lupus 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

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

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

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

Rituximab induced pulmonary fibrosis in a patient with lupus nephritis.

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We describe a 26-year-old woman who was diagnosed eleven years ago with systemic lupus erythematosus and who had suffered multiple relapses. She presented with class IV lupus nephritis with thrombotic microangiopathy, for which she received three doses of rituximab along with plasmapheresis, with no

Lipopolysaccharide induces inducible nitric oxide synthase-dependent podocyte dysfunction via a hypoxia-inducible factor 1α and cell division control protein 42 and Ras-related C3 botulinum toxin substrate 1 pathway.

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Urine protein loss in immune complex-mediated diseases such as lupus nephritis is associated with podocyte foot process effacement (podocytopathy) but is not always dependent on glomerular immune complex deposition. Several murine and human studies have associated lupus nephritis with inducible

Comparative transcriptional profiling of 3 murine models of SLE nephritis reveals both unique and shared regulatory networks.

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OBJECTIVE To define shared and unique features of SLE nephritis in mouse models of proliferative and glomerulosclerotic renal disease. METHODS Perfused kidneys from NZB/W F1, NZW/BXSB and NZM2410 mice were harvested before and after nephritis onset. Affymetrix based gene expression profiles of

What is damaging the kidney in lupus nephritis?

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Despite marked improvements in the survival of patients with severe lupus nephritis over the past 50 years, the rate of complete clinical remission after immune suppression therapy is <50% and renal impairment still occurs in 40% of affected patients. An appreciation of the factors that lead to the

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