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

An atheromatous aorta may be the source of micro-emboli composed of cholesterol crystals. These cholesterol emboli presumably result from dislodgment of atheromatous material occurring either spontaneously, or consecutively to a coronary angiography, an aortic surgery or even an anticoagulant or thrombolytic treatment. Even if the best known clinical feature is the "blue toe" syndrome together with renal insufficiency, the spectrum of disease caused by cholesterol emboli ranges from asymptomatic to rapidly progressive multiple system failure. Therefore cholesterol embolism is a serious complication of aortic atherosclerosis and often holds a poor prognosis. Diagnosis is confirmed by skin or muscle biopsy and fundoscopic examination. The optimal treatment remains to be established.
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PMID:[Cholesterol embolism in the lower limbs]. 772 10

A better understanding of the pathophysiology of progressive renal scarring has emerged from the research undertaken over the last decade. It highlights the respective roles of glomerulosclerosis and tubulo-interstitial fibrosis in the progression of renal insufficiency and scarring. Similarities have been identified between the process of glomerulosclerosis and that of atherosclerosis. In both instances an important role has been attributed to growth promoting factors in particular PDGF and TGF-beta. Similarly, tubulo-interstitial scarring also involves interactions between tubular cells, inflammatory cells and fibroblasts/myofibroblasts mediated by growth factors. The understanding of the contribution of growth factors to experimental renal scarring has led to therapeutic interventions based on their manipulations. It remains to be determined whether such therapeutic approaches will prove beneficial to patients.
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PMID:[Chronic renal insufficiency: from laboratory to clinic]. 789 99

A retrospective study is presented concerning 115 patients submitted to renal artery surgery from 1978 to 1990, and observed during 2 to 15 years. Included are 69 men and 46 women, aged 14 to 84 years (mean: 58.8 years). The underlying occlusive arterial disease was atherosclerosis in 87 patients, fibromuscular dysplasia in 21, and miscellaneous causes in 7 cases. One hundred and one patients (88%) were hypertensive. Some degree of impaired renal excretory function (serum creatinine level above 16 mg/l) was present in 30% (n = 42) of the patients, whereas 11 patients had severe renal insufficiency (creatinemia above 30 mg/l). Primary nephrectomy was performed in 11 patients as sole procedure and was associated with contralateral revascularization in another 9 patients. A variety of types of arterial reconstruction was performed, although more than half of the procedures were aortorenal bypass grafts. Bilateral procedures were performed in 19 cases. Simultaneous extrarenal operations included aortic reconstruction (n = 43), mesenteric arterial repair (n = 8), and carotid endarterectomy (n = 5). Operative mortality (9/115, 7.8%) varied considerably between the subgroups: 4% for group I (hypertension alone, n = 73), 15% for group II (renal impairment with or without hypertension, n = 34), and 12.5% for group III (acute renal failure, n = 8). There were 3 late non procedure-related in-hospital deaths. Preoperative renal insufficiency was the only independent predictive risk factor for operative death. The procedure was curative or led to improved blood pressure control in 79% (80/101) of hypertensive patients. The response rate was better for recent onset hypertension, compared to long-standing hypertension. Of the 42 azotemic patients, 78% had a benefit (improvement in 50%, stabilization in 28%) of renal revascularization. Associated longstanding hypertension had a negative prognostic value. Sequential clinical and functional follow-up evaluations are available on 99 of the 103 surviving patients. Cumulative 5-year survival is 87%. Cardiovascular causes account for most (11/15) of the late deaths.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Surgery for occlusive renal artery disease: immediate and long-term results. 790 Apr 83

Atherosclerosis develops rapidly in patients with diabetes or renal insufficiency. Plasma lipoprotein profiles are frequently abnormal in these conditions and reflect an elevation in the level of the apoprotein B (ApoB)-containing components very low density lipoprotein (VLDL) and low density lipoprotein (LDL). High levels of circulating advanced glycation end products (AGEs) also occur in diabetes and end-stage renal disease (ESRD). These products arise from glucose-derived Amadori products and include AGE-modified peptides (AGE-peptides) which result from the catabolism of AGE-modified tissue proteins. AGE-peptides have been shown to crosslink protein amino groups and to accumulate in plasma as a consequence of renal insufficiency. To address potential mechanisms for the dyslipidemia of diabetes and ESRD, we investigated the possibility that circulating AGEs react directly with plasma lipoproteins to prevent their recognition by tissue LDL receptors. AGE-specific ELISA showed a significantly increased level of AGE-modified LDL in the plasma of diabetic or ESRD patients compared with normal controls. AGE-LDL formed readily in vitro when native LDL was incubated with either synthetic AGE-peptides or AGE-peptides isolated directly from patient plasma. LDL which had been modified by AGE-peptides in vitro to the same level of modification as that present in the plasma of diabetics with renal insufficiency exhibited markedly impaired clearance kinetics when injected into transgenic mice expressing the human LDL receptor. These data indicate that AGE modification significantly impairs LDL-receptor-mediated clearance mechanisms and may contribute to elevated LDL levels in patients with diabetes or renal insufficiency. This hypothesis was further supported by the observation that the administration of the advanced glycation inhibitor aminoguanidine to diabetic patients decreased circulating LDL levels by 28%.
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PMID:Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. 793 86

Available data fail to define the prevalence of ischemic nephropathy or the association of critical renovascular disease (RVD) with renal function in the atherosclerotic population. The data do suggest, however, that critical RVD is prevalent and that the prevalence increases with age, increasing serum creatinine and clinical atherosclerosis at extrarenal sites. Furthermore, our preliminary data suggest that critical RVD may be either the cause or an important superimposed accelerant of renal insufficiency in a larger portion of the atherosclerotic population with renal insufficiency than previously recognized. In this latter group, critical RVD as a cause of renal insufficiency appears to be rapidly progressive and may contribute to end-stage renal disease with increasing frequency. Conclusive definition of the importance of ischemic nephropathy as a contributor to progressive renal insufficiency and end-stage renal disease will require population-based studies that estimate the prevalence of ischemic nephropathy and the natural history of the disease. Presently, renal duplex sonography appears to be the screening test of choice to define critical RVD for such population-based studies.
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PMID:Prevalence of ischemic nephropathy in the atherosclerotic population. 794 19

Increased plasma activity of plasminogen activator inhibitor 1 (PAI-1) is considered as a risk factor for thrombosis associated with atherosclerosis by reduction of fibrinolysis. Since nephropathic patients with non-insulin-dependent diabetes mellitus (NIDDM) are a cardiovascular high-risk group, which has yielded only controversial results as to the regulation of PAI-1, we compared 19 overt nephropathic NIDDM patients (mean age 63 years, serum creatinine 1.9 mg/dl, proteinuria 4.2 g/day) to 17 nondiabetic nephropathic patients with various causes of renal insufficiency (mean age 63 years, serum creatinine 2.8 mg/dl, proteinuria 3.9 g/day). We found normal PAI-1 levels for patients with diabetic nephropathy and significantly elevated PAI-1 levels within the upper normal range for nondiabetic nephropathic patients. Common risk factors in both groups were very high levels of fibrinogen, lipoprotein(a), serum cholesterol, and LDL cholesterol.
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PMID:Plasminogen activator inhibitor 1 activity and lipoprotein(a) in nephropathic patients with non-insulin-dependent diabetes mellitus versus patients with nondiabetic nephropathy. 795 56

The association of apolipoprotein E (apo E) genetic polymorphism, particularly apo E2, with renal failure (plasma creatinine > or = 1.4 mg/dl, and urinary albumin excretion index > or = 300 mg/g.creatinine and/or persistent proteinuria) was investigated in 57 non-insulin-dependent diabetic (NIDDM) patients. Apo E2 allele frequency was significantly higher in diabetic patients with renal failure (9.6%) than in diabetic patients without renal failure (3.2%) and in the general Japanese population (3.7%). This finding suggests that apo E2 is associated with renal failure in NIDDM. In addition, to elucidate the association of apo E2 with lipid abnormalities, plasma lipid and lipoprotein levels were compared among the apo E2 (E2/2 and E3/2) and E3/3 groups of NIDDM with renal failure (n = 27) and the apo E2 (E3/2) and E3/3 groups of NIDDM with normoalbuminuria (n = 34). In diabetic patients, the apo E2 group with renal failure had significantly higher levels of plasma total cholesterol (T-chol), very-low-density lipoprotein (VLDL)-chol, triglyceride (TG), VLDL-TG and apo E than the apo E3/3 group with renal failure, and had significantly higher levels of plasma T-chol, VLDL-chol, TG and VLDL-TG than the apo E2 and E3/3 groups with normoalbuminuria. Furthermore, the apo E2 group with renal failure had significantly higher ratios of VLDL-(chol/TG) and VLDL-chol/TG (an index of remnants in plasma) than the apo E3/3 group with renal failure and the apo E2 and E3/3 groups with normoalbuminuria. These results suggest that apo E2 leads to the accumulation of TG-rich lipoprotein and remnants in plasma. It is concluded that apo E2 is associated with renal insufficiency in NIDDM and that apo E2 may be a factor that aggravates lipid abnormalities in NIDDM with renal failure.
Atherosclerosis 1994 Jun
PMID:Apolipoprotein E2, renal failure and lipid abnormalities in non-insulin-dependent diabetes mellitus. 798 Jun 94

The aim of this study was to determine the prevalence of hyperhomocysteinaemia in cardiac transplant recipients. Three groups of subjects were studied: 27 heart transplant recipients, 14 to 63 months (mean = 36.5) after transplantation; 10 patients with moderate chronic renal insufficiency without clinical evidence of vascular disease; 17 apparently healthy individuals. Twenty-five out of 27 transplanted patients had a coronaroangiography within 6 months of homocysteine measurement. Plasma homocysteine was measured both while the subject was fasting (t0) and 6 h after administration of 0.1 g.kg-1 of methionine (t6). Hyperhomocysteinaemia was present in 14/27 fasting transplanted patients and after methionine loading. Mean plasma levels of homocysteine at t0 were higher (P = 0.03) in transplanted heart recipients (15.4 +/- 7 mumol.l-1) than in the renal patients (9.9 +/- 5 mumol.l-1) despite similar mean plasma creatinin. In eight transplanted patients with angiographic coronary abnormalities of the cardiac graft, homocysteinaemia was at t0 17.1 +/- 9 mumol.l-1 and at t6 47.8 +/- 25 mumol.l-1. In 17 transplanted patients with angiographically normal coronary arteries, plasma homocysteine levels were at t0, 13.2 +/- 4 mumol.l-1 and at t6, 46.8 +/- 25 mumol.l-1. We conclude that hyperhomocysteinaemia is common in transplanted heart recipients, and partly related to renal insufficiency. No correlation was found between hyperhomocysteinaemia and angiographic evidence of coronary atherosclerosis of the graft, but the population of the study was possibly too small to establish this correlation.
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PMID:Hyperhomocysteinaemia in heart transplant recipients. 798 18

Transaortic renal endarterectomy with infra-renal aortic prosthetic graft may be used to treat combined aortic and renal atherosclerosis. We present herein the technics we used in seven patients, which represented 0.4% of our aortic revascularizations and 15% of our combined aortic and renal revascularizations. All these patients were hypertensive and four had a mild preoperative renal insufficiency. Post-operatively there were no death and the morbidity rate was 12%. Morphological assessment showed no renal or limb graft occlusion. During the follow-up there were three deaths, one limb graft occluded. All renal arteries remained patent with improvement of hypertension in 70% and stabilisation of the renal function in all. In carefully selected cases, transaortic renal endarterectomy is a safe and efficient method of treatment of combined aortic and renal atherosclerotic disease.
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PMID:[Bilateral stenosis of the renal arteries: transaortic endarterectomy]. 815 67

Two children with congenital nephrosis of the Finnish type were studied successively at the three stages of the disease: (A) nephrosis, (B) renal insufficiency/peritoneal dialysis and (C) post-transplantation; two additional patients were studied at two stages. Plasma lipoprotein profiles were determined by density gradient ultracentrifugation and lipids by enzymatic methods. Stage A was characterized by hyperchylomicronemia, low high density lipoprotein (HDL) cholesterol and the presence of dense low density lipoprotein (LDL) and HDL particles. Total cholesterol and triglycerides showed great daily variation (5-14 and 5-33 mmol/l, respectively). During stage B, hyperlipidemia weakened. Yet HDL concentration remained low and the concentration of intermediate density lipoproteins (IDL) increased. At stage C, hyperlipidemia had almost subsided, but the presence of IDL persisted. In conclusion, severe hyperlipoproteinemia of congenital nephrosis at the nephrotic stage is attenuated during renal insufficiency and dialysis, and essentially normalizes after kidney transplantation. Yet the presence of IDL implies an increased risk of atherosclerosis.
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PMID:Severe hyperlipoproteinemia in congenital nephrotic syndrome of the Finnish type: effect of dialysis and kidney transplantation. 824 75


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