL-6. CONCLUSIONS Hypertensive renal damage mice display elevated expression of LRG-1 in serum and kidney, and irbesartan can reduce the expression of LRG-1 while alleviating renal damage. The level of serum LRG-1 is positively correlated with the degree of hypertensive renal damage, suggesting that it may participate in the occurrence and development of hypertensive renal damage.
Animals ; Mice ; Mice, Inbred C57BL ; Fibronectins ; Irbesartan ; Creatinine ; Kidney/physiology* ; Hypertension/complications* ; Angiotensin II ; Collagen Type I

Objective:To improve the understanding of hemodialysis complicated with mesenteric artery calcified stenosis and mesenteric ischemia through the analysis of the case and review of related literature.Methods:A case of hemodialysis with intractable abdominal pain as the main manifestation was reported, and its clinical features, diagnosis and treatment were summarized.Results:The case was a maintenance hemodialysis patient with persistent dull pain around the umbilicus, which worsens after meal and hemodialysis. The results showed multiple vascular calcification, superior mesenteric artery stenosis so the patient was diagnosed with chronic mesenteric ischemia. Mesenteric revascularization under intervention was planned but the guide wire failed to enter the superior mesenteric artery after repeated attempts during the operation. Surgical treatment was recommended, but the patient and family refused surgery and were discharged.Conclusions:Dialysis patients with intractable abdominal pain should be carefully identified and alert for mesenteric artery disease and mesenteric ischemia.

BACKGROUND: Ischemic acute kidney injury (AKI) is a common syndrome associated with considerable mortality and healthcare costs. Up to now, the underlying pathogenesis of ischemic AKI remains incompletely understood, and specific strategies for early diagnosis and treatment of ischemic AKI are still lacking. Here, this study aimed to define the transcriptomic landscape of AKI patients through single-cell RNA sequencing (scRNA-seq) analysis in kidneys. METHODS: In this study, scRNA-seq technology was applied to kidneys from two ischemic AKI patients, and three human public scRNA-seq datasets were collected as controls. Differentially expressed genes (DEGs) and cell clusters of kidneys were determined. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, as well as the ligand-receptor interaction between cells, were performed. We also validated several DEGs expression in kidneys from human ischemic AKI and ischemia/reperfusion (I/R) injury induced AKI mice through immunohistochemistry staining. RESULTS: 15 distinct cell clusters were determined in kidney from subjects of ischemic AKI and control. The injured proximal tubules (PT) displayed a proapoptotic and proinflammatory phenotype. PT cells of ischemic AKI had up-regulation of novel pro-apoptotic genes including USP47 , RASSF4 , EBAG9 , IER3 , SASH1 , SEPTIN7 , and NUB1 , which have not been reported in ischemic AKI previously. Several hub genes were validated in kidneys from human AKI and renal I/R injury mice, respectively. Furthermore, PT highly expressed DEGs enriched in endoplasmic reticulum stress, autophagy, and retinoic acid-inducible gene I (RIG-I) signaling. DEGs overexpressed in other tubular cells were primarily enriched in nucleotide-binding and oligomerization domain (NOD)-like receptor signaling, estrogen signaling, interleukin (IL)-12 signaling, and IL-17 signaling. Overexpressed genes in kidney-resident immune cells including macrophages, natural killer T (NKT) cells, monocytes, and dendritic cells were associated with leukocyte activation, chemotaxis, cell adhesion, and complement activation. In addition, the ligand-receptor interactions analysis revealed prominent communications between macrophages and monocytes with other cells in the process of ischemic AKI. CONCLUSION Together, this study reveals distinct cell-specific transcriptomic atlas of kidney in ischemic AKI patients, altered signaling pathways, and potential cell-cell crosstalk in the development of AKI. These data reveal new insights into the pathogenesis and potential therapeutic strategies in ischemic AKI.
Humans ; Mice ; Animals ; Transcriptome/genetics* ; Ligands ; Kidney/metabolism* ; Acute Kidney Injury/metabolism* ; Ischemia/metabolism* ; Reperfusion Injury/metabolism* ; Sequence Analysis, RNA ; Adaptor Proteins, Signal Transducing/metabolism* ; Tumor Suppressor Proteins/metabolism*

OBJECTIVES: Platelet-to-lymphocyte ratio (PLR) has recently been investigated as a new inflammatory marker in many inflammatory diseases, including systemic lupus erythematosus and immunoglobulin A vasculitis. However, there were very few reports regarding the clinical role of PLR in patients with anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis. This study was thus undertaken to investigate the relationship between inflammatory response and disease activity in Chinese patients with myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) associated vasculitis. Furthermore, we evaluated whether PLR predicts the progression of end stage of renal disease (ESRD) and all-cause mortality. METHODS: The clinical, laboratory and pathological data, and the outcomes of MPO-ANCA associated vasculitis patients were collected. The Spearman correlation coefficient was computed to examine the association between 2 continuous variables. Cox regression analysis was used to estimate the association between PLR and ESRD or all-cause mortality. RESULTS: A total of 190 consecutive patients with MPO-ANCA associated vasculitis were included in this study. Baseline PLR was positively correlated with CRP (r=0.333, P<0.001) and ESR (r=0.218, P=0.003). PLR had no obvious correlation with Birmingham Vasculitis Activity Score (BVAS). Patients having PLR≥330 exhibited better cumulative renal survival rates than those having PLR<330 (P=0.017). However, there was no significant difference in the cumulative patient survival rates between patients with PLR≥330 and those with PLR<330 at diagnosis (P>0.05). In multivariate analysis, PLR is associated with the decreased risk of ESRD (P=0.038, HR=0.518, 95% CI 0.278 to 0.963). We did not find an association between PLR with all-cause mortality using multivariate analysis (HR=1.081, 95% CI 0.591 to 1.976, P=0.801). CONCLUSIONS PLR is positively correlated with CRP and ESR. Furthermore, PLR may independently predict the risk of ESRD.
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/diagnosis* ; Antibodies, Antineutrophil Cytoplasmic/analysis* ; China/epidemiology* ; Humans ; Kidney Failure, Chronic/complications* ; Lymphocytes ; Peroxidase ; Retrospective Studies

Objective:Renal involvement in primary Sjogren′s syndrome (pSS) has been considered rare, and recent studies have shown that there was a large difference in the prevalence of the disease, which has been reported to range from 0.03% to 67%. The meta-analysis was to determine the prevalence of renal involvement in pSS patients.Methods:The study on pSS renal involvement was conducted in Pubmed, Embase and Cochrane Library from January 2002 to May 2019. After logarithmic conversion of the prevalence rate, meta-analysis of random effect model was carried out to explore the prevalence of pSS renal involvement. Subgroup analysis and meta regression analysis were used to explore the source of heterogeneity. We also performed sensitivity analysis and assessments of publication bias by Begger′s test.Results:The meta-analysis included eighteen observational studies of 8 888 participants. The result in random effects model showed that the combined prevalence was 9.0% (95% CI: 6.0%-12.0%), with significant heterogeneity between these studies ( I2=97%, P<0.01). The source of heterogeneity was explained by a stratified analysis of region, type of study, and the diagnostic criteria for renal involvement. Sensitivity analysis showed that the result was robust and Begger′s test did not detect the presence of publication bias. Conclusions:The prevalence of renal involvement in pSS is 9.0%. Due to huge heterogeneity, large multicenter prospective studies will be needed to determine its prevalence and the relationship between pSS and kidney.