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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 65-year-old man livedo reticularis occurred in the lower half of the body two days after beginning lysis with streptokinase. This was followed by skin and toe necrosis as well as acute renal failure. Autopsy showed a severe ulcerative atherosclerosis of the aorta with cholesterol crystal embolisation in numerous organs, particularly in both kidneys. The coincidence in time leads one to assume that the streptokinase treatment encouraged acute diffuse embolisation by dissolving the protective thrombi over the ulcerative atheromatous plaques.
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PMID:[Acute renal failure due to diffuse cholesterol crystal embolisation during streptokinase treatment (author's transl)]. 48 51

The evaluation of the results of nearly 800 percutaneous renal biopsies, including biopsies in which insufficient renal tissue was obtained or histologic changes were non-specific, indicated that in 85% of the cases a positive diagnosis could be made. The liberal extension of the indication to percutaneous renal biopsy to include oligosymptomatic renal diseases, the nephrotic syndrome and acute renal failure often resulted in therapeutic and prognostic consequences. Renal biopsy does not facilitate the diagnosis of pyelonephritis. Uremia, severe atherosclerosis, small kidneys, advanced age and lack of cooperation are not contraindications to percutaneous renal biopsy nor do they increase its risk. Severe complications are extremely rare and are always secondary to retroperitoneal hemorrhage. Close observation and prompt treatment can always preclude a fatal outcome. Long-term complications are not to be expected. If the technique of percutaneous renal biopsy and its histologic evaluation are efficiently performed, further extension of the indications to biopsy could be medically sanctioned.
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PMID:[Percutaneous kidney biopsy. Evaluation of a diagnostic method]. 71 Oct 98

Endothelin is a newly discovered potent vasoconstrictive polypeptide released by endothelial cells in response to various stimuli, including vasoactive peptides such as angiotensin II, adrenaline and vasopressin, and thrombocyte products like transforming beta growth factor and thrombin. Endothelin is believed to exert its main effects locally, in a paracrine or autocrine way. In vascular tissue, endothelin induces longlasting contraction of smooth muscle cells, leading to decreased blood flow, especially in the coronary and renal circulation, together with an increase in systemic blood pressure. It acts also mitogenically in vascular smooth muscle cells. Endothelin stimulates release of aldosterone and catecholamines in non-vascular tissue, and inhibits release of renin. A physiological function of endothelin may be to modulate vascular tone, and increased levels of circulating endothelin are seen after the "cold pressor test". Moreover, plasma endothelin concentration is elevated during acute myocardial infarction, in acute renal failure, in patients with hypertension, and during cardiogenic chock. What role endothelin plays in the development of these conditions, and in other disorders such as vascular spasm and atherosclerosis is uncertain.
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PMID:[The endothelial cell as an endocrine organ--endothelin]. 155 33

Surgery of the suprarenal segment of abdominal aorta is characterized by specific problems of operative techniques and of circulatory support during operative procedure. Ischaemic time of kidneys and other viscera has to be limited and use of femoro-femoral bypass allows perfusion of distal aortic branches during performance of the proximal anastomose. Replacement of the suprarenal abdominal aortic segment was performed in 57 consecutive patients (45 with aneurysm and 12 with para- or suprarenal atherosclerosis). Emergent operation was performed in 10 patients (9 with aortic rupture and 1 with acute renal failure by occlusion of the pararenal aortic segment) with early mortality of 50%. Elective operation was much safer with early mortality of 4.3% (2/47 patients). Following procedures were performed to revascularize the kidney and the other visceral arteries: direct replantation with or without endarterectomy (80%), bypass with prosthetic material or saphenous vein (15%), other procedures (5%). Nephrectomy was done in 3 patients. Overall 6-year survival was 64% in patients with aneurysm and 48% in patients with aortic atherosclerosis. 6-year survival was significant (p less than 0.01) higher in patients with normal renal function postoperatively than patients with persisting creatinine value over 200 micromol/l 3 months after operation (68% vs 15%).
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PMID:[Surgery of the suprarenal subdiaphragmatic aorta: early and long-term results]. 164

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

Evidence is increasing that vascular tone is highly dependent on the health of the endothelium and on the delicate balancing act between endothelium-derived relaxing and endothelium-derived contracting factors. Moreover, there is also evidence supporting the notion that the same factors which affect vascular tone also regulate, either in an autocrine or paracrine fashion, changes in vascular architecture. Synthesis and release of both endothelium-derived relaxing and contracting factors are affected by a number of physiologic and therapeutic agents as well as by other factors, among them vascular injury in disease states such as atherosclerosis, hypertension, diabetes, and acute renal failure. A number of trials indicate that therapeutic intervention may be capable of modulating the synthesis and release of these substances and the balance between the two as well as influencing the processes which control vascular remodeling.
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PMID:Mechanisms of vascular injury: the emerging role of the endothelium. 193 39

Transitional metals, particularly iron, markedly potentiate oxidant damage to isolated cell organelles. However, determining the probable importance of iron in damage to intact cells is difficult because of our inability experimentally to increase the cell content of this transition metal. We now report that heme is a uniquely effective iron delivery vehicle, capable of loading large amounts of potentially reactive iron into intact cells. We find that endothelial cells in vitro rapidly incorporate free heme and this heme-loading sensitizes endothelium to oxidant-mediated cytotoxicity caused by hydrogen peroxide, the hypoxanthine/xanthine oxidase system, or phorbol-stimulated PMN. Although the precise mechanism of the heme-aggravated cytotoxicity is not yet known, it closely parallels amplified lipid peroxidation in endothelial cell membranes suggesting the importance of lipid injury. Hemopexin, by complexing heme, protects endothelial cells from activated PMN, but only if added simultaneously. The hydrophobic iron chelator and antioxidant, U74500A, abrogates heme-augmented hydrogen peroxide and PMN-mediated endothelial damage. Such compounds, therefore, may have therapeutic potential in one or more of the listed clinical syndromes. We speculate that exposure of endothelium to free heme may potentiate vascular damage in various clinical syndromes, including acute renal failure after massive intravascular hemolysis, crush injuries, reperfusion after myocardial infarction (perhaps secondary to cardiac myoglobin release), retrolental fibroplasia associated with neonatal hemopexin deficiency, and, perhaps, atherosclerosis involving sites of turbulence that may trigger minor red blood cell lysis.
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PMID:Heme uptake by endothelium synergizes polymorphonuclear granulocyte-mediated damage. 213 29

Between January 1981 and April 1988, histologically proven renal cholesterol embolism was diagnosed in 13 men over 60 years of age with a previous history of hypertension and atherosclerosis. Six patients developed acute renal failure, usually induced by a triggering factor such as angiographic procedure or anticoagulation, and associated with peripheral and visceral cholesterol embolism, eosinophilia and a high sedimentation rate. In this group of patients, whose protean clinical manifestations and laboratory data mimicked necrotizing angiitis despite the absence of antineutrophil cytoplasmic antibodies, skin lesion biopsy established the diagnosis and made renal biopsy unnecessary. Six patients had chronic renal failure and elevated sedimentation rate, and the last patient had isolated microhematuria. In these 7 patients, percutaneous renal biopsy was an adequate procedure for the diagnosis of cholesterol embolism. As medical management of cholesterol embolism is essentially preventive, these unusual presentations must be emphasized.
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PMID:[Renal cholesterol embolism. Apropos of 13 cases]. 214 Nov 58

Hyperlipidemia is usually present in patients with the nephrotic syndrome. The most common lipid abnormality is hypercholesterolemia, although as the disorder progresses, hypertriglyceridemia may develop. Elevated plasma lipids have two potential vascular consequences, namely, atherosclerosis and progression of renal failure. Neither of these complications has been proven with certainty, but there is growing evidence to indicate that both may be long-term consequences of the nephrotic syndrome. Therefore, effective therapy of hyperlipidemia, particularly elevated cholesterol levels, is needed as a protection against these complications. Since nephrotic hypercholesterolemia frequently is severe, dietary therapy, although a valuable adjunct, will not normalize cholesterol levels in most nephrotic patients. Thus, if effective serum cholesterol lowering is to be achieved, drug therapy will be required. Bile acid-binding resins have been shown to lower cholesterol levels in nephrotic patients, but the decline in cholesterol concentrations is usually insufficient to produce a marked reduction in coronary risk. Nicotinic acid theoretically should be useful for treatment of nephrotic hyperlipidemia, but it has not been adequately tested. The new drugs that inhibit cholesterol synthesis, e.g., lovastatin, appear to be highly promising for treating elevations of both serum cholesterol and triglycerides in the nephrotic syndrome. However, testing of these drugs in this condition has been limited, and the possibility of significant side effects in an appreciable portion of patients has not been ruled out. Of particular concern is the development of severe myopathy that can produce myoglobinuria and acute renal failure. This side effect is relatively rare in patients without the nephrotic syndrome, but its prevalence in the latter condition has not been determined. The fibric acids will lower triglyceride levels in nephrotic patients, but they are not effective in lowering cholesterol levels; consequently, they probably have little role in the treatment of nephrotic hypercholesterolemia. Finally, the drug probucol will lower cholesterol levels in nephrotic patients, although not to desirable levels; still, probucol could prove useful in combination with other cholesterol-lowering drugs.
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PMID:Rationale and management of hyperlipidemia of the nephrotic syndrome. 248 42

We evaluated 1525 consecutive patients who had undergone thoracic or thoracoabdominal aortic surgery to ascertain the factors associated with the development of acute renal failure. Complete data were available in 1233 patients who were treated recently, and these were analyzed. Acute renal failure, severe enough to require dialysis, developed in 5.5% of this group (68/1233): 2.3% and 7%, respectively, for descending (9/391) and thoracoabdominal repairs (59/842). Of interest, on multivariate analysis, both renal artery endarterectomy for occlusive disease (p = 0.0006) and chronic dissection (p = 0.03) were associated with significantly less acute renal failure. On multivariate analysis, the significant independent predictors (p less than 0.05) of acute renal failure were preexistent renal dysfunction, evidence of diffuse atherosclerosis, the use of the pump bypass, and markers of hemodynamic instability. Contrary to earlier reports based on a smaller number of patients, we found that neither the use of pump bypass (7% acute renal failure), atriorenal bypass (8% acute renal failure), nor cold Ringer's lactate (3% acute renal failure) appeared to significantly avert the complication of acute renal failure. Indeed, pump bypass appeared to be deleterious (p = 0.0146) and perfusion with cold Ringer's lactate was not without risk. Furthermore, in a prospective evaluation of angiotensin converting enzyme blockers, we were unable to show that they afforded renal protection after transient renal ischemia. This study has clarified the clinical problems associated with acute renal failure and lays the foundation for future research.
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PMID:Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. 277 85


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