An ARF can occur after gadolinium-based contrast agents in patients with moderate to severe chronic renal failure. Risk factors for ARF after gadolinium toxicity include diabetic nephropathy and low GFR.
Although long-term kidney recipients have a relatively high prevalence of RTA, it is usually mild and subclinical. Further studies are needed to clarify long-term effects of RTA in kidney recipients.
Behçet’s disease (BD) is a chronic, relapsing, multisystemic inflammatory disorder with unanswered questions regarding its etiology/pathogenesis and classification. Distinct manifestation based subsets, pronounced geographical variations in expression, and discrepant immunological abnormalities raised the question whether Behçet’s is “a disease or a syndrome”. To answer the preceding question we aimed to display and compare the molecular mechanisms underlying distinct subsets of BD. For this purpose, the expression data of the gene expression profiling and association study on BD by Xavier et al (2013) was retrieved from GEO database and reanalysed by gene expression data analysis/visualization and bioinformatics enrichment tools. There were 15 BD patients (B) and 14 controls (C). Three subsets of BD patients were generated: MB (isolated mucocutaneous manifestations, n = 7), OB (ocular involvement, n = 4), and VB (large vein thrombosis, n = 4). Class comparison analyses yielded the following numbers of differentially expressed genes (DEGs); B vs C: 4, MB vs C: 5, OB vs C: 151, VB vs C: 274, MB vs OB: 215, MB vs VB: 760, OB vs VB: 984. Venn diagram analysis showed that there were no common DEGs in the intersection “MB vs C” ∩ “OB vs C” ∩ “VB vs C”. Cluster analyses successfully clustered distinct expressions of BD. During gene ontology term enrichment analyses, categories with relevance to IL-8 production (MB vs C) and immune response to microorganisms (OB vs C) were differentially enriched. Distinct subsets of BD display distinct expression profiles and different disease associated pathways. Based on these clear discrepancies, the designation as “Behçet’s syndrome” (BS) should be encouraged and future research should take into consideration the immunogenetic heterogeneity of BS subsets. Four gene groups, namely, negative regulators of inflammation (CD69, CLEC12A, CLEC12B, TNFAIP3), neutrophil granule proteins (LTF, OLFM4, AZU1, MMP8, DEFA4, CAMP), antigen processing and presentation proteins (CTSS, ERAP1), and regulators of immune response (LGALS2, BCL10, ITCH, CEACAM8, CD36, IL8, CCL4, EREG, NFKBIZ, CCR2, CD180, KLRC4, NFAT5) appear to be instrumental in BS immunopathogenesis.
Endothelial dysfunction plays an important role in the pathogenesis of preeclampsia. Increased number of circulating endothelial cells (CECs) have previously been reported after various diseases associated endothelial injury. The aim of this study was to evaluate the CECs in patients with preeclampsia and to demonstrate any association between CECs and homocysteine, which is another marker of vascular injury. The study included 20 preeclamptic, 15 hypertensive women, 15 healthy pregnant and 15 healthy non-pregnant women. All subjects had normal renal function. Systolic and diastolic blood pressures, serum homocysteine levels were measured. To isolate CECs, peripheral blood was first incubated with anti-CD-146 antibody and subsequently conjugated to immunomagnetic beads. Cells were stained with acridine and counted. Preeclamptic patients had elevated numbers of CECs (13.275.2 cells/ml) compared with hypertensive patients (6.970.8 cells/ml), healthy pregnants (5.271.4 cells/ml) and non-pregnant controls (4.071.8 cells/ml), (Po0.0001). Serum homocysteine level in preeclamptic patients (9.572.8 lmol/l) was significantly higher compared with healthy pregnants (6.070.6 lmol/l), was not different from hypertensive patients (11.572.3 lmol/l, P40.05), but it was lesser compared with non-pregnant controls (12.273.3 lmol/l, Po0.0001). Also, significant correlation between CECs and systolic blood pressure (Po0.0001, r ¼ 0.63), diastolic blood pressure (Po0.0001, r ¼ 0.64) and serum homocysteine (Po0.01, r ¼ 0.55) levels were found in preeclamptic patients. CECs as a marker of endothelial injury were significantly higher in patients with preeclampsia than in hypertensive patients, healthy pregnants and normal controls. Further studies are needed for the prognostic and potential importance of CECs in preeclampsia.
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