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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite efficient revascularisation procedures for vascular disease, the limb can occasionally be lost following reperfusion. One contributing factor might be the formation of oxygen free radicals. This study attempts to describe the conditions necessary for oxy-radical formation from adenine nucleotide breakdown products and the role of plasma creatine content as a marker of cellular injury. Twelve patients undergoing aortic reconstructive surgery were studied. Only partial ischaemia of the lower limbs was induced by the aortic clamping, since varying degrees of collateral circulation existed. Radial arterial and external iliac venous blood was obtained simultaneously before, during and after cross-clamping of the aorta, and plasma levels of ATP, ADP, hypoxanthine, phosphocreatine, creatine, creatinine and lactate measured using luminescence and spectrophotometry. Venous creatine content increased during ischaemia and was doubled 30 min after recirculation. This increase was possibly due to leakage following cellular injury agreeing with a previously observed decrease in muscle tissue creatine content. The iliac arterio-venous difference of hypoxanthine and lactate markedly increased immediately post-ischaemia, while the phosphocreatine difference decreased. Plasma hypoxanthine was abundant in the leg on reoxygenation. The existence of a xanthine oxidase system in skeletal muscle could produce favourable conditions for oxy-radical formation through hypoxanthine degradation, which may contribute to the known muscle tissue injury.
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PMID:Plasma metabolic disturbances and reperfusion injury following partial limb ischaemia in man. 271 61

Beta-thromboglobulin (beta TG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary beta TG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of beta TG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of beta TG, beta 2-microglobulin and total protein in urine collected for 24 h and creatinine and beta 2 microglobulin in plasma. Survival of indium-111-labeled platelets was measured in nine patients. Urinary beta TG was significantly (p less than 0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 microgram/24 h). There was a strong correlation between urinary beta TG excretion and plasma creatinine concentration (r = 0.8, p less than 0.0001) and plasma beta 2-microglobulin concentration (r = 0.9, p less than 0.0001). Urinary beta TG concentration did not correlate with platelet survival. The results indicate that although urinary beta TG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.
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PMID:Urinary beta-thromboglobulin correlates with impairment of renal function in patients with diabetic nephropathy. 294 92

Plasma oxalate has been measured in 125 patients maintained on continuous ambulatory peritoneal dialysis using an enzyme/bioluminescent assay. Values ranged between 6 and 134 mumol/l, with a positively skewed distribution. Multiple linear regression analysis with plasma oxalate as the dependent variable showed highly significant associations with the dose of ascorbic acid, dose of alfacalcidol, and plasma creatinine, and weaker associations with serum phosphate, serum calcium, and body weight. When the presence of other potential risk factors was taken into account, no significant relationship could be found between the presence of clinically evident cardiac or vascular disease and plasma oxalate.
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PMID:Plasma oxalate in patients receiving continuous ambulatory peritoneal dialysis. 314 Jan 4

Fifty patients, 65 years of age or older, with renovascular disease were evaluated and treated between 1979 and 1981. Twenty-one patients were treated medically, 21 surgically and 8 with percutaneous transluminal angioplasty of the renal arteries. The age, sex, target organ involvement, initial blood pressure and serum creatinine were similar among the three groups. Sixty-six percent of the medical group demonstrated lower blood pressure. Ninety percent of the surgical group demonstrated a cure or improved blood pressure, and 43% of the patients with percutaneous transluminal angioplasty had improved blood pressure. Renal function deteriorated in 50% of the medical group, 19% of the surgical group and 25% of patients in the percutaneous transluminal angioplasty group. There was one operative death in the surgical group and one death related to percutaneous transluminal angioplasty. The data demonstrate that old age itself is not a contraindication to surgery. If hypertension is resistant to medical therapy, if the patient experiences undesirable side effects from the medications or if renal function is jeopardized, surgical therapy should be considered. More experience with percutaneous transluminal angioplasty is necessary to determine its precise role in managing atherosclerotic renal vascular disease in the elderly.
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PMID:Renovascular disease in the elderly: an analysis of 50 patients. 315 38

To explore interrelations between folic acid and methionine metabolism in chronic renal insufficiency, we measured plasma amino acids in 21 patients with mean serum creatinine +/- SD of 560 +/- 240 mumol/L, after a ten-hour overnight fast, before and after administration of 5 mg of oral folic acid daily for 15 +/- 6 days. Mean plasma homocysteine was 12.9 +/- 6.8 mumol/L in the patients and 4.2 +/- 0.8 mumol/L in 24 normal controls (P less than .001), and after folic acid administration it declined in the patients to 6.8 +/- 2.8 mumol/L (P less than .0001) in linear proportion (r = .92) to the prefolate homocysteine level. Methionine concentrations were normal in the patients and did not change after folate administration, nor did elevated cysteine and creatinine. Plasma serine was lower (88.3 +/- 17.2 v 121 +/- 25 mumol/L, P less than .41) and declined further to 67.8 +/- 16.4 (P less than .0001) after folate, while prefolate glycine levels increased from 273.3 +/- 61.2 to 313.2 +/- 97.5 mumol/L (P less than .01). Serum and red-cell folate levels were normal in the patients before treatment. The results show that homocysteine levels are increased in chronic renal insufficiency, but may be lowered by folate enhancement of remethylation of homocysteine to methionine. Since elevated plasma homocysteine is associated with premature vascular disease, folic acid may reduce cardiovascular risk in chronic renal insufficiency.
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PMID:Folic acid lowers elevated plasma homocysteine in chronic renal insufficiency: possible implications for prevention of vascular disease. 338 35

In recent years, the prognosis for a successful pregnancy has greatly improved for women with insulin-dependent diabetes mellitus (IDDM) who are under good glycemic control and free of complications such as vascular disease and nephropathy. We report the rapid development of severe nephrotic syndrome, malignant hypertension, and microangiopathic hemolytic anemia during the first trimester of pregnancy in a 29-yr-old woman with IDDM of 18 yr duration. Our patient had no pregestational history of retinopathy or hypertension and only minimal proteinuria. Significant improvement in blood glucose levels had been achieved over the 6 mo before conception. Kidney biopsy performed before the termination of pregnancy at 10 wk gestation revealed diabetic nephropathy. No other etiology for her renal disease could be found. An arteriole was noted to have entrapped red blood cell fragments and platelet thrombi, revealing the probable source of her hemolytic process. By 8 wk postpartum, her nephrotic syndrome and hemolysis had completely resolved. At 3 mo postgestation, the patient's hypertension was still present but less severe. Her serum creatinine has continued to decrease toward normal. This is the first report of a woman with IDDM in White's classification C who developed a toxemia-like syndrome during the first trimester of pregnancy, attributable to the underlying diabetic state.
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PMID:Rapid development of nephrotic syndrome, hypertension, and hemolytic anemia early in pregnancy in patients with IDDM. 339 Oct 92

A correlation between increased platelet adhesiveness and aggregation and the development of angiopathy in diabetes mellitus can be made. Thromboxane produced by platelets represents a potent platelet aggregation factor. We studied the platelet TXB2 production during blood coagulation in carefully selected patients with type II diabetes mellitus in good metabolic control and the results were correlated with the presence or absence of microangiopathy, fasting blood glucose levels, type of therapy, age, duration of diabetes and the most important hematochemical parameters. No statistically significant differences were found between serum TXB2 concentrations in diabetic patients and control subjects, in diabetics with or without microangiopathy and in diabetics on insulin therapy or on oral hypoglycemic agents. We did not observe any correlation between TXB2 production and age, duration of diabetes, sex, basal blood glucose levels, total and HDL-cholesterol, triglycerides, blood creatinine and blood electrolytes. The thromboxane production may be a not important factor for determining the increased platelet aggregation which is at the origin of the angiopathy in diabetes mellitus.
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PMID:Thromboxane production in diabetes mellitus. 357 51

This report summarizes the major design features, methods, and baseline characteristics of patients enrolled in a Veterans Administration Cooperative Study. In eleven V.A. centers, 231 male diabetic patients who had either a recent amputation for gangrene (N = 207) or active gangrene (N = 24) were randomly assigned to a group which received aspirin (325 mg t.i.d.) plus dipyridamole (75 mg t.i.d.) (N = 110) or two placeboes t.i.d. (N = 121). Major end point were vascular death and amputation of the opposite extremity for gangrene. Forty-one percent of the 563 patients screened were enrolled during a 39 month period. Enrollment errors were found in 8.7%. Historically, the two groups were well matched regarding the following variables: age, duration of diabetes, insulin therapy, previous oral agent therapy, hypertension, myocardial infarction, congestive heart failure, renal disease, sensory neuropathy, and smoking. The drug therapy group had an increased frequency of a history of cerebrovascular disease (19% vs 7%, p = 0.01). The groups were well matched regarding amputation site, obesity, extent of lower extremity vascular disease, retinopathy, and neuropathy upon examination. Their baseline fasting values of glucose, cholesterol, triglycerides, and creatinine were also comparable. We conclude that this study should provide definitive data on the efficacy of these antiplatelet agents in preventing further vascular disease in this patient group. It should also provide new prospective data on the natural history of vascular disease, and the association of vascular risk factors with subsequent vascular events in this patient population.
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PMID:V.A. Cooperative Study on antiplatelet agents in diabetic patients after amputation for gangrene: III. Definitions and review of design and baseline characteristics. 390 83

To investigate whether the elevation of factor VIII coagulant activity observed in children with poor control of diabetes is due to increased levels of the factor VIII coagulant moiety of the factor VIII complex or reflects activation of the factor VIII coagulant moiety, factor VIII coagulant activity (VIII C), factor VIII coagulant antigen (VIII C:Ag), and factor VIII-related antigen (VIII R:Ag) were determined in 75 insulin-dependent children. All children were without signs of vascular disease based on negative funduscopy, negative fluorescein angiography, normal serum creatinine levels, and absence of proteinuria. Children with poor actual control of diabetes had significantly higher VIII C values than did children with good actual control of diabetes based on HbA1 values, but VIII C:Ag values did not differ in children with good or poor actual control of diabetes. A significant elevation of VIII C over VIII C:Ag values was observed in children with poor actual control of diabetes, but no elevation of VIII C over VIII C:Ag was found in children with good actual control. VIII R:Ag values were higher in children with poor actual control. VIII C, VIII C:Ag, and VIII R:Ag did not differ significantly in children with short or long duration of clinical diabetes. Our observation of significantly higher VIII C values than VIII C:Ag levels strongly suggests intravascular activation of the factor VIII coagulant moiety during poor diabetes control. The process leading to activation of the coagulant moiety seems to be different from the process leading to the elevation of the other moiety of the factor VIII complex, the factor VIII-related antigen, in diabetic subjects.
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PMID:Elevation of Factor VIII coagulant activity over Factor VIII coagulant antigen in diabetic children without vascular disease. A sign of activation of the Factor VIII coagulant moiety during poor diabetes control. 391 55

The development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3-day MHY and 3-day BHY animals. Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non-renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12-day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.
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PMID:Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension. 636 44


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