Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Report of necropsy findings of a 17 years old girl with a progeria syndrome. There was a high degree of generalized atherosclerosis, involving the visceral arteries, chiefly those to the kidneys. The patient died of nephrosclerosis with uraemia. The aetiology of progeria syndrome remains obscure, single findings (lipoprotein- and amino-acid metabolism) may be understood as an inborn error of metabolism.
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PMID:[Morphologic contribution to a progeria syndrome (Hutchinson-Gilford) (author's transl)]. 744 1

Cardiovascular complications are the main cause of mortality in patients with chronic renal failure. Hypertension and lipid abnormalities which often lead to left ventricular hypertrophy and accelerated atherosclerosis as well as coronary artery disease are a common cause of death. On the other hand uremia often causes pericarditis and thereby may lead to cardiac tamponade and constrictive pericarditis. Renal failure can also cause secondary hyperparathyroidism, amyloidosis, hemosiderosis and oxalosis which can produce visceral infiltrations and lead to a variety of disturbances of cardiovascular functions. Life-threatening arrhythmias are one of the major cardiovascular complications during maintenance dialysis as their occurrence might result in sudden death. The aim of cardiologic management which includes the complex of preventive and therapeutic measures is to reduce the morbidity and mortality and to improve the quality of life.
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PMID:[Cardiologic management in patients on a long-term dialysis program]. 763 9

Dyslipidemia is commonly observed in nephrotic syndrome, in chronic renal failure, and after renal transplantation. The patterns of dyslipidemia, however, differ among these three conditions, and the origins and mechanisms responsible for abnormalities in lipoprotein metabolism in each are not well understood. Whether these dyslipidemias contribute to the development of atherosclerosis and coronary heart disease is uncertain, but it is probable that they do. Important questions are whether an attempt should be made to treat the various renal dyslipidemias, and if so, by what means. Also of current interest are dyslipidemias in the nephrotic syndrome, chronic renal failure (uremia), and the post-renal transplantation state.
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PMID:Mechanisms and treatment of dyslipidemia of renal diseases. 792 19

Atherosclerotic cardiovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. It is unclear, however, if atherosclerosis in fact occurs at a higher incidence compared with the nonuremic population matched for age, hypertension, and diabetes mellitus or if it occurs at an accelerated rate following the onset of end-stage renal disease. The extent of true atherosclerotic lesions, versus clinically diagnosed "atherosclerosis," in patients with chronic renal failure is equally unclear. Potentially, the uremic state per se, the dialysis treatment, and factors unrelated to renal failure may participate in atherogenesis. The relative contribution of each of these factors is unknown. In this review, we discuss the pathology of "atherosclerotic" lesions in patients with chronic renal failure and the putative factors involved in atherogenesis in this population and describe the results of available studies examining the issue of accelerated atherosclerosis in uremia.
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PMID:Atherosclerosis in chronic renal failure. 792 27

28 patients treated by programmed hemodialysis (PH) were followed up from 1985 to 1991. All the patients were over 60 years old. 16 patients died within month 1-60 since PH initiation. Overall PH duration for the whole group reached 24.6 +/- 3.58 months. Pretreatment urea and creatinine in plasma of senile patients were significantly lower than in young patients not resulting, though, in uremia reduction. The findings show that it is not valid to consider creatinine a determinant for starting hemodialysis in senile patients. Despite multimorbidity, more rapid progression of atherosclerosis and complicated establishment of the vascular approach, senile patients successfully adapt to PH regimen, need less numerous weekly PH hours. By anemia manifestations, incidence of hyperparathyroidism and polyneuropathy, senile patients did not differ much from their younger counterparts.
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PMID:[Programmed hemodialysis in middle and old age]. 794 Mar 70

Due to the incidence of symptomatic atherosclerosis in uremic patients, hemostasis-derived cardiovascular risk factors, basal plasma concentrations of some endothelial-derived glycoproteins and desmopressin-induced variations of endothelial-derived proteins were studied in 22 uremic patients on prolonged maintenance hemodialysis with no cardiovascular antecedent. Compared to control subjects, patients had increased predialysis hemostasis-related cardiovascular risk factors: high fibrinogen, proconvertin, and type 1 plasminogen activator inhibitor plasma concentrations; low albumin values; generally low antithrombin III values but sometimes high. They had high predialysis plasma concentrations of endothelium-derived glycoproteins: von Willebrand factor, tissue-type plasminogen activator and urokinase-type plasminogen activator, which are secreted by endothelial cells, but also soluble thrombomodulin, a marker of endothelial cell injury. The desmopressin-induced release of tissue-type plasminogen activator and of von Willebrand factor were lower than in controls. High fibrinogen, type 1 plasminogen activator inhibitor and low albumin plasma concentrations may be linked to repeated acute phase reactions associated with hemodialysis. Data concerning endothelium-related proteins are concordant with the co-existence of a chronic in vivo endothelial activation and endothelial injury in uremia. This could be linked to the initiation and progression of atherosclerosis.
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PMID:Increased cardiovascular risk factors and features of endothelial activation and dysfunction in dialyzed uremic patients. 799 2

The clearance of low-density lipoprotein (LDL) isolated from uremic patients (autologous-LDL) and from a control subject (control-LDL) was studied in 12 uremic patients on conservative management and compared to the LDL clearance in control subjects. The clearances of autologous-LDL and control-LDL were almost the same in the patients. However, the fractional catabolic rate (FCR) of the autologous-LDL (0.307 +/- 0.094 pools/day, mean +/- SD) and the control-LDL (0.289 +/- 0.081 pools/day) were significantly lower (P < 0.05 and P < 0.01, respectively) than the FCR for LDL in the control subjects (0.376 +/- 0.045 pools/day). Moreover, one-half of the patients had an abnormally low LDL clearance rate ranging from 0.146 to 0.282 pools/day. The FCR for the autologous-LDL varied from 0.146 to 0.416 pools/day between the patients and was negatively related (r = -0.68, P = 0.02) to the serum urea concentration (from 11.8 to 39.2 mmol/liter) and tended to correlate positively with the glomerular filtration values (from 9.2 to 48.3 ml/min/1.73 m2; r = 0.57, P = 0.096, non-linear relationship). In conclusion, the clearance of LDL in patients with advanced uremia on conservative management is frequently decreased. This alteration in the metabolism of the most atherogenic particle in plasma may contribute to the accelerated atherosclerosis in uremic patients.
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PMID:Decreased clearance of low-density lipoprotein in patients with chronic renal failure. 816 46

Non-enzymatic protein glycosylation is the first stage of the reaction described by L.C. Maillard. When the reaction progresses beyond that stage the long half-life molecules are damaged by formation of intermolecular crosslinking. The recent discovery of pentosidine, a crosslink between lysine and arginine residues, has demonstrated that advanced Maillard reaction is accelerated in diabetic patients with severe complications. Moreover, high tissue and plasma levels of pentosidine have been found in uraemia. The formation of advanced Maillard end-products (AGE) in plasma proteins constitutes a source of cell stimulation which induces macrophages to secrete cytokines, interleukin-1 and tumoral necrosis factor. Similarly, endothelial cells are induced to increase the permeability and production of the procoagulant factor. These mechanisms are thought to play an important role in the pathogenesis of atherosclerosis, nephropathy and thromboembolic disorders of diabetes. The discovery of beneficial effects of amino-guanidine, an inhibitor of advanced Maillard reaction, in the prevention of experimental diabetic complications opens a new line of investigation and new hopes for diabetics.
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PMID:[Non-enzymatic glycosylation of proteins. Complications of diabetes mellitus, aging and kidney failure]. 824 84

Serum Apolipoproteins (Apo) and lipids were determined in 20 patients with uremia. The results were compared with those obtained in sex and age matched controls. The patients had significantly reduced level of Apo AI and ratio of Apo AI/Apo B100, and increased levels of Apo CII, Apo CIII. It was also found that the patients had normal levels of TC, TG and significant decrease of HDL-C, HDL2-C. These findings suggested that Chinese uremic patients had wide extensive Apo abnormalities which could induce disturbances of lipid metabolism and development of atherosclerosis although serum lipid levels were normal, and that Apo might be better predicators of cardiovascular complications than lipids in Chinese patients with uremia.
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PMID:[Serum apolipoproteins in uremic patients]. 827 22

A retrospective multi-institutional study was performed to document and characterize the arterial vascular disease in the hypogastric-cavernous arterial bed and/or veno-occlusive dysfunction of the corpora cavernosa in patients with end stage renal disease. We evaluated 20 impotent patients (mean age 40 +/- 9 years) with chronic renal failure using pharmaco-cavernosometry and pharmacocavernosography (4 also underwent pharmaco-arteriography). Patients were divided into groups based on the treatment (14 with renal transplantation and 6 with hemodialysis or peritoneal dialysis), as well as by history of vascular risk factors (16 with and 4 without risk factors). Of the patients 19 revealed abnormal intracavernous pressure responses to repeated intracavenous injections of vasoactive agents implying vascular disease of the penis. Cavernous artery occlusive disease was found in 78% of the patients. All patients who underwent arteriography had diffuse atherosclerotic disease of the distal penile arteries. Corporeal veno-occlusive dysfunction was found in 90% of the patients, of whom 60% had diffuse pan-cavernous leakage involving the dorsal, cavernous and crural veins, glans penis and corpus spongiosum. This renal failure-associated vascular disease of the penis was found to occur independently of the presence of known systemic atherosclerotic vascular risk factors. Patients who underwent early treatment of the uremia by renal transplantation had vasculogenic impotence only in the case of rejection of the renal transplant, suggesting that early renal transplantation may delay or prevent the development of the penile vasculopathy. The most likely pathophysiology of the vascular impairment includes renal failure-associated atherosclerosis, and renal failure-associated hypoxia changes of the contractile (smooth muscle) and structural (collagen/elastin) components of the erectile tissue. Strategies for future research and clinical therapies are suggested.
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PMID:Impotence and chronic renal failure: a study of the hemodynamic pathophysiology. 830 70


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