Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein lipid analysis has been carried out in 39 women and 28 men with chronic renal failure on haemodialysis. The results have been analysed in relation to the etiology of the renal disease and compared with those obtained in age- and sex-matched controls and in triglyceride-matched controls. Serum cholesterol was normal or low in glomerulonephritis but was normal in analgesic nephropathy. Serum triglycerides and VLDL lipids were raised uniformly regardless of the etiology of the renal disease. LDL triglyceride and HDL triglyceride were also raised. LDL cholesterol and phospholipid were low in glomerulonephritis but were normal in analgesic nephropathy. HDL cholesterol was reduced in both male and female patients regardless of etiology, statistical significance was not reached for the women. The ratio of esterified to free cholesterol tended to be reduced in all the lipoproteins regardless of sex or etiology but the changes were not significant in all groups. Comparison of the lipid abnormalities with those found in other hyperlipidaemic states suggests that the lipid disorders found in chronic renal failure are probably insufficient to explain the rapid development of vascular disease which has been reported.
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PMID:Lipoprotein lipids in chronic renal failure and haemodialysis. The influence of etiology and implications for atherogenesis. 22 78

A patient with cutaneous necrotizing vasculitis had chronic urticaria associated with multiple system involvement including arthralgias, glomerulonephritis, myositis, pseudotumor cerebri, and adenopathy. Persistent hypocomplementemia is noted with classic pathway activation. The syndrome recognized in this patient and those few individuals reported previously seems to constitute a distinct category of collagen-vascular disease.
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PMID:Vasculitis with urticaria, hypocomplementemia, and multiple system involvement. 98 89

Spontaneous eosinophilic chemotactic activity (SECA) present in human sera can mediate the directed movement of normal human eosinophils. Our data utilize normal peripheral blood eosinophils obtained from subjects with 500 eosinophils/m3 or less. SECA is defined as that chemotactic activity for eosinophils present in serum that has been heat-inactivated immediately after collection. It was demonstrated in patients with severe chronic eczema with eosinophilia (20 to 30%); mixed collagen vascular disease with vasculitis; clinical serum sickness; acute glomerulonephritis, and chronic membranoproliferative glomerulonephritis. Control sera were obtained from normal, healthy individuals. The data indicated: (1) that SECA in patient sera was significantly higher than in control sera; (2) when activated by endotoxin, no additional chemotactic activity was generated from patient sera over that spontaneously present--by contrast, addition of endotoxin to control sera did result in increased chemotactic activity; (3) sera from patients with extrinsic bronchial asthma had no SECA.
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PMID:SECA, a new mediator of the human eosinophil response. 117 23

The several kinds of mice that spontaneously develop acute systemic lupus erythematosus (SLE)--BXSB males, MRL/l males and females, and (NZB X W)F1 females--have a 15-20% incidence of degenerative vascular disease (DVD) and myocardial infarcts (MI) in which the affected coronaries contain deposits of immunoreactants, presumably in the form of immune complexes. Among the F1 hybrid crosses of SLE mice, only the (NZW X BXSB)F1, (W X B)F1 male has a significantly higher incidence of DVD/MI (80%). Search for possible causes of this high incidence of myocardial infarcts revealed several unique features of this mouse: hypertension, thrombocytosis, and early onset of circulating immune complexes and glomerulonephritis. Our attempts to prevent this DVD/MI focused on: reduction of hypertension, prevention of thrombosis, and immunosuppression. Immunosuppression by Cytoxan resulted in almost complete prevention of both the SLE disease and DVD/MI. Administration of bretylium, an antihypertensive and anti-arrhythmic agent, resulted in reduction of blood pressure and the severities of glomerulonephritis, DVD, and MI; it also slightly reduced the levels of circulating immune complexes and leukocytosis. Of the 4 antithrombotic agents used, only aspirin showed some reduction in the incidence of DVD/MI and delay of glomerulonephritis-associated mortality.
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PMID:The role of hypertension in the vascular disease and myocardial infarcts associated with murine systemic lupus erythematosus. 663 92

Although most forms of glomerulonephritis in man are thought to have an immunopathogenesis, certain clinical and experimental observations support the role of other non-immunologic mechanisms in the progression of these diseases. 1. Intra-renal vascular disease thought to be secondary to hypertension, may be responsible for ischemic glomerular sclerosis. 2. Hypertension may damage the diseased glomerulus directly, as has been demonstrated in experimental glomerulonephritis, in the remnant kidney, and in experimental diabetes mellitus. 3. Alterations in glomerular structure and function in the remnant kidney suggest that adaptations to nephron loss may contribute to further renal damage. 4. Glomerular sclerosis occurs under circumstances where immunologic mechanisms are highly unlikely, such as aging, reflex nephropathy, chronic aminonucleoside administration, and protein loading. 5. Preservation of renal function can be achieved by phosphorus restriction in the remnant kidney and in nephrotoxic serum nephritis.
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PMID:Mechanisms of progression in glomerulonephritis. 703 41

Fibronectin (Fn) plays an important role in tissue remodeling during embryogenesis, wound repair, and vascular disease, and is thought to regulate cellular processes such as cell adhesion, migration, proliferation, and differentiation through specialized domains within the molecule. In addition, Fn can be alternatively spliced at three regions: extradomains EIIIA, EIIIB, and a variable segment V, potentially giving rise to functionally distinct variants of the molecule. We have previously shown a sequential expression of cellular Fn first by platelets, followed by macrophages, then mesangial cells in habu snake venom-induced proliferative glomerulonephritis (Am J Pathol 145: 585-597, 1994). These studies examined the cellular sources and glomerular localization of Fn in general but did not distinguish between the various alternatively spliced isoforms. In this study, we examine by in situ hybridization and immunohistochemistry the temporal expression and cellular sources of EIIIA, EIIIB, and V in a model of proliferation glomerulonephritis that has cell migration, proliferation, and extracellular matrix synthesis as features of tissue remodeling. Macrophages were the first cells to express Fn mRNA showing an EIIIA+, EIIIB-, and V95+ pattern beginning at 8 hours after habu snake venom injection. Migrating mesangial cells at the margins of early lesions (8 and 24 hours) did not overexpress mRNA encoding these Fn variants, but immunofluorescence microscopy revealed V95 and EIIIA protein at the margins of lesions. EIIIB was absent in lesions at this time. At 48 hours and peaking at 72 hours after habu snake venom injection, mesangial cells in central aspects of glomerular lesions expressed abundant mRNA and protein for V95 and EIIIA. EIIIB mRNA and protein was slight in the mesangium at these times. Parietal epithelial cells, particularly adjacent to glomerular lesions, also expressed abundant mRNA and protein for all three variants throughout the course of the disease, beginning at 24 hours after habu snake venom injection. Expression of mRNA and protein for all three isoforms declined by 2 weeks after habu snake venom injection. These studies show that migrating mesangial cells do not require their own synthesis of Fn and suggest that they might rely on exogenous sources of Fn, particularly V95+ and EIIIA+ forms. Commencement of enhanced expression of EIIIA and EIIIB mRNA and protein by resident glomerular cells coincided with the temporal course of cell proliferation, acquisition of alpha-smooth muscle cell actin phenotype, and matrix synthesis, suggesting that Fn isoforms have specific functions during the course of glomerular remodeling.
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PMID:Expression of alternatively spliced fibronectin variants during remodeling in proliferative glomerulonephritis. 748 99

The incidence of renal failure due to vascular diseases is increasing. Two reasons for this are the epidemic of atherosclerotic vascular disease in the aging population and the widespread use of vasoactive drugs that can adversely affect renal function. These vascular causes of renal failure include vasomotor disorders such as that associated with nonsteroidal antiinflammatory drugs, small-vessel diseases such as cholesterol crystal embolization, and large-vessel diseases such as renal artery stenosis. These causes of azotemia are less familiar to physicians than more classic causes, such as acute tubular necrosis, and are less likely to be recognized in their early stages. This article describes the various vascular diseases that impair renal function and outlines the steps necessary to identify them. Although some of these conditions, such as renal artery stenosis, can gradually impair function, the vascular causes of acute renal failure are emphasized in this article. Because the vasculitides primarily cause renal failure through secondary glomerulonephritis, they are mentioned only briefly. Extensive testing is rarely necessary because the cause is usually suspected through syndrome recognition. The diagnosis can then be confirmed by the results of one or two additional tests or by improved renal function after treatment.
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PMID:Diagnosing vascular causes of renal failure. 867 77

In order to examine the clinical features of pulmonary involvement in patients with myeloperoxidase specific-antineutrophil cytoplasmic antibody (MPO-ANCA), 46 MPO-ANCA positive patients with collagen-vascular disease and glomerulonephritis were investigated. Twenty eight patients (60.8%) had pulmonary involvement without tumor and infection, 20 (43.5%) of MPO-ANCA positive patients had interstitial pneumonitis, 11 (23.9%) had pulmonary hemorrhage, 3 had asthma (6.5%) and 7 had both interstitial pneumonitis and pulmonary hemorrhage. Patients with pulmonary involvement were older (mean age 61.1) and they had higher inflammatory acute phase reactants and higher mortality (42.9%) than patients without pulmonary involvement. Pulmonary hemorrhage revealed on both lung fields in 10 patients, 7 patients required artificial respirator and 6 died. Titer of MPO-ANCA increased paralleled with progression of pulmonary hemorrhage. Interstitial fibrosis revealed predominantly lower and lateral side of the lung. It is suggested that MPO-ANCA may be closely related to the pathogenesis of pulmonary hemorrhage and interstitial pneumonia. Careful management is needed in patients with pulmonary involvement, especially pulmonary hemorrhage in patients with MPO-ANCA.
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PMID:[Pulmonary involvement in patients with myeloperoxidase specific-antineutrophil cytoplasmic antibody]. 773 90

Age-specific and cumulative incidence rates were calculated for entry into Australian end-stage renal failure programmes from 1972 to 1991, as a result of all causes, or from analgesic nephropathy, glomerulonephritis, hypertension and vascular disease, or diabetes. Three different trends were demonstrated. A rising recorded incidence of renal failure occurred throughout the period of observation in those aged 0-4 years (all causes) and in those aged 55 years and over (all categories, least in analgesic nephropathy) principally attributable to a falling fraction of patients not accepted for treatment. Falling incidence rates indicating a real reduction in the burden of disease were seen for analgesic nephropathy (at least up to the age of 64 years) and hypertension and vascular disease (only up to the age of 54 years). In young adults the unchanging incidence of renal failure due to all causes, glomerulonephritis and diabetes probably reflect nearly complete acceptance rates into end-stage renal failure programmes, and therefore approximate the true burden of disease. In end-stage renal failure, age-specific or age-standardized cumulative rates are required to distinguish rising or falling incidence of disease from trends due to changing medical practice.
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PMID:Trends in incidence of end-stage renal failure in Australia, 1972-1991. 781 48

Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease with myocardial infarction (CVD). To determine whether this murine lupus-associated CVD could be transferred to otherwise autoimmune-resistant (C57BL/6 x C3H/He)F1 (B6C3F1) mice via W/BF1 T-cell-depleted marrow (TCDM) transplants, or conversely whether the CVD of W/BF1 mice could be prevented by the reciprocal transplant, reciprocal haploidentical transplants of TCDM were performed. CVD developed only in mice with systemic autoimmunity. Mice that developed lupus had glomerulonephritis and thrombocytopenia and also had elevated titres of autoantibodies to double-strand DNA, cardiolipin, and platelets and elevated levels of circulating immune complexes. Of control W/BF1 mice, 80% developed lupus, and of these, 81% developed CVD with a mean grade of 2.5 +/- 0.8. Engraftment of W/BF1 mice with B6C3F1 marrow protected 90% of the recipients from the development of lupus, and none developed CVD. Engraftment of B6C3F1 mice with W/BF1 marrow induced lupus in 60% of the recipients, and of those, 33% developed CVD with a mean grade of 1.3 +/- 0.3. The B6C3F1 recipients of W/BF1 marrow which developed CVD had significantly higher titres of autoantibodies to cardiolipin (aCL; P < .01). These findings show that genetic abnormalities present in the W/BF1 hematopoietic stem cells contribute to autoantibody development, including aCL, and suggest that thrombogenic mechanisms induced by aCL may contribute to the development of CVD in this form of murine lupus erythematosus.
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PMID:Prevention and induction of occlusive coronary vascular disease in autoimmune (W/B)F1 mice by haploidentical bone marrow transplantation: possible role for anticardiolipin autoantibodies. 821


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