Effect of tumor necrosis factor α and vascular permeability growth factor on albuminuria in rats

Laflam, Paul; Garin, Eduardo H.

doi:10.1007/s00467-005-2078-3

Cited by 16 publications

(11 citation statements)

References 24 publications

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“…However, VEGF does not appear to have a role in proteinuria, as proteinuria is governed primarily by the integrity of the slit diaphragm of the podocyte [8]. Moreover, the infusion of VEGF in rats does not induce proteinuria [5,6].…”

Section: Cytokines As Factors That Increase Glomerular Permeability Tmentioning

confidence: 96%

“…A favorite candidate has been vascular endothelial growth factor (VEGF) [5,6], as it is known to induce capillary permeability by stimulating the release of nitric oxide (a vasodilator) and by inducing endothelial cell fenestration. However, in the kidney, VEGF is constitutively expressed, and both glomerular and peritubular capillary endothelial cells are already in a fenestrated state.…”

Section: Cytokines As Factors That Increase Glomerular Permeability Tmentioning

confidence: 99%

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A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome

et al. 2006

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Idiopathic minimal lesion nephrotic syndrome (IMLNS) was proposed to be a disorder of T-cell dysfunction by Shalhoub in 1974. The mechanisms by which T-cells increase glomerular permeability have remained elusive (and unproven). There is evidence that IMLNS may be due to a circulating factor released from activated T-cells. In recent years, efforts have been made to identify this pathogenetic cytokine as well as to understand the mechanism(s) for the increased release of this factor. This review attempts to critically analyze the available published data. Using different methodologies, investigators have focused on the production of cytokines in patients with IMLNS during relapse and remission. This has resulted in a plethora of data without definitive conclusions. The pathogenetic cytokine has not been identified, and it is questionable whether there is a Th2 dominance in IMLNS. The review of the available data illustrates the difficulties encountered when one is studying the cytokine secretory pattern in patients with IMLNS. Differences in patient population, type of cells studies, sample preservation, and methodology used to measure cytokines are some of the factors that could account for the disparity of observed results.

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Section: Cytokines As Factors That Increase Glomerular Permeability Tmentioning

confidence: 96%

Section: Cytokines As Factors That Increase Glomerular Permeability Tmentioning

confidence: 99%

A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome

et al. 2006

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“…TNF-α has apoptotic and proinflammatory properties and patients with glomerulosclerosis and glomerular endothelial dysfunction have high urinary TNF-α levels (25). Infusion of TNF-α in rat exacerbates glomerular injury and albuminuria (26).…”

Section: Tnf-αmentioning

confidence: 99%

Obesity-Related Glomerulopathy

Mohamed¹

2017

Electron J Gen Med

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Obesity is a major risk factor for renal disease and can cause de novo glomerulopathy. The characteristic finding of obesity-induced renal injury includes glomerular hypertrophy, glomerular basement membrane thickening, mesangial matrix expansion, and increased renal inflammation. These changes may lead to albuminuria, a progressive impairment of renal function, glomerulosclerosis and tubulointerstitial fibrosis. The mechanisms of obesity-related glomerulopathy (ORG) are not well understood however, several mechanisms acting singly or in combination have been suggested as excess excretory load, excess renal sodium retention and insulin resistance (IR) and hyperinsulinemia, increased monocyte chemoattractant protein 1 (MCP-1) expression, Lipotoxicity in proximal tubular cells, increased inflammatory cytokine production such as Interleukin (IL) IL-6, IL-1, and tumor necrosis factor (TNF-α). Activation of NFκB transcription, increase Leptin levels, reduction in plasma adiponectin expression with its anti-inflammatory effects, decrease nitric oxide (NO) level, increase reactive oxygen species (ROS) generation, Hyperlipidemia, and increases in plasma renin activity, angiotensinogen, angiotensin-converting enzyme activity, and circulating AngII. Many lines of treatment are suggested for ORG as Peroxisome proliferator-activated receptors (PPAR) Agonistic, Statins, anti-inflammatory therapy, and antioxidants are under trial. Weight loss decreases of proinflammatory factors, increase of anti-inflammatory molecules and reduces oxidative stress state in obesity, which may protect renal function. This review discusses recent data about ORG, the characteristics of pathogens and possible interventions to prevent kidney injury in obesity.

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“…Both depressed and enhanced cell-mediated immunity has been observed during relapses. Experimental studies have shown that peripheral blood mononuclear cells (PBMCs) and T cell hybridomas made from patients with MCNS released proteinuria-inducing factors in rats [6,7,8]. Various cytokines released by PBMCs from MCNS patients have also been demonstrated in vivo and in vitro [9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Genome-Wide Analysis of Histone H3 Lysine 4 Trimethylation in Peripheral Blood Mononuclear Cells of Minimal Change Nephrotic Syndrome Patients

Zhang¹,

Dai²,

Peng³

et al. 2009

Am J Nephrol

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Background: Studies of the epigenome have attracted some interest in nephrology. However, to date, our knowledge about the alterations in histone modification in minimal change nephrotic syndrome (MCNS) is unknown. This study aimed to investigate the variations in histone H3 lysine 4 trimethylation (H3K4me3) in peripheral blood mononuclear cells of patients with MCNS. Methods: H3K4me3 variations were analyzed in peripheral blood mononuclear cells, from 15 MCNS patients and 15 healthy subjects, using the ChIP-chip approach. ChIP real-time PCR is used to validate the microarray results. In addition, mRNA expression and DNA methylation status can also be further analyzed by quantitative (q) RT-PCR and methyl-DNA immunoprecipitation-q PCR, respectively. Results: 848 increased and 231 decreased H3K4me3 probes displaying significant H3K4me3 differences were found in MCNS patients compared with healthy subjects. The results of ChIP real-time PCR coincided well with the microarray. Expression analysis by qRT-PCR revealed positive correlations between mRNA and H3K4me3 levels. DNA methylation alterations were found on selected positive genes (IL4R, HIVEP3, HPSE2, CDH13 and PRKD2). In addition, we also found that there is an inverse relationship between H3K4me3 and promoter DNA methylation in MCNS patients. Conclusion: Our studies indicate that there are significant alterations of H3K4me3 in MCNS patients. These significant H3K4me3 candidates may help to explain the immunological disturbance involved in MCNS patients.

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Effect of tumor necrosis factor α and vascular permeability growth factor on albuminuria in rats

Cited by 16 publications

References 24 publications

A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome

A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome

Obesity-Related Glomerulopathy

Genome-Wide Analysis of Histone H3 Lysine 4 Trimethylation in Peripheral Blood Mononuclear Cells of Minimal Change Nephrotic Syndrome Patients

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