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)

Over a 16-year period, 205 patients with hypertension were shown to have a renovascular aetiology. Of these, 125 (61 per cent) had Takayasu's arteritis, 58 (28.3 per cent) had fibromuscular dysplasia, 16 (7.8 per cent) had atherosclerosis, five (2.4 per cent) had polyarteritis nodosa and one (0.5 per cent) had renal artery aneurysm. Among patients with Takayasu's arteritis, males were affected as commonly as females. The mean age of these patients at the time of detection was 26.8 +/- 8.6 years (range 5-52 years). Type I arteritis was seen in nine (7.2 per cent), Type II in 40 (32 per cent) and Type III in 76 (60.8 per cent) patients. The abdominal aorta was involved in 117 (93.3 per cent) patients. Takayasu's arteritis was associated with ulcerative colitis in two patients and with renal amyloidosis and focal segmental glomerulosclerosis with a nephrotic syndrome in one patient each. Surgical intervention consisting of bypass procedures, autotransplantation or nephrectomy was performed in 17 (13.6 per cent) and angioplasty in nine (7.2 per cent) patients. Cure and improvement in blood pressure was observed in 82.4 per cent and 77.8 per cent respectively. Adequate control of blood pressure was achieved with drugs only in 22 (22.2 per cent) patients. A definite cause and effect relationship could not be established between any infective or immunological disorder and Takayasu's arteritis. Takayasu's arteritis is a far more common cause of renovascular hypertension in Indian population than fibromuscular dysplasia or atherosclerosis, which are more common in the western population.
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PMID:Renovascular hypertension due to Takayasu's arteritis among Indian patients. 136 62

Experimental evidence suggests a pathogenetic role for lipids in focal glomerulosclerosis (FGS) analogous to atherosclerosis. As foam cells (FC) are an important factor in atherosclerosis, a retrospective comparative study was done to evaluate the significance of intraglomerular FC in human FGS. Glomerular FC infiltration was evaluated in 115 biopsies of FGS, 120 biopsies of membranous glomerulonephritis (MGN) and 50 biopsies of minimal-change disease (MCD). Selected clinical and laboratory data collected at about the time of biopsy were reviewed. The proportion of biopsies showing glomerular FC was much higher in FGS (70%) than in either MGN (12%) or MCD (0%) p less than 0.001. The mean percent (+/- SD) of glomeruli with FC per biopsy was significantly greater in FGS (7.9 +/- 9.9) than in MGN (2.0 +/- 7.8; p less than 0.0001). Of the 14 MGN biopsies with FC, 13 showed superimposed FGS. Mean serum total cholesterol and triglyceride were not significantly higher in FGS than in either MGN or MCD. The results demonstrate a close association of glomerular FC infiltration with FGS.
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PMID:Intraglomerular foam cells and human focal glomerulosclerosis. 143 3

A universal underlying abnormality in the pathogenesis of hypertension, atherosclerosis, myocardial dysfunction, and diabetic glomerulosclerosis involves alteration in smooth muscle cell structure, function, and growth. Angiotensin II, through its effects on contractility, growth, and the sympathetic nervous system, may potentially play a key role in this pathologic process and, thus, contribute to the development of these cardiovascular and renal complications of diabetes mellitus. Angiotensin-converting enzyme inhibitors and some direct renin inhibitors prevent or slow the progression of some of these complications, which further suggests a pathologic role for the reninangiotensin system in diabetes mellitus.
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PMID:Effect of the renin-angiotensin system in the vascular disease of type II diabetes mellitus. 158 Feb 75

Recently, much experimental evidence has accumulated contending that hypercholesterolemia is an aggravating factor in the progression of initial glomerular injury to glomerulosclerosis. Many of the features of progressive glomerular disease share biological properties with those of atherosclerosis, and data suggesting a noxious role for oxidized low-density lipoprotein in the glomerulosclerosis process are emerging. This review discusses these issues and examines the pathobiology of cholesterol-induced glomerular injury.
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PMID:A putative role of hypercholesterolemia in progressive glomerular injury. 158 Jun 8

Hypertension is a major factor that contributes to the development of the vascular complications of diabetes mellitus, which primarily include atherosclerosis, nephropathy, and retinopathy. The mechanism of the pathophysiological effects of hypertension lies at the cellular level in the blood vessel wall, which intimately involves the function and interaction of the endothelial and vascular smooth muscle cells. Both hypertension and diabetes mellitus alter endothelial cell structure and function. In large and medium size vessels and in the kidney, endothelial dysfunction leads to enhanced growth and vasoconstriction of vascular smooth muscle cells and mesangial cells, respectively. These changes in the cells of smooth muscle lineage play a key role in the development of both atherosclerosis and glomerulosclerosis. In diabetic retinopathy, damage and altered growth of retinal capillary endothelial cells is the major pathophysiological insult leading to proliferative lesions of the retina. Thus, the endothelium emerges as a key target organ of damage in diabetes mellitus; this damage is enhanced in the presence of hypertension. An overall approach to the understanding and treatment of diabetes mellitus and its complications will be to elucidate the mechanisms of vascular disease and endothelial cell dysfunction that occur in the setting of hypertension and diabetes.
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PMID:Hypertension, the endothelial cell, and the vascular complications of diabetes mellitus. 163 68

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Risk factors for renal and cardiovascular disease in diabetic patients. 165 64

Proliferation of vascular smooth muscle cells is postulated to be one of the key events in the pathogenesis of atherosclerosis or during the development of focal glomerular sclerosis. Several studies have suggested that the antiproliferative effects of heparin appear to be regulated by different structural determinants. Our experiments show that dextrans substituted with carboxylic and benzylamide sulphonate groups markedly inhibit the growth of smooth muscle cells in vitro. Studies on the structure-function relationships of these products to their effect on rat aorta smooth muscle cells are reported. The antiproliferative capacity is similar to that of heparin.
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PMID:Derivatized dextran inhibition of smooth muscle cell proliferation. 172 99

It has been recently suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Obese Zucker (OZ) rats spontaneously develop hyperlipidemia, proteinuria and FGS. To evaluate the role of the monocyte (MO) and its derivatives in the pathogenesis of the lesion, 30 OZ rats and 15 lean littermates (LZ) were followed for up to 240 days of age. At 75, 120 and 240 days of age, groups of 10 OZ and 5 LZ were assessed with respect to serum total and free cholesterol (TC and FC), triglyceride, lipoprotein electrophoresis, renal histology, histochemistry and immunohistochemistry. All serum lipids were raised at 75 days in OZ rats and increased progressively at 120 and 240 days. The early lesions of FGS were first demonstrated in OZ at 120 days with more advanced lesions at 240 days. FGS was seen in LZ only at 240 days when their serum lipids were raised. Intraglomerular MO infiltration was significantly higher in OZ than in LZ at all time periods (p less than 0.01) and greater in glomeruli with FGS lesions than in those without (p less than 0.01 and 120 days and p less than 0.05 at 240 days). Staining for ED1 and Ia antigens with monoclonal antibodies demonstrated increasing numbers of intraglomerular ED1+ and Ia+ cells with increasing age and extent of FGS. The findings suggest a role for intraglomerular macrophages in the pathogenesis of FGS in OZ.
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PMID:Monocytes and macrophages in focal glomerulosclerosis in Zucker rats. 194 26

This paper attempts to further delineate the similar pathobiologic mechanisms involved in the atherosclerosis and glomerulosclerosis processes. In particular, recent experimental data in models of both processes have focused on the roles of hypercholesterolemia and the monocyte/macrophage in propagating these lesions. In a nonimmune toxic glomerulopathy, chronic aminonucleoside nephrosis, our laboratory has demonstrated an important role for the glomerular macrophage, which is increased in number in temporal association with the onset of albuminuria, in propagating initial glomerular injury to glomerulosclerosis. In addition, a superimposition of dietary hypercholesterolemia further augments this heightened glomerular macrophage number and activates systemic macrophages. These data suggest a synergistic role between the hypercholesterolemia of nephrosis and the surge in glomerular macrophage number following initial glomerular injury in establishing a cascade of intercellular events that culminates in glomerulosclerosis. The intriguing histologic and immunohistochemical similarities between the evolving fatty streak in the atherosclerotic vessel wall and the progressive glomerular lesion leading to glomerulosclerosis suggest analogous pathobiologic mechanisms.
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PMID:Analogous pathobiologic mechanisms in glomerulosclerosis and atherosclerosis. 204 67

It is proposed that the systemic hyperinsulinemia and hepatic portal hypoinsulinemia that occurs with conventional injectable preparations of insulin currently used in the treatment of patients with diabetes mellitus is largely responsible for the morbidity associated with this disease. Epidemiological evidence and animal experimentation strongly support systemic hyperinsulinemia as a major factor in genesis of atherosclerosis in diabetic patients. In addition, in vitro studies demonstrate a direct effect of insulin on endothelial cell and arterial smooth muscle proliferation. On the other hand, inadequate hepatic delivery of insulin is associated with overproduction of renal vasoregulatory factors leading to glomerular hyperfiltration and ultimately to glomerulosclerosis and its clinical endpoint--end-stage renal disease. In the absence of widespread success of pancreatic and islet-cell transplantation as a means to deliver insulin physiologically into the hepatic portal circulation, methods must be devised and perfected to accomplish such delivery using approaches such as orally administering insulin in intestinal-enzyme protected capsules. Until such methods of delivery are available for safe and widespread use, one should abandon the illusory goal of rigid glucose control in favor of methods that reduce insulin requirement. Along these lines, dietary restriction and aerobic exercise should be the major life style changes advised for diabetic patients. Reduction of glomerular hyperfiltration in diabetic patients can be promoted with the use of low protein diets and/or angiotensin converting enzyme inhibitors.
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PMID:Hypothesis: insulin is responsible for the vascular complications of diabetes. 205 21


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