nephritis/hypoxia

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Detection of Renal Hypoxia in Lupus Nephritis Using Blood Oxygen Level-Dependent MR Imaging: A Multiple Correspondence Analysis.

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OBJECTIVE Nephrologists have pursued ideal, dynamic and noninvasive methods for assessing renal function and disease progression. Blood oxygen level dependent (BOLD) imaging is a useful technique for assessing renal disease. This current study was performed to explore the correlation between the

Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis.

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OBJECTIVE Tubulointerstitial hypoxia in the kidney is considered a hallmark of injury and a mediator of the progression of tubulointerstitial fibrosis. Hypoxia-inducible factor-1alpha (HIF-1alpha), a master transcription factor in cellular adaptation to hypoxia, regulates a wide variety of genes,

Hypoxia inducible factor-1 alpha promotes mesangial cell proliferation in lupus nephritis.

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BACKGROUND Evidence has accumulated that hypoxia plays a significant role in the pathogenesis and progression of both acute renal injury and chronic renal disease. However, little was known about the effects of hypoxia on lupus nephritis (LN). In the current study, we investigated the expression of

P-selectin blockade ameliorates lupus nephritis in MRL/lpr mice through improving renal hypoxia and evaluation using BOLD-MRI.

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Lupus nephritis is one of the most common and severe complications of systemic lupus erythematosus, of which poor prognosis is indicated by aggravated renal hypoxia and tubulointerstitial fibrosis. Cell adhesion molecules play a key role in the progression of lupus nephritis

Hsa‑miR‑371‑5p inhibits human mesangial cell proliferation and promotes apoptosis in lupus nephritis by directly targeting hypoxia‑inducible factor 1α.

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MicroRNAs (miRNAs/miR) have emerged as a novel class of gene expression modulators in kidney disease. Lupus nephritis (LN) is the predominant cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Hsa‑miR‑371‑5p has previously been reported to be dysregulated in LN

Genome-wide profiling identifies associations between lupus nephritis and differential methylation of genes regulating tissue hypoxia and type 1 interferon responses.

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OBJECTIVE Previous studies have shown that differential DNA methylation is associated with SLE susceptibility. How DNA methylation affects the clinical heterogeneity of SLE has not been fully defined. We conducted this study to identify differentially methylated CpG sites associated with nephritis

Kidney tissue hypoxia dictates T cell-mediated injury in murine lupus nephritis.

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The kidney is a frequent target of autoimmune injury, including in systemic lupus erythematosus; however, how immune cells adapt to kidney's unique environment and contribute to tissue damage is unknown. We found that renal tissue, which normally has low oxygen tension, becomes more hypoxic in lupus

Inhibition of Endothelial PHD2 Suppresses Post-Ischemic Kidney Inflammation through Hypoxia-Inducible Factor-1.

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Prolyl-4-hydroxylase domain-containing proteins 1-3 (PHD1 to PHD3) regulate the activity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transcription factors that are key regulators of hypoxic vascular responses. We previously reported that deficiency of endothelial HIF-2

The role of hypoxia in the pathogenesis of lupus nephritis

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[A case of lupus nephritis resistant to steroid pulse therapy markedly improved by bolus intravenous cyclophosphamide therapy].

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Bolus intravenous cyclophosphamide therapy (IVCY) has recently been the subject of considerable attention because it is occasionally very effective in the treatment of severe lupus nephritis. However only a few reports on this form of therapy have been noted in Japan. Described here is a patient

Mononuclear phagocytes orchestrate prolyl hydroxylase inhibition-mediated renoprotection in chronic tubulointerstitial nephritis.

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Prolyl hydroxylase domain enzyme inhibitors (PHDIs) stabilize hypoxia-inducible factors (HIFs), and are protective in models of acute ischemic and inflammatory kidney disease. Whether PHDIs also confer protection in chronic inflammatory kidney disease models remains unknown. Here we investigated

Molecular studies of lupus nephritis kidneys.

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Lupus nephritis is a devastating complication of systemic lupus erythematosus (SLE) for which current therapies are insufficiently effective. Histologic evaluation of renal biopsies is a poor predictor of therapeutic response or outcome. Integrated immunologic, genomic and proteomic approaches may

Pathogenesis of tubular interstitial nephritis.

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Injury to the interstitium of the kidney is regarded as a common pathway leading to end-stage renal insufficiency, regardless of etiology. Tubular interstitial nephritis is characterized histologically by inflammatory changes in the tubulointerstitial compartment, such as interstitial edema,

[The modulation of renal tubular epithelial cells treated with hypoxia on renal interstitial fibroblasts in coculture].

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To clarify cell-cell interaction in the pathogenesis of renal tubulointerstitial nephritis (TIN), the effect of renal tubular epithelial cells (TEC) on renal interstitial peritubular fibroblasts (PTF) was examined in cell coculture system without direct contact. TEC and PTF were prepared from the

Identification of stage-specific genes associated with lupus nephritis and response to remission induction in (NZB × NZW)F1 and NZM2410 mice.

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OBJECTIVE To elucidate the molecular mechanisms involved in renal inflammation during the progression, remission, and relapse of nephritis in murine lupus models using transcriptome analysis. METHODS Kidneys from (NZB × NZW)F1 (NZB/NZW) and NZM2410 mice were harvested at intervals during the disease

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