PubMed Health⌕ Search

Biomedical subjects

Efrain Reisin

Publications and source records attributed to Efrain Reisin.

15 recordsLinked to original sources
PubMed2006

Functional and structural renal changes in the early stages of obesity.

Obesity is an epidemic of colossal proportion, and the healthcare system has been singularly unable to abate this growing threat to society. Two-thirds of US adults are now overweight or obese. Also, the incidence of obesity is increasing in children and adolescents at an alarming rate. The mechanisms of kidney damage, can be both direct and consequential from hypertension and diabetes mellitus. Both hemodynamic and hormonal effects of obesity are discussed. Benefits of weight loss and pharmacological treatment are evaluated.

Animals↗
PubMed2005

Independent and additive impact of blood pressure control and angiotensin II receptor blockade on renal outcomes in the irbesartan diabetic nephropathy trial: clinical implications and limitations.

Elevated arterial pressure is a major risk factor for progression to ESRD in diabetic nephropathy. However, the component of arterial pressure and level of BP control for optimal renal outcomes are disputed. Data from 1590 hypertensive patients with type 2 diabetes in the Irbesartan Diabetic Nephropathy Trial (IDNT), a randomized, double-blind, placebo-controlled trial performed in 209 clinics worldwide, were examined, and the effects of baseline and mean follow-up systolic BP (SBP) and diastolic BP and the interaction of assigned study medications (irbesartan, amlodipine, and placebo) on progressive renal failure and all-cause mortality were assessed. Other antihypertensive agents were added to achieve predetermined BP goals. Entry criteria included elevated baseline serum creatinine concentration up to 266 micromol/L (3.0 mg/dl) and urine protein excretion >900 mg/d. Baseline BP averaged 159/87 +/- 20/11 mmHg. Median patient follow-up was 2.6 yr. Follow-up achieved SBP most strongly predicted renal outcomes. SBP >149 mmHg was associated with a 2.2-fold increase in the risk for doubling serum creatinine or ESRD compared with SBP <134 mmHg. Progressive lowering of SBP to 120 mmHg was associated with improved renal and patient survival, an effect independent of baseline renal function. Below this threshold, all-cause mortality increased. An additional renoprotective effect of irbesartan, independent of achieved SBP, was observed down to 120 mmHg. There was no correlation between diastolic BP and renal outcomes. We recommend a SBP target between 120 and 130 mmHg, in conjunction with blockade of the renin-angiotensin system, in patients with type 2 diabetic nephropathy.

Amlodipine↗
PubMed2005

Definition of the metabolic syndrome: current proposals and controversies.

Metabolic syndrome includes a clustering of metabolic derangements that cause affected subjects to have an increased risk for developing diabetes, cardiovascular disease, and, according to recent epidemiologic studies, chronic kidney disease. The present review discusses four definitions of metabolic syndrome published by different national and international committees. In an effort to bridge the differences existent in those classifications, a unified definition that recognizes the increased biologic activity of the upper visceral fatty tissue and the strong association of abdominal obesity as a leading part of metabolic syndrome is proposed herein. The diagnosis of metabolic syndrome is reserved for pre-diabetic patients who share the risk of becoming diabetic or developing cardiovascular or chronic kidney disease.

Adipose Tissue↗
PubMed2005

Hypertension and the metabolic syndrome.

The cause of hypertension in the metabolic syndrome is complex and multifactorial and all of the elements of the metabolic syndrome, including obesity, insulin resistance, and the characteristic dyslipidemia probably are involved in mediating changes ultimately resulting in hypertension and modifying its course. Of these elements, obesity may play the most important and pivotal role in creating the conditions that lead to hypertension in the metabolic syndrome. This is not to say that the other elements of the syndrome are less important, and, as we gain more insight into the processes involved, we should be able to better manage the disease and tailor our therapeutic interventions appropriately.

Dyslipidemias↗
PubMed2005

Kidney disease and the metabolic syndrome.

The epidemic of metabolic syndrome contributes to the rapid growth of cardiovascular and renal diseases. Hyper-hemodynamics, impaired pressure natriuresis, excess excretory load, insulin resistance, endothelial dysfunction, chronic inflammation, and prothrombotic status individually and interdependently initiate renal injury in metabolic syndrome. The prevention and treatment of kidney disease require a multifactorial approach. Weight loss through diet control and exercise can reverse many pathophysiologic processes. Pharmacologic intervention includes insulin sensitizers, tight glycemic and lipid control, blockage of renin angiotensin aldosterone system, and anti-inflammatory and antithrombotic therapies. Each peroxisome proliferator-activated receptor isoform plays a distinct role in metabolic syndrome, and their agonists may prevent or reverse the early renal injuries.

Cardiovascular Diseases↗
PubMed2005

The heart in obesity-hypertension.

There is growing recognition that obesity is reaching epidemic proportions throughout the world. In adults, obesity is associated with increased cardiovascular morbidity and mortality. A series of endocrine, metabolic and hemodynamic mechanisms have been responsible for the development of obesity-hypertension. These mechanisms include: a suppressed biologic activity and availability of natriuretic peptide, increased sympathetic adrenergic activity, release of angiotensin ll from adipocytes and activation of the renin-angiotensin-aldosterone system, leptin resistance, chronic hyperleptinemia and hyperinsulinemia. The systemic hemodynamic profile of obesity includes high intravascular volume, increased cardiac output and inappropriately normal peripheral resistance. The cardiovascular adaptations to these changes include changes in vascular responsiveness and concentric-eccentric left ventricular hypertrophy, and may be responsible for increased risk of congestive heart failure, arrhythmia and sudden death.

Adaptation, Physiological↗
PubMed2004

The prevalence of reduced glomerular filtration rate in older hypertensive patients and its association with cardiovascular disease: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.

BACKGROUND: The prevalence of reduced glomerular filtration rate (GFR) in older hypertensive patients and the relationship between level of GFR and cardiovascular disease (CVD) and its risk factors are not well known. METHODS: We evaluated baseline renal function in 40 514 hypertensive patients 55 years or older who were enrolled in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). We used the simplified Modification of Diet in Renal Disease study equation to estimate GFR and examined the prevalence of CVD in patients with different levels of GFR. RESULTS: Fifty-seven percent of patients had mild (60-89 mL/min per 1.73 m(2)), 17.2% had moderate (30-59 mL/min per 1.73 m(2)), and 0.6% had severe (<or=29 mL/min per 1.73 m(2)) reductions in GFR. Compared with patients with normal or mildly reduced GFR, patients with moderate or severe reductions in GFR were more likely to have had a prior myocardial infarction or stroke (19.2% and 23.4% vs 28.7% and 26.9%, respectively), have ischemic changes on electrocardiography (ECG) (16.0% and 18.9% vs 24.6% and 34.1%, respectively), and have left ventricular hypertrophy on ECG (ECG-LVH) (3.9% and 4.2% vs 6.0% and 11.2%, respectively). A decrease in GFR of 10 mL/min per 1.73 m(2) was independently associated with a 6% higher risk for CVD and 14% higher risk for ECG-LVH. The increase in risk was marked at a GFR of approximately 60 to 70 mL/min per 1.73 m(2). CONCLUSIONS: The prevalence of reduced GFR is high in older hypertensive patients. Patients with moderate or severe reduction in GFR are more likely to have a history of CVD and ECG-LVH. Even modest reductions in GFR are independently associated with a higher prevalence of CVD and ECG-LVH.

Cardiovascular Diseases↗
PubMed2004

Kidney transplantation: the evolving challenges.

Kidney transplantation is the treatment of choice for patients with end stage renal disease. Kidney transplantation not only improves the quality of life but also prolongs life. Over the last decade, the short-term allograft survival rate has been improved dramatically. Chronic allograft nephropathy and death from cardiovascular diseases become predominant causes of later graft loss. Prevention and treatment of these disease processes require a comprehensive approach. The ever-increasing shortage of organ supply becomes the greatest challenge for the transplant community and modern medicine. More and more patients are waiting for organs; many of them are dying while waiting. Xenotransplantation and organ engineering and cloning are promising techniques and can potentially provide organs for transplantation in the future.

Animals↗
PubMed2004

Interferon-alpha-associated sarcoidosis responsive to infliximab therapy.

Sarcoidosis, a multisystem disease characterized by noncaseating granulomas, has been reported to be associated with interferon alpha (IFN-alpha) therapy for hepatitis C infection. INF-alpha is known to stimulate T helper cells with a Th1 profile immune response, which is the key immunologic event of a sarcoid granuloma formation. We report a patient treated with IFN-alpha who developed hypercalcemia and renal insufficiency as presenting clinical manifestation of sarcoidosis. Prednisone therapy was effective in controlling hypercalcemia but had to be discontinued due to an increase in hepatitis C viral RNA count. Infliximab, a chimeric monoclonal antibody directed against tumor necrosis factor alpha was used as therapy in our patient for its known potent anti-inflammatory effects. The patient received three doses of infliximab (5 mg/kg) and achieved a rapid decline in serum calcium to normal levels in 7 days; the serum calcium level has remained normal 3 months after the last infusion.

Antibodies, Monoclonal↗
PubMed2003

Leptin: sympathetic and cardiovascular effects.

Shortly after leptin was first discovered, it was hailed as the key to understanding obesity. However, it didn't take long for investigators to realize that the hormone was more than a feedback signal to inhibit further food intake. Since those early days, leptin has been well characterized in rodents. It exerts an influence in many physiologic processes, including food intake, thermoregulation, fertility, thyroid function, adrenal function, sympathetic nerve activation, renal function, blood vessel tone, and blood pressure. No longer a satiety hormone, it is being looked at from many different perspectives. One such perspective is its influence on the cardiovascular system. This review highlights some of the work in this area.

Animals↗
PubMed2003

Regression of left ventricular hypertrophy is a key goal of hypertension management.

Left ventricular hypertrophy (LVH) in patients with hypertension is associated with an increased risk for many cardiovascular events and predicts a higher mortality rate. The pathogenesis of LVH is complicated. In addition to the hemodynamic burden (pressure or volume overload) and demographic factors, several trophic humoral factors, such as angiotensin II, aldosterone, endothelin, leptin, and catecholamines, may also contribute to the development and progression of LVH. Effective antihypertensive therapy can reverse LVH as well as prevent its development. Regression of LVH decreases subsequent cardiovascular morbidity and mortality. The commonly used drugs have various effects on LVH. Angiotensin receptor blockers and angiotensin-converting enzyme inhibitors seem most effective. Several new agents, including direct antifibrotic drugs, aldosterone blockade, vasopeptidase inhibitors, and endothelin receptor antagonists that more specifically target the underlying pathogenesis of LVH may provide us with innovative approaches to treat LVH.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2003

Hypertension in chronic dialysis patients: pathophysiology, monitoring, and treatment.

The prevalence of hypertension in the population with ESRD is very high, approaching 100% in some populations, and may account for the fact that cardiovascular disease continues to be the leading cause of morbidity and mortality in ESRD. The pathophysiology of hypertension in ESRD is reviewed, suggesting multifactorial causes; a dominant cause is that of volume expansion and an inappropriate increase in systemic vascular resistance because of activation of the renin-angiotensin system. The primary goal in the treatment of hypertension should be to attain a dry-weight and maintain volume control through limiting salt and fluid intake and ultrafiltration of excess fluids. If this approach is unsuccessful, an array of antihypertensive medications are available to help control blood pressure in patients with ESRD.

Antihypertensive Agents↗
PubMed2003

Hypertension after kidney transplantation: impact, pathogenesis and therapy.

Hypertension (HTN) contributes to the high incidence of cardiovascular disease mortality as well as chronic allograft nephropathy (CAN) and late graft failure in renal transplant recipients. The mechanisms are complex and may involve pathogenic factors attributable to the host, allograft, and immunosuppressive drugs. Calcium channel blockers should be used to ameliorate the nephrotoxicity of calcineurin inhibitors in the early years after transplantation. Angiotensin-converting enzyme inhibitors and angiotensin-2 type-1 receptor blockers are safe and effective, have antiproteinuric effects, slow the progression of CAN, and may provide survival benefits. Diuretics and/or beta-adrenergic receptor blockers are frequently added in combination regimen. Appropriate adjustment of the immunosuppressive drugs should also be considered for the long-term care of kidney recipients with HTN.

Antihypertensive Agents↗
PubMedDate not supplied

Characteristics and lipid distribution of a large, high-risk, hypertensive population: the lipid-lowering component of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) consisted of 42,418 participants randomized to one of four antihypertensive treatment groups: chlorthalidone, amlodipine, lisinopril, or doxazosin. A subset of these participants with fasting low-density lipoprotein cholesterol levels 100-189 mg/dL were randomized into a lipid-lowering component: 5170 to receive pravastatin (40 mg daily) and 5185 to receive usual care. This report describes the characteristics and lipid distribution of these participants. There were no important differences between the randomized treatment groups. Women had higher total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol than men. There was a similar finding for black participants compared with whites, except blacks had lower triglycerides. Diabetics had lower high-density lipoprotein cholesterol and higher triglycerides than nondiabetics, and patients with body mass index <25 kg/m(2) had higher high-density lipoprotein cholesterol but lower low-density lipoprotein cholesterol and triglycerides than patients with higher body mass index. The success of the randomization of this large, diverse population and the differences in the lipid distributions among its subgroups will allow further understanding of optimal lipid-lowering treatment.

Aged↗