Publications by authors named "Shoujun Bai"

Background: Pulmonary hypertension (PH) is common in peritonealdialysis (PD) patients and is associated with increased morbidity and mortality. However, the specific risk factors for PH and its prognostic impact remain underexplored, particularly in suburban populations. This study aimed to investigate the risk factors for PH and evaluate its impact on long-term all-cause and cardiovascular mortality in PD patients.

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Persistent inflammation plays a pivotal role in the initiation and progression of renal fibrosis. Activation of the pattern recognition receptor retinoic acid-inducible gene-I (RIG-I) is implicated in the initiation of inflammation. This study aimed to investigate the upstream mechanisms that regulates the activation of RIG-I and its downstream signaling pathway.

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Ischemia‑reperfusion injury‑induced acute kidney injury (IRI‑AKI) involves inflammatory cell infiltration and increased apoptosis, although the potential association between these processes remains unclear. The aim of the present study was to assess the impact of β‑elemene treatment on the IRI‑AKI using both and models, reverse transcription‑quantitative PCR, western blot assays, hematoxylin and Eosin (H&E) staining, Immunohistochemical staining and TUNEL staining. β‑elemene significantly decreased morphological and pathological kidney inflammation in mice caused by IRI.

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Introduction: To investigate the effect of continuous renal replacement therapy (CRRT) in patients with severe acute kidney injury (AKI) by using Nafamostat Mesilate (NM).

Methods: Eighty patients with AKI who underwent CRRT from March 2022 to January 2022 were divided into control group (n = 40, treated with unfractionated heparin) and Observation group (n = 40, treated with NM). The duration of the first filter use, the number of filters used 72 hours after treatment, coagulation and renal functions, adverse reactions, bleeding events, length of stay in intensive care unit (ICU) and survival status at 28 days were compared between the two groups.

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Background: Gallstone disease (GSD) is associated with obesity. The Cardiometabolic Index (CMI), a metric that accurately assesses central adiposity and visceral fat, has not been extensively studied in relation to GSD risk. This study investigates the link between CMI and GSD incidence in U.

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Background: Whether angiotensin receptor-neprilysin inhibitor (ARNI) can reduce the incidence of cardiovascular events and improve peritoneal function in peritoneal dialysis (PD) patients remains unclear. Thus, this study aims to clarify the role of ARNI in PD patients.

Methods: This was a multicenter retrospective study.

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Background: Few clinical studies compare the long-term remission, relapse, and safety of rituximab (RTX) or a combination of intermittent intravenous infusion of cyclophosphamide (CTX) and oral corticosteroid for primary membranous nephropathy (PMN) patients.

Methods: We collected multicenter retrospective data on PMN patients with nephrotic syndrome who received RTX or intermittent intravenous CTX with oral corticosteroids between 1 January 2019 and 31 January 2024. Patients were followed up until two years after receiving immunotherapy.

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Background: The treatment of refractory nephrotic syndrome (RNS) is full of challenges and the role of rituximab (RTX) is not well-established, thus this study aims to demonstrate the role of RTX in RNS.

Methods: This was a multicenter retrospective study of all adult patients receiving RTX for RNS. Patients enrolled were divided into two groups according to pathological pattern: 20 patients as a group of podocytopathy (including minimal change disease [MCD] and focal and segmental glomerulosclerosis [FSGS]), and 26 patients as membranous nephropathy (MN) group.

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Background: Left ventricular hypertrophy is associated with adverse outcomes among peritoneal dialysis patients. The aim of this study was to evaluate the prognostic impact of baseline left ventricular hypertrophy and its relationship with baseline peritoneal transfer characteristics in peritoneal dialysis patients.

Methods: We enrolled 151 incident peritoneal dialysis patients to perform a multicentric retrospective cohort study since January 1, 2017 to January 31, 2021.

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Diabetic nephropathy (DN) is still on the rise worldwide, and millions of patients have to be treated through dialysis or transplant because of kidney failure caused by DN. Recent reports have highlighted circRNAs in the treatment of DN. Herein, we aimed to investigate the mechanism by which high glucose-induced exo-circ_0125310 promotes diabetic nephropathy progression.

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Background: Diabetic nephropathy (DN) is the most common causes of end-stage renal disease. Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) is connected with the development of DN, but the role of CDKN2B-AS1 in DN has not been entirely elucidated.

Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to measure CDKN2B-AS1 and miR-98-5p levels.

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Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The association between epithelial-mesenchymal transition (EMT) and fibrosis is quite ascertained, but its link to eventual tubule dysfunction is missing. Here, we show that human microRNA- (hsa-miR-) 199b-3p protects renal tubules from diabetic-induced injury by repressing KDM6A, a histone lysine demethylase regulating E-cadherin expression.

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Cisplatin is a commonly used chemotherapy drug in cancers, which can lead to acute kidney injury (AKI). AKI can occur in almost one third of tumor patients, who receive cisplatin treatment. microRNAs (miRNAs) are significant tools in regulating the expression of crucial factors in multiple diseases, but little is known about their biological roles in AKI.

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Diabetic nephropathy (DN) is the most common cause of end-stage renal disease. Although numerous reports have demonstrated a correlation between epithelial-mesenchymal transition (EMT) and renal fibrosis, how these processes lead to tubular dysfunction remains unclear. Here, we show that FOXO3a protects kidneys from injury in type II DN by increasing Sirt6 expression, which deacetylates Smad3 and inhibits its transcriptional activity.

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Acute kidney injury (AKI) is a complex renal disease. Long non-coding RNAs (lncRNAs) have frequently been associated with AKI. In the present study, we aimed to investigate the molecular mechanism(s) of LINC00052 in AKI.

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Diabetic kidney disease (DKD) is closely associated with the high risk of cardiovascular disease and mortality. Exosomal circRNAs can exert significant roles in the pathology of various diseases. Nevertheless, the role of exosomal circRNAs in DKD progression remains barely known.

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Article Synopsis
  • Diabetic nephropathy (DN) is a serious kidney disease linked to diabetes, where abnormal processes in mesangial cells worsen the condition.
  • The study found that MIAT is up-regulated in DN patients and high glucose-treated mesangial cells, and silencing MIAT reduces abnormal cell growth and fibrosis triggered by high glucose levels.
  • MIAT acts as a sponge for miR-147a, which is reduced in DN, and the loss of MIAT rescues the effects of high glucose, highlighting a pathway where MIAT promotes harmful cell behavior by regulating miR-147a and its target, E2F transcription factor 3 (E2F3).
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The study explored the correlations of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) gene polymorphisms with susceptibility and the condition of primary nephrotic syndrome. A total of 200 patients with primary nephrotic syndrome in Qilu hospital were collected as disease group, and 200 healthy people were selected as control group. Genomic deoxyribonucleic acids (DNAs) of nucleated cells in the peripheral blood were extracted to detect the gene polymorphisms of TNF-α (rs1799724 and rs1800629) and IL-10 (rs1800872 and rs141219090).

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The current study aimed to investigate the role and underlying mechanisms of circ_LARP4 in diabetic nephropathy (DN). Here, mouse mesangial cells (SV40-MES13) were cultured with 30 mM glucose to establish a DN cellular model. The qRT-PCR results indicated that circ_LARP4 expression was downregulated in the DN cellular model compared to that in the control cells.

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Article Synopsis
  • Diabetic nephropathy is a major global cause of severe kidney disease, with circular RNAs (circRNAs) playing a significant but unclear role in its progression.
  • This study specifically examines the circ-AKT3/miR-296-3p/E-cadherin network, demonstrating that circ-AKT3 can reduce fibrosis-related proteins and cell death in mesangial cells exposed to high glucose levels, common in diabetes.
  • Findings suggest that circ-AKT3 helps prevent damage by regulating the interaction between miR-296-3p and E-cadherin, potentially leading to new strategies for diagnosing and treating diabetic nephropathy.
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Acute kidney injury (AKI) is a common kidney disease that markedly affects public health. To date, the roles of long noncoding RNA XIST in AKI are poorly understood. Here, we investigated the biological functions of XIST in AKI.

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Recently, microRNAs have been recognized as crucial regulators of diabetic nephropathy (DN) development. Epithelial-to-mesenchymal transition (EMT) can play a significant role in tubulointerstitial fibrosis, and it is a hallmark of diabetic nephropathy progression. Nevertheless, the function of miR-98-5p in the modulation of EMT and renal fibrosis during DN remains barely investigated.

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Background: Renal anemia is one of the most important complications in patients on maintenance hemodialysis (MHD). Telehealth-based dialysis registration systems have the advantage of real-time monitoring and have gradually been applied to the management of chronic diseases.

Objective: The objective of our study was to evaluate the impact of a telehealth-based dialysis registration system on patients on MHD in terms of renal anemia control.

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Long non-coding RNAs (lncRNAs) play vital roles in diabetic nephropathy (DN). This research aimed to study the potential role and underlying molecular mechanisms of long non-coding RNA MEG3 in DN. We found that MEG3 was upregulated in DN in vivo and in vitro and could enhance cell fibrosis and inflammatory response in DN.

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