UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antineutrophil cytoplasmic autoantibodies (ANCA) are commonly associated with a necrotizing and crescentic glomerulonephritis (GN) that is pauci-immune, with few or no glomerular immune complex deposits detectable by immunofluorescence (IF) or electron microscopy (EM). Immunoglobulin A (IgA) nephropathy may also be manifest as a crescentic GN, but it is characterized by mesangial immune complex deposits containing IgA and is rarely associated with myeloperoxidase (MPO)- or proteinase 3 (PR3)-specific ANCA when an enzyme immunoassay is used to detect these antibodies. This report describes six patients with severe crescentic GN with mesangial IgA deposits by IF and mesangial electron-dense deposits by EM in patients with positive ANCA serological test results (four patients, anti-PR3; one patient, anti-MPO; one patient, anti-PR3 and anti-MPO). Patients presented with acute or progressive renal insufficiency, hematuria, proteinuria (nephrotic range in two patients), and hypertension. Three patients had evidence of systemic vasculitis: two patients at initial presentation and one patient later in the clinical course. Renal biopsy specimens showed crescents in greater than 50% of glomeruli in all cases, but only mild, focal and segmental mesangial and endocapillary hypercellularity, more typical of ANCA-associated crescentic GN than of crescentic IgA nephropathy without associated ANCA. Semiquantitative analysis of mesangial and endocapillary cellularity performed on renal biopsy slides from these six patients and from eight ANCA-negative patients with IgA nephropathy and crescents in greater than 50% of glomeruli showed significantly greater hypercellularity in the ANCA-negative cases. Three of five ANCA-positive patients for whom follow-up clinical data were available showed improved renal function after treatment with cyclophosphamide and corticosteroids and have not developed end-stage renal disease 17, 20, and 25 months postbiopsy. The remaining two patients were dialysis dependent at the time of biopsy and have remained so despite treatment with cyclophosphamide and corticosteroids. The findings suggest an overlap syndrome of ANCA-associated crescentic GN and IgA nephropathy that resembles the former both histologically and in its potential to respond to aggressive therapy if detected relatively early in its course.
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PMID:ANCA-associated crescentic glomerulonephritis with mesangial IgA deposits. 1100 72

Risk factors for cardiovascular disease have been shown to exacerbate the inflammatory response and microvascular dysfunction that is normally associated with ischemia-reperfusion. The objective of this study was to determine whether hypercholesterolemia and/or hypertension alter I/R-induced expression of P-selectin in the intestinal vasculature. Male control and hypertensive (HTN) rats were placed on either a normal diet or high cholesterol diet (HCD) for at least 3 weeks resulting in hypercholesterolemia (HC). Ischemia was induced by occlusion of the superior mesenteric artery for 15 min, followed by either 30 min or 4 h of reperfusion. The dual radiolabeled antibody technique was used to quantify the rapid (30 min) and transcription-dependent (4 h) expression of P-selectin. Tissue myeloperoxidase (MPO) was used to quantify neutrophil infiltration. The constitutive (basal) expression of P-selectin did not differ among the experimental groups. Although I/R significantly increased P-selectin expression in control, HC, and HTN+HC, P-selectin expression did not increase in HTN. The HC group exhibited the largest increments in P-selectin expression and tissue MPO after I/R. The increment in P-selectin expression was not significantly attenuated in HC rats that were rendered thrombocytopenic with anti-platelet serum. Treatment with an anti-P-selectin antibody largely prevented the exaggerated MPO increase noted in HC. These findings indicate that hypercholesterolemia in contrast to hypertension enhances the expression of P-selectin in the postischemic intestinal vasculature.
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PMID:Influence of hypercholesterolemia and hypertension on ischemia-reperfusion induced P-selectin expression. 1116 66

A 74-year-old male was referred for the sudden onset of bilateral sudden deafness. The patient had no history of any disease or trauma to the head. Pure tone audiometry revealed bilateral moderate, to severe, sensorineural hearing loss. Auditory brain stem responses (ABRs) showed normal peak and interpeak latencies. These audiological findings suggested that his hearing loss could be attributed to inner ear lesions. However, we felt an alternative explanation for this sudden deafness was likely to exist because the patient also had a month-long fever of unknown origin (FUO) and weight loss of 5 kg/month. Using the criteria of The American College of Rheumatology, we made the diagnosis of polyarteritis nodosa (PAN). Serum MPO-ANCA was positive (x 661). For treatment, the patient was begun on prednisolone and cyclophosphamide. Nine months later, fever, hypertension, nephritis, pneumonitis, and arthritis had completely resolved, the MPO-ANCA became negative (MPO-ANCA < x 10). Furthermore, his hearing improved.
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PMID:Sensorineural hearing loss as the initial manifestation of polyarteritis nodosa. 1127 37

Increased LDL oxidation is associated with coronary artery disease. The predictive value of circulating oxidized LDL is additive to the Global Risk Assessment Score for cardiovascular risk prediction based on age, gender, total and HDL cholesterol, diabetes, hypertension, and smoking. Circulating oxidized LDL does not originate from extensive metal ion-induced oxidation in the blood but from mild oxidation in the arterial wall by cell-associated lipoxygenase and/or myeloperoxidase. Oxidized LDL induces atherosclerosis by stimulating monocyte infiltration and smooth muscle cell migration and proliferation. It contributes to atherothrombosis by inducing endothelial cell apoptosis, and thus plaque erosion, by impairing the anticoagulant balance in endothelium, stimulating tissue factor production by smooth muscle cells, and inducing apoptosis in macrophages. HDL cholesterol levels are inversely related to risk of coronary artery disease. HDL prevents atherosclerosis by reverting the stimulatory effect of oxidized LDL on monocyte infiltration. The HDL-associated enzyme paraoxonase inhibits the oxidation of LDL. PAF-acetyl hydrolase, which circulates in association with HDL and is produced in the arterial wall by macrophages, degrades bioactive oxidized phospholipids. Both enzymes actively protect hypercholesterolemic mice against atherosclerosis. Oxidized LDL inhibits these enzymes. Thus, oxidized LDL and HDL are indeed antagonists in the development of cardiovascular disease.
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PMID:Oxidized LDL and HDL: antagonists in atherothrombosis. 1164 Dec 34

A Japanese girl aged 13 years with myeloperoxidase anti-neutrophil cytoplasmic antibodies(MPO-ANCA)-associated glomerulonephritis(GN) progressed to end-stage renal failure after 7 years' clinical observation. She had been suffering from recurrent disease flare associated with serum MPO-ANCA elevation(i.e. 153 EU/ml, 208 EU/ml and 358 EU/ml, maximum at each of the episodes, normal < 10 EU/ml). Each flare was treated successfully with prednisolone combined with cyclophosphamide and azathioprine. However, her renal function gradually deteriorated, and peritoneal dialysis(PD) was initiated 7 years after the onset of the disease. During the clinical course, no extrarenal manifestations were observed. Due to subsidence of the serum MPO-ANCA titer(10 EU/ml) after starting PD, prednisolone and azathioprine were tapered thereafter. Her daily urine volume was preserved at approximately 600 ml at that time. She suddenly developed fatigue with severe anemia, oliguria and hypertension 4 months after discontinuation of immunosuppressive therapy. The serum titer of MPO-ANCA increased to 100 EU/ml. These clinical observation suggests that disease flare may occur in selected patients with MPO-ANCA-associated GN, who develop end-stage renal failure requiring PD. Although recurrent flare associated with an increased serological activity in a proportion of patients with lupus nephritis who have received dialysis has been reported to date, to our knowledge, a similar clinical observation in the MPO-ANCA-associated GN has not been reported. Selected patients with the disease should be followed with close observation after undergoing dialysis.
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PMID:[A case of ANCA-associated glomerulonephritis without extrarenal symptoms with disease flare after starting dialysis]. 1221 82

A 58-year-old woman with Goodpasture syndrome and active ulcerative colitis is described. On admission, the patient had exertional dyspnea, hemoptysis, severe hypertension, and peripheral edema. Her serum levels of urea nitrogen and creatinine were increased, and her hemoglobin concentration was reduced. The patient had a rapidly progressive glomerulonephritis with acute renal failure. She was treated with methylprednisolone, cyclophosphamide, and plasmapheresis but failed to regain renal function. Circulating anti-glomerular basement membrane (anti-GBM) antibody was positive; however, serum antinuclear antibody, proteinase-3-antineutrophil cytoplasm antibody and myeloperoxidase-antineutrophil cytoplasm antibody were negative. Nineteen months after initial presentation, she developed abdominal pain and severe diarrhea. These symptoms did not improve with conventional treatment. Colonoscopy performed after 3 months showed multiple ulcers in the colon. She was diagnosed with ulcerative colitis. She underwent granulocyte and monocyte adsorption apheresis once per week for 5 weeks. At 8 weeks, her symptoms had improved; her stool number was markedly decreased, and the bloody stools and abdominal pain disappeared. These results suggest that granulocyte and monocyte apheresis may be of benefit in the therapy of a patient with ulcerative colitis who previously had Goodpasture syndrome
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PMID:Granulocyte and monocyte adsorption apheresis in a patient with antiglomerular basement membrane glomerulonephritis and active ulcerative colitis. 1279 51

Vascular NAD(P)H oxidase-derived reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) have emerged as important molecules in the pathogenesis of atherosclerosis, hypertension, and diabetic vascular complications. Additionally, myeloperoxidase (MPO), a transcytosable heme protein that is derived from leukocytes, is also believed to play important roles in the above-mentioned inflammatory vascular diseases. Previous studies have shown that MPO-induced vascular injury responses are H2O2 dependent. It is well known that MPO can use leukocyte-derived H2O2; however, it is unknown whether the vascular-bound MPO can use vascular nonleukocyte oxidase-derived H2O2 to induce vascular injury. In the present study, ANG II was used to stimulate vascular NAD(P)H oxidases and increase their H2O2 production in the vascular wall, and vascular dysfunction was used as the vascular injury parameter. We demonstrated that vascular-bound MPO has sustained activity in the vasculature. MPO could use the vascular NAD(P)H oxidase-derived H2O2 to produce hypochlorus acid (HOCl) and its chlorinating species. More importantly, MPO derived HOCl and chlorinating species amplified the H2O2-induced vascular injury by additional impairment of endothelium-dependent relaxation. HOCl-modified low-density lipoprotein protein (LDL), a specific biomarker for the MPO-HOCl-chlorinating species pathway, was expressed in LDL and MPO-bound vessels with vascular NAD(P)H oxidase-derived H2O2. MPO-vascular NAD(P)H oxidase-HOCl-chlorinating species may represent a common pathogenic pathway in vascular diseases and a new mechanism involved in exacerbation of vascular diseases under inflammatory conditions.
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PMID:Interaction of myeloperoxidase with vascular NAD(P)H oxidase-derived reactive oxygen species in vasculature: implications for vascular diseases. 1461 14

Acutely increased intra-abdominal pressure (IAP) may lead to abdominal compartment syndrome (ACS), which ischaemia/reperfusion (I/R) injury plays an important role. The main goal of the management of ACS is to lower the intra-abdominal pressure despite reperfusion injury. Octreotide (OCT), a synthetic somatostatin analogue, lowers the splanchnic perfusion. The aim of this study was to investigate whether OCT improves the reperfusion injury after decompression of acute abdominal hypertension.Under anesthesia, a catheter was inserted intraperitoneally and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1h. In the I/R group, pressure applied for an hour was decompressed and 1h reperfusion period was allowed. In another group of I/R, OCT was administered (50 microg/kg i.p.) immediately before the decompression of IAP. The results demonstrate that kidney and lung tissues of malondialdehyde (MDA; an end product of lipid peroxidation) levels and myeloperoxidase (MPO; index of tissue neutrophil infiltration) activity were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in I/R group (P<0.001). Moreover, OCT treatment applied in the I/R group reduced the elevations in blood urea nitrogen (BUN) and serum creatinine levels. Our results implicate that IAP causes oxidative organ damage and OCT, by reducing splanchnic perfusion and controlling the reperfusion of abdominal organs, could improve the reperfusion-induced oxidative damage. Therefore, its therapeutic role as a "reperfusion injury-limiting" agent must be further elucidated in IAP-induced abdominal organ injury.
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PMID:Octreotide: a new approach to the management of acute abdominal hypertension. 1470 53

Ischemia/reperfusion injury plays an important role in the pathogenesis of abdominal compartment syndrome, which is characterized by increased intra-abdominal pressure. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the reperfusion injury after decompression of acute abdominal hypertension. This study was carried out in Wistar albino rats. With the rats under anesthesia, an arterial catheter was inserted intraperioneally and with the use of an aneroid manometer connected to the catheter, intra-abdominal pressure was kept at 20 mm Hg (ischemia group) for 1 hour. In the ischemia/reperfusion group, pressure applied for 1 hour was decompressed and a 1-hour reperfusion period was allowed. In another ischemia/reperfusion group, octreotide was administered (50 microg/kg intraperitoneally) immediately before the decompression of intra-abdominal pressure. At the end of the experiment, liver and intestinal tissues were taken and malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity were estimated. The results demonstrated that tissue levels of malondialdehyde and myeloperoxidase activity were elevated, whereas glutathione levels were reduced in both the ischemia and ischemia/reperfusion groups. Octreotide treatment reversed these oxidant responses. In conclusion, increased intra-abdominal pressure causes oxidative organ damage and octreotide, by controlling the reperfusion of abdominal organs and inhibiting neutrophil infiltration, could improve the reperfusion-induced oxidative damage. Therefore its therapeutic role as a "reperfusion injury-limiting" agent must be further elucidated in intra-aortic pressure-induced abdominal organ injury.
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PMID:Octreotide improves reperfusion-induced oxidative injury in acute abdominal hypertension in rats. 1474 43

Cardiovascular disease is common in patients with chronic kidney disease (CKD). As renal function fails, many patients become progressively malnourished, as evidenced by reduced levels of albumin, prealbumin, and transferrin. Malnourished patients have increased levels of C reactive protein (CRP), interleukin-6 (IL-6), and concomitant cardiovascular disease when they reach end stage. Many diseases that cause CKD, diabetes, and hypertension are also associated with cardiovascular disease. Thus the direct effect of renal failure per se directly contributing to the inflammation-malnutrition-atherosclerosis paradigm is not completely established in early stages of CKD. Some aspects of progressive renal failure, however, cause changes in plasma composition and endothelial structure and function that favor vascular injury. As renal function fails, hepatic apo A-I synthesis decreases and HDL levels fall. HDL is an important antioxidant and defends the endothelium from the effects of cytokines. Inflammation causes further structural and functional abnormalities in HDL. Apolipoprotein C III (apo C III), a competitive inhibitor of lipoprotein lipase is increased in CKD. Serum triglyceride levels increase as a result of accumulation of intermediate-density lipoprotein (IDL) comprising VLDL and chylomicron remnants. These impede vascular relaxation and are associated with cardiovascular disease. Activation of the renin angiotensin axis is a component of many renal diseases and adaptation to loss of renal mass. Angiotensin II (AngII) activates NADPH oxidases, leading to production of the superoxide anion and decreased availability of nitric oxide (NO), further impairing vascular function. H(2)O(2), produced as a consequence of superoxide dismutation, stimulates vascular cell proliferation and hypertrophy. Leukocyte-derived myeloperoxidase functions as an "NO Oxidase" in the inflamed vasculature and contributes to decreased NO bioavailability and compromised vascular reactivity. The changes in lipoprotein composition and structure as well as AngII-mediated alterations in endothelial function amplify the effect of subsequent inflammatory events.
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PMID:The role of oxidative stress-altered lipoprotein structure and function and microinflammation on cardiovascular risk in patients with minor renal dysfunction. 1497 55

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