Publications by authors named "Houyong Dai"

Objective: To evaluate the potential application of tubularinterstitial biomarkers in the differential diagnosis of diabetic kidney disease (DKD) from non-diabetic kidney disease (NDKD), as well as investigate key clinical and pathological parameters to help improve the stratification of patients according to end-stage renal disease risk.

Methods: 132 type 2 diabetic patients with chronic kidney disease were enrolled. Patients were categorized into 2 groups according to the renal biopsy results: DKD (n = 61) and NDKD (n = 71).

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Introduction: Among maintenance hemodialysis (MHD) patients, ones with diabetes mellitus (DM) are known to have the worst outcome.

Methods: A total of 263 MHD patients were included, a dynamic nomogram was established based on multivariable Cox regression analysis.

Results: The median overall survival (OS) time was 46 months.

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Objective: To establish a simple model for predicting postoperative acute kidney injury (AKI) requiring renal replacement therapy (RRT) in patients with renal insufficiency (CKD stages 3-4) who underwent cardiac surgery.

Methods: A total of 330 patients were enrolled. Among them, 226 were randomly selected for the development group and the remaining 104 for the validation group.

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Background: The objective of this study was to examine the clinical characteristics of patients with different cumulative hemodialysis (HD) durations, so as to improve their survival rate.

Methods: In this cross-sectional study, we extracted background information and relevant clinical data from 145 patients who were undergoing maintenance HD three times a week at the Affiliated Hospital of Nantong University between January 1998 and January 2019. The study subjects were divided into four groups according to the duration of their HD: <5 years, 5-10 years, 10-15 years, and >15 years of HD.

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BACKGROUND The aim of this study was to observe the concentration of serum anti-PLA2R antibody in idiopathic membranous nephropathy (IMN) patients and analyze its relationship with clinical and laboratory parameters. MATERIAL AND METHODS We treated 72 patients with idiopathic membranous nephropathy diagnosed by renal biopsy; all these patients who presented nephrotic syndrome were enrolled for investigation, and then underwent combination therapy with prednisone and cyclosporine A for 6 months. We collected data on 24-h total proteinuria (TUpro), creatinine clearance rate (Ccr), and serum albumin (Alb) levels before and after immunosuppressive treatment.

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Klotho is highly expressed in the kidney, while soluble Klotho is detectable in the blood, urine, and cerebrospinal fluid, and has multiple hormone-like functions. The role of Klotho in kidney injury has attracted more and more attentions from researchers. Emerging evidence revealed that the transient deficiency of Klotho is an early event of acute kidney injury (AKI), whereas, in chronic kidney disease, this deficiency is sustained not only in the kidney, but also in other organ systems.

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Rationale: It is reported that successful pregnancies in dialyzed uremic women are rare. Over the past years, despite advances in clinical management and technology in dialysis for pregnancy in patients receiving maintenance hemodialysis, uremia remains a high risk factor for adverse outcomes in mother and fetus.

Patient Concerns: In this article, we present a case of pregnancy in a 34-year-old uremic woman on dialysis.

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Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays a pivotal role in the pathogenesis of hypertension and renal fibrosis. GSK-3β contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo-induced hypertension, and renal damage is not clear. In the present study, rats were treated with Aldo combined with SB-216763 (a GSK-3β inhibitor) for 4 weeks.

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Renal Ischemia-Reperfusion Injury (IRI) is one of the main causes of Acute Kidney Injury (AKI), and may lead to chronic kidney disease. The high mortality rate of AKI has not changed in the last 5 decades due to non-recognition, nephrotoxin exposure, delayed diagnosis and lack of specific intervention. Complement activation plays important roles in IRI-induced AKI because of its association with immunity, inflammation, cell death and tissue repair.

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Despite substantial progress in medical care, the morbidity rate of diabetic nephropathy (DN) remains high in patients with diabetes. Evidence suggests that connective tissue growth factor (CTGF) induced podocyte injury may contribute to DN and CTGF inhibition could reduce albuminuria. However, to date the mechanisms involved in the effect of CTGF on podocyte injury have not been fully understood.

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Objective: It is known that connective tissue growth factor (CTGF) and β-catenin are involved in DN; however, the underlying molecular mechanisms remain unknown. Here we hypothesized that podocytes undergo epithelial-mesenchymal transition (EMT) in high-glucose condition and CTGF mediates high-glucose induced EMT by activating β-catenin in podocytes.

Methods: The differentiated podocytes were cultured and divided into three groups: the normal glucose group (5 mmol/L glucose), the high-glucose group (30 mmol/L glucose), and the osmotic control group (5 mmol/L glucose supplemented with 25 mmol/L mannitol).

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Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays an important role in the pathogenesis of hypertension and renal fibrosis. Toll-like receptor 4 (TLR4) signaling contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo-induced hypertension and renal damage is not clear. In the current study, rats were treated with Aldo-salt combined with TAK-242 (a TLR4 signaling antagonist) for 4 weeks.

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Background: Cardiovascular damage and diabetic nephropathy are major complications in patients with Type 2 diabetic nephropathy (T2DN); however, the role of renal damage on cardiac remodeling is not yet fully known.

Methods: A retrospective research was conducted in 254 T2DN patients. All were divided into three groups according to urinary albumin excretion (UAE): the normoalbuminuria group (UAE < 30 mg/g, n = 18), the microalbuminuria group (UAE 30 - 300 mg/g, n = 99) and the macroalbuminuria group (UAE > 300 mg/g, n = 137).

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Background: The initiation and progression of diabetic nephropathy (DN) is complex. Quantification of mRNA expression in urinary sediment has emerged as a novel strategy for studying renal diseases. Considering the numerous molecules involved in DN development, a high-throughput platform with parallel detection of multiple mRNAs is needed.

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Background: Integrin-linked kinase (ILK) dysregulation is involved in the progression of diabetic nephropathy (DN). The aim of this study was to investigate the effects of angiotensin II receptor blocker (ARB), irbesartan, on ILK expression and podocyte injury in DN.

Methods: DN was induced by the combined feeding of high-sucrose, high-fat diet and intra-peritoneal injection of low dose of streptozotocin (35 mg/kg) in spontaneously hypertensive rats.

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Emerging evidence has suggested that podocytes undergo epithelial-mesenchymal transition (EMT) in diabetic nephropathy (DN). Connective tissue growth factor (CTGF) and integrin-linked kinase (ILK) are involved in the progression of DN. However, the underlying mechanisms of EMT are not well understood.

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Background: Emerging evidence has indicated that the endothelial-to-mesenchymal transition (EndMT) is a crucial event during early stages of cardiac fibrosis. In the present study, we first investigated the influence of Irbesartan (Irb) on myocardial EndMT in diabetic rats.

Methods: Diabetic rats were divided into two groups: the diabetic group (DM) and the Irb-treated group (DM+Irb).

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Background: Emerging evidence suggests that podocyte injury is a crucial event in the stage of diabetic nephropathy (DN), a process in which angiotensin II is implicated. In this study, the authors investigated the influence of irbesartan, an angiotensin receptor blocker, on the phenotypic alterations of podocytes in experimental DN.

Methods: DN was induced by combination of high-sucrose, high-fat diet and intraperitoneal injection of low dose of streptozotocin (35 mg/kg) in spontaneously hypertensive rats.

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Background: Substantial evidence suggests that high glucose (HG) causes endothelial cell damage; however, the potential mechanism therein has yet to be clarified. The aim of this study was to investigate the influence of HG on the endothelial-to-mesenchymal transition (EndMT) and its relevance to the activation of the renin-angiotensin system.

Methods: Primary human aortic endothelial cells (HAECs) were divided into three groups: a normal glucose (NG) group, HG group, and irbesartan (1 microM)-treated (HG+irbesartan) group.

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