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Biomedical subjects

Pantelis A Sarafidis

Publications and source records attributed to Pantelis A Sarafidis.

10 recordsLinked to original sources
PubMed2007

Antihypertensive therapy in the presence of proteinuria.

The presence of proteinuria is a well-known risk factor for both the progression of renal disease and cardiovascular morbidity and mortality, and decreases in urine protein excretion level were associated with a slower decrease in renal function and decrease in risk of cardiovascular events. Increased blood pressure has a major role in the development of proteinuria in patients with either diabetic or nondiabetic kidney disease, and all recent guidelines recommend a blood pressure goal less than 130/80 mm Hg in patients with proteinuria to achieve maximal renal and cardiovascular protection. Drugs interfering with the renin-angiotensin system, ie, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, should be used as first-line antihypertensive therapy in patients with proteinuria because they seem to have a blood pressure-independent antiproteinuric effect, and if blood pressure levels are still out of goal, a diuretic should be added to this regimen. A combination of an angiotensin-converting enzyme inhibitor with an angiotensin receptor blocker or other classes of medications shown to decrease protein excretion, such as nondihydropyridine calcium antagonists or aldosterone receptor blockers, should be considered to decrease proteinuria further. This review provides an extended summary of current evidence regarding the associations of blood pressure with proteinuria, the rationale for currently recommended blood pressure goals, and the use of various classes of antihypertensive agents in proteinuric patients.

Angiotensin Receptor Antagonists↗
PubMed2006

Review: Insulin and endothelin: an interplay contributing to hypertension development?

CONTEXT: The aim of this article was to review the existing data on the interactions among insulin, insulin resistance, and endothelin and how those contribute to the development of hypertension in insulin-resistant states. EVIDENCE ACQUISITION: A literature search of MEDLINE database was performed to identify English-language articles published during the last 20 yr. Search terms used were endothelin, insulin, insulin resistance, and hyperinsulinemia in combination with blood pressure and hypertension. Reference lists of retrieved articles were also evaluated for relevant information. EVIDENCE SYNTHESIS: Several mechanisms connect insulin resistance and compensatory hyperinsulinemia with blood pressure elevation in the context of the metabolic syndrome, i.e. sodium retention, sympathetic activation, and impairment of endothelial nitric oxide production. Accumulating evidence suggests that activation of the endothelin system seems to be another important, yet less discussed, mechanism. In vitro studies have shown that insulin stimulates both endothelin-1 production and action on the vascular wall. In vivo, high levels of insulin result in increase in circulating endothelin-1 in healthy individuals, and this effect is also seen in insulin-resistant subjects, a relationship not observed with nitric oxide production. Moreover, endothelin receptor antagonism effectively reduces blood pressure in animal models of insulin resistance and hypertension. On the other hand, elevation of endothelin-1 levels can further increase insulin resistance, forming possibly a deleterious circle. CONCLUSIONS: Endothelin-1 may play a crucial role in the pathogenesis of hypertension in insulin-resistant states. Future research should examine the potential of endothelin receptor antagonism to help blood pressure control in patients with insulin resistance.

Animals↗
PubMed2006

Insulin resistance, hyperinsulinemia, and renal injury: mechanisms and implications.

Most of the basic components of the metabolic syndrome, namely type 2 diabetes mellitus, hypertension, obesity, or low high-density lipoprotein cholesterol levels, apart from being major risk factors for cardiovascular disease have been also associated with an increased risk of chronic kidney disease. However, several epidemiologic studies conducted over the past years suggest that the central component of the syndrome, insulin resistance, as well as compensatory hyperinsulinemia are independently associated with an increased prevalence of chronic kidney disease. In addition, background studies support the existence of several pathways linking insulin resistance and hyperinsulinemia with kidney damage. Insulin per se promotes the proliferation of renal cells and stimulates the production of other important growth factors such as insulin-like growth factor-1 and transforming growth factor beta. Insulin also upregulates the expression of angiotensin II type 1 receptor in mesangial cells, thus enhancing the deleterious effects of angiotensin II in the kidney, and stimulates production and renal action of endothelin-1. Moreover, insulin resistance and hyperinsulinemia are associated with decreased endothelial production of nitric oxide and increased oxidative stress which have been also implicated in the progression of diabetic nephropathy. This review analyzes the above and other potential mechanisms, through which insulin resistance and hyperinsulinemia can contribute to renal injury.

Animals↗
PubMed2006

Gender disparity in outcomes of care and management for diabetes and the metabolic syndrome.

Although diabetes lies among the major risk factors for cardiovascular disease (CVD) in both men and women, current evidence suggests that it has a much stronger effect on the risk of coronary heart disease (CHD) in women than in men. Moreover, diabetic women have not experienced the decline in CHD mortality observed in diabetic men and individuals without diabetes over the past three decades. Apart from a more pronounced direct effect of diabetes on the vascular wall, this greater impact of diabetes on CHD risk in women could be associated with a heavier burden of other traditional cardiovascular risk factors within the context of the metabolic syndrome, a stronger effect of the metabolic syndrome on CVD, and a less aggressive management of the various risk factors in diabetic women compared with men. This article discusses the recent evidence on the gender differences in the outcomes of CVD and the management of risk factors associated with diabetes and the metabolic syndrome, highlighting the need for better treatment strategies of diabetes and the other components of the metabolic syndrome in diabetic women.

Cardiovascular Diseases↗
PubMed2006

Microalbuminuria.

Microalbuminuria, originally described more than 3 decades ago as a predictor of nephropathy in patients who had type 1 diabetes mellitus and associated with higher cardiovascular risk, is now linked with increased risk for cardiovascular events rather than progression to end-stage kidney disease. This article reviews the role of microalbuminuria in the context of atherosclerotic vascular disease. It presents the methods for microalbuminuria assessment in clinical practice, its relations with other cardiovascular risk factors, and the pathophysiologic associations between microalbuminuria and vascular damage. In addition, this article discusses the prognostic significance of microalbuminuria for cardiovascular disease as well as existing therapeutic interventions for reducing urine albumin excretion in patients who are at high cardiovascular risk.

Albuminuria↗
PubMed2006

The effects of thiazolidinediones on blood pressure levels - a systematic review.

Insulin resistance has been proposed to be the underlying disorder of the so-called metabolic or insulin resistance syndrome, which represents the clustering in the same individual of several cardiovascular risk factors, such as type 2 diabetes mellitus, hypertension, abdominal obesity, elevated triglycerides and low high-density lipoprotein-cholesterol. As far as the connection of insulin resistance and compensatory hyperinsulinaemia with hypertension is concerned, a number of mechanisms possibly linking these disturbances have been described, such as activation of sympathetic nervous system, enhancement of renal sodium reabsorption, or impairment of endothelium-dependent vasodilatation. Thiazolidinediones (TZDs) constitute a class of oral antihyperglycaemic agents that act by decreasing insulin resistance, and apart from their action on glycaemic control, they have been also reported to exert beneficial effects on other parameters of the metabolic syndrome. In particular, during recent years a considerable number of animal and human studies have shown that the use of TZDs was associated with usually small but significant reductions of blood pressure (BP) levels. Since a possible beneficial action of these compounds on BP could be of particular value for patients with the metabolic syndrome, this review aimed to summarize and evaluate the literature data in the field, derived either from studies that just examined BP levels among other parameters or from studies that were specifically designed to determine the effect of a TZD on BP.

Blood Pressure↗