Atherosclerosis renal artery

Increased production of ET-1 has been implicated in a variety of cardiovascular diseases, including hypertension, cardiac hypertrophy, heart failure, atherosclerosis, coronary artery disease, and myocardial infarction. ET-1 also participates in pulmonary diseases, including asthma and pulmonary hypertension, as well as in several renal diseases. 

Renal artery stenosis (whether unilateral, bilateral renal or suspected from the presence of generalised atherosclerosis) an ACE inhibitor may cause renal failure and is contraindicated. 

Familial dysbetalipoproteinemia (type III) is characterized by the accumulation of chylomicron and VLDL remnants, which are enriched in cholesterol compared to their precursors. The primary molecular cause of familial dysbetalipoproteinemia (type III) is the homozygous presence of the apolipoprotein E2 (apoE2) isoform, which is associated with recessive inheritance of the disorder [62]. However, only 1 in 50 homozygotes for apoE2 will develop type III hyperlipoproteinemia, which is clinically characterized by palmar and tuberous xanthomas, arcus lipoides, and premature atherosclerosis of coronary, peripheral, and cerebral arteries. Precipitating factors include diabetes mellitus, renal disease, hemochromatosis, but also familial hypercholesterolemia. In addition, some rare mutations in the apoE gene have been found to cause dominant and more penetrant forms of type III hyperlipoproteinemia. 

Cardiovascular diseases are the leading cause of death in the Western world. Basically, atherosclerosis manifests itself in three major organs and thereby leads to severe secondary diseases. Coronary disease results from atherosclerosis of the coronary arteries and culminates in myocardial infarction when vessels are occluded by a thrombus. In the brain, atherosclerosis gives rise to arterial thrombi or ruptures that result in a stroke. Atherosclerosis in the kidney leads to renal failure. Since these diseases significantly lower life expectancy, early recognition and elimination of risk factors (hypertension, diabetes mellitus, hyperlipidemia, and smoking) that promote atherosclerosis are essential. 

Aberrant thrombus formation and deposition on blood vessel walls imderlies the pathogenesis of acute cardiovascular disease states which remain the principal cause of morbidity and mortality in the industrialized world [1,2,3]. Plasma proteins, proteases and specific cellular receptors that participate in hemostasis have emerged as important risk considerations in thrombosis and thromboembolic disorders. The clinical manifestations of the above disease states include acute coronary artery and cerebrovascular syndromes, peripheral arterial occlusion, deep vein thrombosis and pulmonary/renal embolism [3]. The most dilabilitating acute events precipitated by these disorders are myocardial infarction and stroke. In addition, the interplay between hemostatic factors and hypertension (4) or atherosclerosis (5) dramatically enhances the manifestation of these pathologic states. 

Diabetes mellitus is now recognized as one of the most common and significant diseases facing Americans. It is estimated that I of 4 children bom today will become diabetic in their lifetime because of obesity and inactivity. Also, it has been noted that diabetes has a severe effect on blood vessels, particularly in the pathogenesis of atherosclerosis (blockage of arteries by lipids and plaque), which can lead to myocardial infarction or stroke. Diabetes mellitus is treated as equivalent to a prior cardiovascular event in its risk for future atherosclerotic disease. Diabetes is also associated with immunosuppression, renal insufficiency, blindness, neuropathy, and other metabolic disorders. 

The rationale underlying the treatment of chronic HTN concerns its association with atherosclerosis and the increased risk of stroke, heart failure, renal diseases, peripheral vascular disease, and coronary artery disease. Except in severe HTN, there is no rash to start drug Rx prior to lifestyle changes because the goals are long term. Factors in hypertension include decreases in vagal tone, increases in sympathetic tone, increased renin-angiotensin activity, and water retention. 

Somewhere in the mosaic of atherosclerosis, vascular sensitivity and reaction resembling an allergic response may occur. Hypertension of renal origin may be paralleled by the contribution of some component by the kidney (or by some sources excited by the hypertension or Injured kidney) that causes a predisposition of the arterial wall toward atherosclerosis. Vascular Injury of the "serum sickness" type from vascular... 

---