摘要:

Renovascular disease, particularly when associated with atherosclerosis, is a common cofactor in accelerating hypertension and deteriorating renal function. With increased longevity and effective antihypertensive medications, the prevalence of vascular lesions affecting renal viability is increasing, possibly accounting for 15% of end-stage renal disease. Renal vascular lesions alter renin release and multiple associated mechanisms related to adrenergic and vascular regulation. Several new diagnostic modalities, including captopril renography, duplex ultrasonography, and magnetic resonance angio-graphy, are being applied for noninvasive diagnosis. Advances in interventional radiologic procedures, including endovascular stents and surgical revascularization, offer the potential for both improved blood pressure management and salvage of renal function. Optimal management of renovascular disease depends on careful assessment of the progression of each patient and associated risk of intervention.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

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.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The majority of hemodialysis patients die from cardiovascular disease. However, the contribution of myocardial infarction to mortality is relatively minor, despite the fact that coronary artery disease is common in uremic patients. Hypertension seems to be the major risk factor for the development of atherosclerosis in hemodialysis patients, although abnormalities of the lipid spectrum, characterized by an increase in triglycerides and very low density lipoprotein levels and a decrease in high-density lipoprotein levels, are frequent in hemodialysis patients. The existence of left ventricular (LV) hypertrophy is a serious risk factor for morbidity and mortality in hemodialysis patients. LV hypertrophy can present as a dilated cardiomyopathy or as concentric or asymmetric septal hypertrophy. Loss of myocardial contractility by coronary artery disease or carnitine deficiency can lead to systolic LV dysfunction with a compensatory dilated cardiomyopathy. Furthermore, the presence of a hypercirculation in uremic patients, resulting from anemia, the arteriovenous fistula, or fluid overload, can also lead to a dilated cardiomyopathy. Systolic LV dysfunction occurs when the increase in LV wall thickness is inadequate for the increase in LV radius, which might be caused by increased levels of parathyroid hormone. LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. Therefore, in uremic patients, anemia should be corrected and hypertension adequately treated early in the development of renal failure. Chronic fluid overload should be prevented by adequate estimation of optimal dry weight. Whether normalization of the lipid profile will prevent atherogenesis is dubious. In patients with LV dysfunction, rapid changes in plasma volume should be avoided.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The pathogenesis of renal sodium and water retention in cardiac failure, cirrhosis, and the nephrotic syndrome may be explained by the unifying hypothesis of body fluid volume regulation. According to this hypothesis, underfilling of the arterial vascular compartment initiates a sequence of events, including activation of various neurohormonal vasoconstrictor systems, which results in enhanced renal sodium and water reabsorption, the failure to escape from the sodium-retaining effect of aldosterone, and renal resistance to atrial natriuretic peptide. In patients with low-output cardiac failure, a decrease in cardiac output results in arterial underfilling. Peripheral arterial vasodilation diminishes the fullness of the arterial vascular compartment in patients with high-output cardiac failure and cirrhosis. In the nephrotic syndrome, the decrease in plasma oncotic pressure due to hypoalbuminemia initiates arterial underfilling. The factors that are responsible for the peripheral arterial vasodilation in patients with cirrhosis remain obscure. Diuretics are initially effective in reducing the excess of total-body sodium and water in edematous patients. Loop diuretics, with or without metolazone or a thiazide diuretic, are quite useful in patients with heart failure. In cirrhosis and the nephrotic syndrome, the specific aldosterone antagonist spironolactone, alone or in combination with other diuretics, has proven to be highly efficacious. However, in all instances, the emergence of diuretic resistance represents a major limitation of diuretic therapy for the edematous patient. This diuretic resistance may be mediated by further activation of vasoconstrictor, antinatriuretic neurohormones.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID