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Management of Hypertension in Diabetic Patients With Chronic Kidney Disease. Diabetes Spectrum. 21(1):30-36.Winter 2008.
Diabetes is associated with markedly increased cardiovascular risk, a risk that is made worse by the presence of chronic kidney disease (CKD), a common complication of diabetes. More than 80 percent of people with diabetes and CKD have hypertension. This review, from a special section about managing patients with diabetes and CKD, discusses the evidence regarding one of the most important treatment targets for patients with CKD: control of blood pressure to less than 130/80 mmHg. The author provides detailed information about appropriate blood pressure measurement and treatments to best achieve that target. Careful blood pressure measurement, a multiple risk factor modification strategy, and persistent and judicious renin-angiotensin-aldosterone system (RAAS) blockade in combination with diuretics and add-ons should result in good blood pressure control in most patients. In addition, engaging patients and their families through home-based blood pressure measurement (HBP), lifestyle modification, and collaboration with clinic nurses, pharmacists, and other health care providers will facilitate success. 2 tables. 57 references.
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Management of Hypertension in Diabetic Patients With Chronic Kidney Disease. Diabetes Spectrum. 21(1): 30-36. Winter 2008.
Diabetes is associated with markedly increased cardiovascular risk, a risk that is made worse by the presence of chronic kidney disease (CKD), a common complication of diabetes. More than 80 percent of people with diabetes and CKD have hypertension. This review from a special section on managing patients with diabetes and CKD, called diabetic kidney disease (DKD), discusses the evidence regarding one of the most important treatment targets for these patients, namely, control of blood pressure to less than 130/80 millimeters of mercury (mmHg). The author provides detailed information about appropriate blood pressure measurement and treatments to best achieve that target. Careful blood pressure measurement, a multiple risk factor modification strategy, and persistent and judicious renin-angiotensin-aldosterone system (RAAS) blockade in combination with diuretics and add-ons should result in good blood pressure control in a majority of patients. In addition, engaging patients and their families through home-based blood pressure measurement (HBP), lifestyle modification, and collaboration with clinic nurses, pharmacists, and other health care providers will facilitate success. 2 tables. 57 references.
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Endocrine Hypertension. IN: Gardner, D.; Shoback, D., eds. Greenspan’s Basic and Clinical Endocrinology. 8th ed. Columbus, OH: McGraw Hill. 2007. pp 396-420.
This chapter about endocrine hypertension is from a textbook about endocrinology that describes the scientific principles and clinical management of patients with endocrine-related diseases and disorders. The authors note that although the kidney is not an endocrine organ per se, its role as both the origin of and target tissue for the hormones that comprise the renin-angiotensin-aldosterone system make hypertensive disorders of kidney origin an appropriate subject for a chapter on endocrine hypertension. Hypertension can be a prominent feature of other endocrine disorders, including acromegaly, thyrotoxicosis, hypothyroidism, and hyperparathyroidism, but these are discussed elsewhere in the text. In this chapter, the authors discuss the synthesis, metabolism, and action of mineralocorticoid hormones; the pathogenesis of mineralocorticoid hypertension; aldosterone and the heart; primary aldosteronism; syndromes due to excess deoxycorticosterone production; Cushing’s syndrome; pseudohyperaldosteronism; hypertension of renal origin; the renin-angiotensin system and hypertension; and other hormone systems and hypertension, including insulin, the natriuretic peptides, nitric oxide, endothelin, the kallikrein-kinin system, and the sympathetic nervous system. The chapter includes numerous black-and-white photographs and illustrations; a list of abbreviations is provided. 11 figures. 1 table. 15 references.
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American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Hypertension. Endocrine Practice. 12(2): 193-222. March-April 2006.
This article presents the American Association of Clinical Endocrinologists (AACE) medical guidelines for clinical practice for the diagnosis and treatment of hypertension. The guidelines focus on identifying and managing hypertension secondary to or coincident with endocrinopathies, such as diabetes mellitus. The AACE contends that understanding the associated pathophysiologic features of hypertension will guide appropriate treatment and thus help physicians anticipate the usefulness of evolving therapies, such as blockade of the renin-angiotensin systems for retarding the progression of retinopathy and nephropathy in patients with diabetes. The objectives of the guidelines are to indicate when to suspect the presence of and pursue further testing for secondary hypertension; provide appropriate examples of the most common causes of endocrine-associated hypertension that physicians my encounter; elucidate the cause of each endocrine disorder underlying hypertension; describe the tests used to confirm each diagnosis; identify the appropriate management options for each condition based on the available evidence and known pathophysiologic changes; and discuss outcomes and potential side effects associated with each management option. In addition to diabetes, the guidelines cover coronary or peripheral vascular disease; glucocorticoid excess (Cushing’s syndrome); genetic diseases; disorders of the adrenal, thyroid, parathyroid, and pituitary glands; abnormal renal tubular sodium handling; and renin-secreting tumors. 3 figures. 7 tables. 187 references.
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Angiotensin II and Its Receptors in the Pathogenesis of Diabetic Nephropathy. IN: Cortes, P. and Mogensen, C.E., eds. Diabetic Kidney. Totowa, NJ: Humana Press. 2006. pp. 3-21.
This chapter on angiotensin II and its receptors in the pathogenesis of diabetic nephropathy is from a clinical textbook on the diabetic kidney. After a brief introduction, the authors cover the renin-angiotensin system (RAS) in diabetes, angiotensin II receptors, the mechanisms of action of angiotensin II receptors, and future directions for research in this area. Diabetic nephropathy (DN) is characterized by the accumulation of extracellular matrix (ECM) in the kidney. The peptide angiotensin II has many hemodynamic and biochemical effects that could contribute to DN. The authors conclude that recent research suggests that angiotensin II may act as a signaling peptide to initiate transcriptional changes for particular genes. In view of these findings, it is imperative to study the localization of nuclear angiotensin II receptors and their role in the regulation of gene transcription and expression of matrix proteins in glomerular mesangial cells. The chapter begins with an outline of the topics covered and ends with an extensive list of references. 10 figures. 1 table. 95 references.
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Diabetic Renal and Related Heart Disease: ACE Inhibitors and/or Angiotensin Receptor Blockers: Does It Matter?. IN: Cortes, P. and Mogensen, C.E., eds. Diabetic Kidney. Totowa, NJ: Humana Press. 2006. pp. 437-452.
This chapter on diabetic renal and related heart disease is from a clinical textbook on the diabetic kidney. After a brief introduction, the authors focus on the role of Angiotension-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). Topics include the use of ACE inhibitors versus beta blockers and diuretics, antihypertensives that may confer an increased risk for the development of new diabetes, strategies to prevent microalbuminuria in diabetes, research studies of the impact of ACE inhibitors and ARBs on renal outcomes and mortality, and the use of ACE inhibitors or ARBs in patients with congestive heart failure. The authors conclude that although any type of blood pressure reduction is important in patients with diabetes, blocking the renin-angiotensin system (RAS) is the most important strategy in both type 1 and type 2 diabetes patients. Both classes of drugs discussed (ACE inhibitors and ARBs) provide the same benefits, preventing progression of renal disease. Regarding heart failure, ACE inhibition is a well-established part of heart failure treatment, but the role of ARBs is not fully determined. The chapter begins with an outline of the topics covered and ends with an extensive list of references. 3 tables. 67 references.
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Disorders of the Adrenal Cortex. IN: Jameson, J.L., ed. Harrison's Endocrinology. Columbus, OH: McGraw Hill. 2006. pp 113-150.
This chapter on disorders of the adrenal cortex is from a textbook that offers a comprehensive, practical look at the field of endocrinology. The adrenal cortex produces three major classes of steroids: glucocorticoids, mineralocorticoids, and adrenal androgens. Thus, normal adrenal function is involved in modulating intermediary metabolism and immune responses; blood pressure, vascular volume, and electrolytes; and secondary sexual characteristics in females. The authors discuss biochemistry and physiology, the laboratory evaluation of adrenocortical function, hyperfunction of the adrenal cortex including Cushing's syndrome and aldosteronism, hypofunction of the adrenal cortex, hypoaldosteronism, and the pharmacologic clinical uses of adrenal steroids. Specific topics covered include steroid nomenclature, the biosynthesis of adrenal steroids, steroid transport, steroid metabolism and excretion, adrenocorticotropic hormone (ACTH) physiology, renin-angiotensin physiology, glucocorticoid physiology, mineralocorticoid physiology, and androgen physiology. The chapter includes full-color illustrations and black-and-white photographs. 11 figures. 11 tables. 16 references.
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Do Oral Contraceptives Pose a Risk to Diabetic Kidneys?. Consultant. 46(1): 14. January 2006.
This brief article considers the interplay of oral contraceptives and kidney complications of diabetes mellitus (diabetic nephropathy). The author first reviews the benefits of certain antihypertensive medications, notably ACE inhibitors and angiotensin receptor blockers (ARBs), for inhibiting the renin-angiotensin system and thus protecting the kidneys. In contrast, oral contraceptives can activate the renin-angiotensin system in healthy women and they might therefore have adverse effects on the kidneys of women with diabetes. The author reports on a study in which macroalbuminuria (protein in the urine) developed in 18 percent of women with diabetes who were on oral contraceptives, compared with 2 percent of nonusers. The author concludes that a large prospective trial is required to determine definitively whether the risk of renal disease is real enough to lead to a change in the way in which oral contraceptives are prescribed for women with diabetes. 3 references.
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Hypertension and the Kidney. Seminars in Nephrology. 25(4): 236-245. July 2005.
Hypertension (high blood pressure) is an important and widely prevalent risk factor for the development of chronic kidney disease (CKD), which can subsequently progress to end stage renal disease (ESRD). This article reviews the impact of hypertension on the kidney, with an emphasis on patients with diabetes mellitus. The authors note that diabetes is another cause of CKD and that aggressive control of hypertension and diabetes is indicated to reduce the risk for kidney disease in the community. The concept of decreasing the systemic blood pressure as well as the intraglomerular (within the kidney) pressure has led to the application of rational treatment options in patients with chronic renal insufficiency (CRI). The authors stress that antihypertensive agents that also block the renin-angiotensin system have been shown to have special renal (kidney) and cardiovascular benefits. Early detection and treatment of microalbuminuria (microscopic protein in the urine) is an important part of disease management. Topics discussed include primary glomerular disease, hypertensive nephrosclerosis, cardiovascular disease risk, nonpharmacologic (lifestyle) treatment strategies, monitoring blood pressure response, and hypertension in patients on hemodialysis. 3 figures. 3 tables. 101 references.
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Hypertension in Hemodialysis. In: Clinical Dialysis. 4th ed. New York, NY: McGraw-Hill. 2005. pp. 755-776.
Hypertension occurs very frequently in chronic kidney disease (CKD) and is nearly universal in patients who reach end stage renal disease (ESRD). This chapter on hypertension in hemodialysis is from a comprehensive textbook on the clinical management of patients on dialysis. The author discusses the etiology of hypertension, rationalizes the measurement of blood pressure (BP), discusses the relationship between BP and adverse outcomes, and outlines the pharmacologic and nonpharmacologic therapies used to control hypertension in this patient population. Specific topics include increased cardiac output due to increased sodium and extracellular fluid volume, the renin-angiotensin system, circulating inhibitors of nitric oxide, the role of erythropoietin, vascular changes as a basis of systolic hypertension, cardiovascular changes in hemodialysis hypertension, sources of error in the measurement of BP in hemodialysis patients, the assessment of interdialytic BP in hemodialysis patients, factors that modify the relationship between BP and mortality, the role of increased frequency and duration of dialysis, and the benefits of treating hypertension. The author calls for immediate quality control and improvement programs to more accurately monitor BP in hemodialysis patients. 6 figures. 204 references.
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Hypertension Treatment Guidelines: Practical Implications. Seminars in Nephrology. 25(4): 198-209. July 2005.
The goal of lowering blood pressure (BP) levels is to prevent or reduce the risk for cardiovascular and renal (kidney) events. This article reviews the major guidelines on blood pressure goals, with an emphasis on their application to patients with kidney disease. Guidelines reviewed include those from the Seventh Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-7), the American Diabetes Association, the European Society of Hypertension, and the Kidney Disease Outcomes Quality Initiative. The goal BP in the majority of patients with hypertension (high blood pressure) should be less than 140/90 mm Hg, with a lower goal of less than 130/80 mm Hg in patients with diabetes or kidney disease. The presence of 1 gram or more of proteinuria (protein in the urine) mandates a BP approaching 115 mm Hg to slow the progression of advanced nephropathy (kidney disease) adequately. Compelling indications also exist for the use of certain antihypertensive agents in the setting of kidney dysfunction, diabetes, heart failure, and coronary artery disease. Initiation with 2 antihypertensive agents should be considered strongly for patients with a BP of more than 20 mm Hg greater than the systolic BP goal. In patients with kidney disease, reaching the BP goal requires multiple agents that should include an appropriate diuretic and an agent that blocks the renin-angiotensin-aldosterone system to slow the progression of kidney disease. 2 figures. 6 tables. 86 references.
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Management of Hypertension in Diabetes. Diabetes Spectrum. 19(1): 25-31. Winter 2005.
Untreated or poorly controlled hypertension (high blood pressure) can significantly accelerate the development and progression of both the microvascular and macrovascular complications of diabetes. This article reviews the recommendations for the management of hypertension in diabetes. The authors discuss the epidemiology and complications of hypertension in diabetes; the effectiveness of hypertension treatment in diabetes, along with recommended goals; diagnostic issues; nonpharmacologic treatment of hypertension in diabetes; drug therapy, including the role of renin-angiotensin-aldosterone axis blockade, diuretics, CCBs, and beta-blockers; and patient management strategies. The authors emphasize that aggressive blood pressure control improves patient outcomes and reduces health care costs. Effective antihypertensive regimens maximize nonpharmacological therapies, minimize adverse effects on glucose control, lessen the risk of medication-related side effects, and provide adequate cardiac and renal protection. One patient care algorithm is included for management of hypertension in diabetes in patients who do not have heart failure and who are not post-myocardial infarction. 1 figure. 1 table. 61 references.
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Prevention of Progression in Diabetic Nephropathy. Diabetes Spectrum. 19(1): 18-24. Winter 2005.
Diabetic nephropathy (kidney disease associated with diabetes) is the most common cause for end-stage renal disease (ESRD) and for patients entering into chronic dialysis care. This article reviews what is known about the major mechanisms and risk factors promoting renal injury in diabetes. The author summarizes the evidence-based recommendations for preventing progression of this problem. Risk factors for diabetic nephropathy include hyperglycemia, hypertension, genetic predisposition, glomerular hyperfiltration, proteinuria, the renal renin-angiotensin system, advanced glycation end-products, and possibly reduced nephron number and lipid disorders. Progression of diabetic kidney injury may be prevented or delayed by tight control of diabetes, blood pressure treatment to systolic pressure of less than 130 mmHg, reduction of proteinuria, and treatment with drugs that inhibit the renin-angiotensin system. The author notes that the protective effect of ACE inhibition or ARB therapy has been shown to be the result of both blood pressure reduction and direct drug effect. 2 tables. 64 references.
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Optimizing Therapy in the Diabetic Patient with Renal Disease: Antihypertensive Treatment. Journal of the American Society of Nephrology. 15(1): S6-S11. January 2004.
Hypertension (high blood pressure), impaired renal (kidney) function, and proteinuria (protein in the urine) are commonly associated to the presence of diabetes. They play a major role in the development of cardiovascular and renal damage. Effective antihypertensive treatment reduces the progression of diabetic nephropathy (kidney disease associated with diabetes) and improves cardiovascular prognosis. This article describes strategies to optimize antihypertensive therapy in the diabetes patient with renal disease. The pharmacologic blockade of the renin-angiotensin-aldosterone system has been shown to convey greater renal and cardiovascular protection compared with other classes of drugs. In particular, studies focusing on renal end point suggest that ACE inhibitors are the first-choice drugs in type 1 diabetes. The authors conclude by noting that to achieve maximal renal and cardiovascular protection, most patients with diabetes require integrated therapeutic intervention, including not only several antihypertensive drugs, but statins and antiplatelet therapy as well. 1 table. 55 references.
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Pathogenesis, Prevention, and Treatment of Diabetic Nephropathy. In: Johnson, R.J. and Feehally, J. Comprehensive Clinical Nephrology. 2nd ed. Orlando, FL: Mosby, Inc. 2003. p. 439-450.
Diabetic nephropathy (kidney disease associated with diabetes mellitus) is the single largest cause of end stage renal (kidney) disease (ESRD) in American and European adults, accounting for over one third of all patients beginning renal replacement therapy (dialysis and transplantation). Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria (protein in the urine). Patients invariably develop associated hypertension (high blood pressure), a progressive increase in proteinuria, and a predictable and relentless decline in glomerular filtration rate (GFR, a measure of kidney function). This chapter on the pathogenesis, prevention, and treatment of diabetic nephropathy is from a comprehensive textbook that covers every clinical condition encountered in nephrology (the study of kidney disease). The authors of this chapter cover genetic and environmental factors, the role of glucose control, the hemodynamic changes in diabetic nephropathy, renal hypertrophy, microalbuminuria and proteinuria, mesangial expansion and nodule formation, tubulointerstitial fibrosis, mechanisms by which hyperglycemia mediates diabetic nephropathy, and the renin-angiotensin system. Prevention and treatment issues discussed include glycemic control in diabetes, antihypertensive therapy, ACE inhibitors, dietary protein intake, lipids, and management strategies for the patient with diabetes. The chapter is clinically focused and extensively illustrated in full color. 9 figures. 3 tables. 47 references.
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Renal and Electrolyte Disorders, Sixth Edition. Philadelphia, PA: Lippincott Williams and Wilkins. 2003. 703 p.
This textbook on renal (kidney) pathophysiology is designed for physicians in training who wish to maintain a current knowledge base and update their clinical skills. The text features clinically focused coverage of kidney pathophysiology. Fifteen chapters cover disorders of water metabolism; renal sodium excretion, edematous disorders, and diuretic use; the pathogenesis and management of metabolic acidosis and alkalosis; the pathogenesis and management of respiratory and mixed acid-base disorders; disorders of potassium metabolism; disorders of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) activity; normal and abnormal magnesium metabolism; disorders of the renin-angiotensin-aldosterone system; the kidney in hypertension (high blood pressure); the pathogenesis, diagnosis, and management of acute renal failure (ARF); the manifestations and pathogenesis of chronic renal failure (CFR); obstructive nephropathy; renal function in pregnancy; proteinuria and the nephrotic syndrome; and the glomerulopathies. Each chapter concludes with a lengthy reference list and the text concludes with a detailed subject index.
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Chronic Renal Diseases: Renoprotective Benefits of Renin Angiotensin System Inhibition. Annals of Internal Medicine. 136(8): 604-615. April 16, 2002.
Progression to renal parenchymal (the body of the kidney organ) damage and end stage renal disease (ESRD), which seems to be largely independent of the initial insult (disease, trauma, toxicity), is the final common pathway for chronic, proteinuric nephropathies (kidney diseases characterized by spill of protein into the urine) in animals and humans. This review article considers the protective benefits for the kidneys of drugs that inhibit the renin-angiotensin system. The authors first describe the progression to ESRD. The key event is enhanced glomerular capillary pressure (high blood pressure in the filtering units of the kidney); this impairs glomerular permeability to proteins and permits excessive amounts of proteins to reach the lumen of the proximal tubule. The secondary process of reabsorption of filtered proteins can contribute to renal interstitial injury by activating intracellular events, including upregulation of the genes encoding vasoactive and inflammatory mediators. Both interstitial inflammation and progression of disease can be controlled by such drugs as angiotensin converting enzyme (ACE) inhibitors, which strengthen the glomerular permeability barrier to proteins and thereby limit proteinuria and filtered protein dependent inflammatory signals. Clinical data strongly suggest that remission can now be achieved in some patients with chronic renal disease. Because of the current lag time between starting treatment and remission, however, a substantial proportion of patients still progress to ESRD before renal function begins to stabilize. The authors conclude that a multimodal approach that centers on reducing or removing all risk factors associated with the progression of renal disease may decrease the time to remission of the disease for most patients with proteinuric nephropathies.
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Clinical Management of Cardiovascular Risk Factors in Diabetes. Caddo, OK: Professional Communications, Inc. 2002. 240 p.
This handbook offers a concise overview of the clinical management of cardiovascular risk factors in diabetes. The handbook includes twelve chapters: epidemiology and the scope of the problem; diabetes in the United States; risk factors for cardiovascular disease in patients with diabetes; pathophysiologic and metabolic interactions between diabetes and cardiovascular disease; the renin-angiotensin-aldosterone system in diabetes; results of hypertension (high blood pressure) treatment trials in patients with diabetes; cardiovascular risk reduction in people with diabetes and hypertension; lipid lowering therapy; antiplatelet therapy; control of diabetes; risk reduction in special populations; and a summary of cardiovascular risk reduction in people with diabetes. Each chapter includes references for suggested additional reading and a subject index concludes the handbook. The handbook is a small size (4 inches by 7 inches), for ease of use.
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Kidney Disease in African Americans: Genetic Considerations. Journal of the National Medical Association. 94(8 Supplement): 16S-27S. August 2002.
African Americans shoulder a disproportionately high burden of kidney disease when compared with white Americans. While environmental factors such as poverty and poor health habits, and the high prevalence of risk factors such as obesity, contribute to the high rate of kidney disease in this population, genetic factors may also contribute. This article reviews the genetic considerations related to kidney disease in African Americans. Studies of polymorphisms in genes encoding the proteins of the renin-angiotensin-aldosterone system have identified alleles that are associated with kidney disease or changes in renal function in some populations. A higher prevalence of such alleles in African Americans may contribute to the increased prevalence of kidney disease. Diabetes mellitus and hypertension (high blood pressure), the main causes of end stage renal disease (ESRD) in the United States, are more prevalent in African Americans. However, no direct links between diabetic or hypertensive kidney disease and any genetic polymorphisms seen in African Americans have been identified. The authors conclude that further research is required to elucidate the genetic components that contribute to the high prevalence of kidney disease in African Americans. 2 figures. 106 references.
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Renin-Angiotensin-Aldosterone System in Diabetes. In: Moser, M. and Sowers, J.R. Clinical Management of Cardiovascular Risk Factors in Diabetes. Caddo, OK: Professional Communications, Inc. 2002. p.61-70.
This chapter on the renin-angiotensin-aldosterone system (RAAS) in diabetes is from a handbook that offers a concise overview of the clinical management of cardiovascular risk factors in diabetes. The RAAS appears to play an important role in the development of hypertension (high blood pressure) in patients with diabetes. RAAS exerts its hypertensive action via stimulation of salt and water retention, increasing vascular tone, and interference with the vasorelaxing action of insulin. Topics include how the RAAS works, the effect of ACE inhibition on insulin resistance and the development of diabetes, ACE inhibitors and vascular health in the diabetes patient with hypertension. 1 figure. 9 references.
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Using ACE Inhibitors Appropriately. American Family Physician. 66(3): 461-468. August 1, 2002.
When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension (high blood pressure that is resistant to regular therapy). Since then, they have been shown to reduce morbidity (related illness) or mortality (death) in congestive heart failure, myocardial infarction (heart attack), diabetes mellitus, chronic renal (kidney) insufficiency, and atherosclerotic cardiovascular disease. Pathologies underlying these conditions are, in part, attributable to the renin-angiotensin-aldosterone system. Angiotensin II contributes to endothelial dysfunction, altered renal hemodynamics, and vascular and cardiac hypertrophy. ACE inhibitors attenuate these effects. Clinical outcomes of ACE inhibition include decreases in myocardial infarction (fatal and nonfatal), reinfarction, angina, stroke, end stage renal disease (ESRD), and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. This article reviews the appropriate use of ACE inhibitors. 1 figure. 2 tables. 31 references.
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Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. 458 p.
With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This textbook offers practicing physicians the day to day practical knowledge about cardiovascular disease and diabetes. The 24 chapters in the book focus on either clinical or basic aspects of diabetes and cardiovascular disease. Part I, pathophysiology, reviews the mechanisms and risk factors for diabetic cardiovascular disease. Specific topics include the effects of insulin on the vascular system, vascular abnormalities in the prediabetic state, diabetes and advanced glycation end products, diabetes and hypertension (high blood pressure), the renin-angiotensin system, diabetes and dyslipidemia (disordered levels of fats in the blood), diabetes and thrombosis (blood clotting), diabetes and atherosclerosis (hardening and narrowing of the arteries), and nitric oxide and its role in diabetes mellitus. Part II focuses on the heart in diabetes mellitus, including coronary artery disease and congestive heart failure, including the preoperative assessment and perioperative management of the surgical patient with diabetes mellitus. Part III, the peripheral vascular system, addresses epidemiology (incidence and prevalence), mechanisms, methods of assessment, and treatment of this macrovascular disease. Specific topics include diabetes and arterial stiffness, methods for assessing large vessel pathophysiology, and peripheral vascular disease in patients with diabetes mellitus. And Part IV reviews the different microvascular effects in individuals with diabetes mellitus, including retinopathy (eye disease), nephropathy (kidney disease), neuropathy (nerve disease), and microcirculation of the diabetic foot. Each chapter includes extensive references and a subject index concludes the text.
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Diabetes and Hypertension: How Low Should You Go and with Which Drugs?. American Journal of Hypertension. 14(5 Part 2): 17S-26S. May 2001.
Diabetes and hypertension (high blood pressure) are the most common causes of end stage renal disease (ESRD) in the United States. This article considers both experimental and clinical studies that have demonstrated the importance of more intensive control of systolic blood pressure (SBP) in delaying the progression of renal (kidney) disease, particularly in diabetic patients with macroproteinuria. Although traditional recommendations have suggested that reducing systolic levels to less than 140 mm Hg is appropriate, there is consistent evidence in clinical trials demonstrating that, in the presence of diabetes, macroproteinuria, and impaired renal function, reducing systolic levels to less than 125 mm Hg will result in a more successful attenuation of the rate of progression of renal disease. In addition, there is convincing evidence demonstrating that blockade of the renin angiotensin system, particularly with ACE inhibitors, results in an improved opportunity to delay progression of renal disease. Despite the advantages of ACE inhibitors, most patients will require three to five medications to achieve optimal levels of goal SBP to attenuate the rate of progression of renal disease. The author even concludes that in patients with diabetes, controlling blood pressure may be a more important predictor of delaying kidney disease (nephropathy) than is intensive glycemic (blood glucose) control. 5 figures. 5 tables. 42 references.
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Effect of Irbesartan on the Development of Diabetic Nephropathy in Patients with Type 2 Diabetes. New England Journal of Medicine. 345(12): 870-877. September 20, 2001.
Microalbuminuria (microscopic protein in the urine) and hypertension (blood pressure) are risk factors for diabetic nephropathy (diabetes associated kidney disease). Blockade of the renin angiotensin system slows the progression to diabetic nephropathy in patients with type 1 diabetes, but similar data are lacking for hypertensive patients with type 2 diabetes. This article reports on a study that evaluated the renoprotective effect of the angiotensin II receptor antagonist irbesartan in hypertensive patients with type 2 diabetes and microalbuminuria. A total of 590 patients were enrolled in the study, at a dose of either 150 milligrams daily or 300 milligrams daily, and were followed for two years. The primary outcome was the time to the onset of diabetic nephropathy, defined by persistent albuminuria in overnight specimens, with a urinary albumin excretion rate that was greater than 200 micrograms per minute and at least 30 percent higher than the baseline level. The baseline characteristics in the three groups were similar. Ten of the 194 patients in the 300 milligram group (5.2 percent) and 19 of the 195 patients in the 150 milligram group (9.7 percent) reached the primary end point, as compared with 30 of the 201 patients in the placebo group (14.9 percent). Serious adverse events were less frequent among the patients treated with irbesartan. The authors conclude that iresartan is renoprotective (protects the kidney) independently of its blood pressure lowering effect in patients with type 2 diabetes and microalbuminuria. 3 figures. 2 tables. 33 references.
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Effect of Irbesartan on the Development of Diabetic Nephropathy in Patients with Type 2 Diabetes. New England Journal of Medicine. 345(12): 870-878. September 20, 2001.
Microalbuminuria (microscopic amounts of protein in the urine) and hypertension (high blood pressure) are risk factors for diabetic nephropathy (kidney disease associated with diabetes mellitus). Blockade of the renin-angiotensin system slows the progression of this disease in patients with type 1 diabetes, but similar data are lacking for hypertensive patients with type 2 diabetes. This article reports on a study undertaken to evaluate the renoprotective (protective of the kidney) effect of the angiotensin II receptor antagonist irbesartan in this population. A total of 590 hypertensive patients with type 2 diabetes and microalbuminuria were enrolled at a dose of either 150 milligrams or 300 milligrams of irbesartan daily, or a placebo; patients were followed for 2 years. Ten of the 194 patients in the 300 milligram group (5.2 percent) and 19 of the 195 patients in the 150 milligram group (9.7 percent) reached the primary endpoint (onset of diabetic nephropathy), as compared with 30 of the 201 patients in the placebo group (14.9 percent). Serious adverse events were less frequent among the patients treated with irbesartan. The authors conclude that irbesartan is renoprotective independently of its blood pressure lowering effect in patients with type 2 diabetes and microalbuminuria. 3 figures. 2 tables. 33 references.
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Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy. New England Journal of Medicine. 345(12): 861-869. September 20, 2001.
Diabetic nephropathy (diabetes associated kidney disease) is the leading cause of end stage renal disease (ESRD). Interruption of the renin angiotensin system slows the progression of renal (kidney) disease in patients with type 1 diabetes, but similar data are not available for patients with type 2, the most common form of diabetes. This article reports on a study that assessed the role of the angiotensin II receptor antagonist losartan in patients with type 2 diabetes and nephropathy. A total of 1,513 patients were enrolled in this randomized, double blind study comparing losartan (50 to 100 milligrams once daily) with placebo, both taken in addition to conventional antihypertensive treatment (calcium channel antagonists, diuretics, alpha blockers, beta blockers, and centrally acting agents) for a mean of 3.4 years. The primary outcome was the composite of a doubling of the baseline serum creatinine concentration, end stage renal disease, or death. Secondary end points included a composite of morbidity (related illness or complications) and mortality from cardiovascular causes, proteinuria, and the rate of progression of renal disease. A total of 327 patients in the losartan group reached the primary end point, as compared with 359 in the placebo group. Losartan reduced the incidence of a doubling of the serum creatinine concentration and end stage renal disease, but had no effect on the rate of death. The benefit exceeded that attributable to changes in blood pressure. The composite of morbidity and mortality from cardiovascular causes was similar in the two groups, although the rate of first hospitalization for heart failure was signficantly lower with losartan. The level of proteinuria (protein in the urine) declined by 35 percent with losartan. The authors conclude that losartan conferred significant renal benefits in patients with type 2 diabetes and nephropathy, and it was generally well tolerated. 3 figure. 3 tables. 34 references.
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Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy. New England Journal of Medicine. 345(12): 861-869. September 20, 2001.
Diabetic nephropathy (kidney disease associated with diabetes mellitus) is the leading cause of end stage renal disease (ESRD). Interruption of the renin-angiotensin system slows the progression of this disease in patients with type 1 diabetes, but similar data are lacking for hypertensive patients with type 2 diabetes. This article reports on a study undertaken to evaluate the renoprotective (protective of the kidney) effect of the angiotensin II receptor antagonist losartan in this population. A total of 1513 patients were enrolled in the study and randomized to 50 to 100 milligrams once daily of losartan, or placebo. Both groups also took conventional antihypertensive treatment for a mean of 3.4 years. The primary outcome was the composite of a doubling of the baseline serum creatinine concentration, ESRD, or death. Secondary end points included a composite of morbidity (illness) and mortality (death) from cardiovascular causes, proteinuria (protein in the urine), and the rate of progression of renal disease. A total of 327 patients in the losartan group reached the primary end point, as compared with 359 in the placebo group. Losartan reduced the incidence of a doubling of the serum creatinine concentration and ESRD, but had no effect on the rate of death. The benefit exceeded that attributed to changes in blood pressure. The authors conclude that losartan conferred significant renal benefits in patients with type 2 diabetes and nephropathy, and it was generally well-tolerated. 3 figures. 3 tables. 34 references.
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Reduction of ACE Activity Is Insufficient to Decrease Microalbuminuria in Normotensive Patients with Type 1 Diabetes. Diabetes Care. 24(5): 919-924. May 2001.
This article describes a study that determined whether the reduction of urinary albumin excretion rate (UAER) in normotensive patients with type 1 diabetes is dependent on changes of blood pressure or if interference with the renin-angiotensin system is sufficient to explain the effects of angiotensin converting enzyme (ACE) inhibition on UAER. The study was conducted in six centers in Sweden. Ramipril was administered double blind at a dose of 1.25 mg to 19 patients and a dose of 5.0 mg to 18 patients and compared with placebo in 18 patients after a single blind placebo period of 1 to 4 weeks. The 55 patients were followed for 2 years. ACE activity and plasma renin activity (PRA) were measured to document an effect on the renin-angiotensin system. In addition, 24 hour ambulatory blood pressure was recorded at baseline and repeated after 1 and 2 years using an ambulatory blood pressure recording device. The study found that both doses of ramipril were sufficient to reduce ACE activity and to increase PRA significantly as compared with placebo. However, neither ambulatory nor clinic blood pressure was affected by either dose of ramipril compared with the placebo group. There was no progression of UAER in the placebo group during the 2 years of the study. Analysis of covariance showed no differences in UAER between the three treatment groups at year 1 or year 2, after adjusting for baseline. Furthermore, there were no statistically significant changes from baseline UAER within any of the three treatment groups. The article concludes that treatment with ramipril did not affect microalbuminuria or clinic or ambulatory blood pressure. On the basis of the present study, researchers question the clinical use of ACE inhibitors in stably normotensive patients with type 1 diabetes and microalbuminuria in whom a concomitant reduction in blood pressure is not demonstrated. 1 figure. 3 tables. 32 references. (AA-M).
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Renin-Angiotensin System in Diabetic Cardiovascular Complications. In: Johnstone, M.T. and Veves, A. Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. p. 103-121.
With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This chapter on the renin-angiotensin system in diabetes cardiovascular complications is from a textbook that offers physicians practical knowledge about cardiovascular disease and diabetes. This chapter is in Part I, which focuses on pathophysiology, including the mechanisms and risk factors for diabetic cardiovascular disease. The author notes that the renin-angiotensin system (RAS) plays an integral role in blood pressure regulation and also exerts a diverse range of direct effects on vascular (blood vessel) homeostasis. The author discusses the effect of RAS inhibition on diabetic vascular complications; the role of the RAS in glycemic control, insulin sensitivity, and diabetes onset; the effect of diabetes on the RAS; and vascular effects of the RAS in diabetes. Existing clinical data indicate that ACE inhibition provides protective effects against cardiovascular outcomes in diabetes patients. These beneficial effects appear to apply to both type 1 and type 2 diabetes. A key question is whether ACE inhibition alleviates some of the vasculopathies specific to diabetes or whether ACE inhibitors primarily affect mechanisms of cardiovascular disease common to both diabetic and nondiabetic patients. 3 figures. 154 references.
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ACE Inhibition or Angiotensin Receptor Blockade: Impact on Potassium in Renal Failure. Kidney International. 58(5): 2084-2092. November 2000.
Inhibition of the renin angiotensin system is known to raise serum potassium (K+) levels in patients with renal insufficiency or diabetes. This study evaluates the comparative effects of an angiotensin converting enzyme (ACE) inhibitor versus an angiotensin receptor blocker (ARB) on the changes in serum K+ in people with renal (kidney) insufficiency. A total of 35 people (21 males and 14 females, 19 African Americans and 16 Caucasians, mean age 56 years plus or minus 2 years) participated in the double crossover study. For the total group serum potassium level changes were not significantly different between the lisinopril (an ACE inhibitor) and valsartan (an ARB) treatments. The subgroup with glomerular filtration rate (a measure of kidney function) values of less than 60 milliliters per minute per 1.73 m-squared who received lisinopril demonstrated significant increases in serum potassium above the mean baseline. This increase in serum potassium was also accompanied by a decrease in plasma aldosterone. The lower GFR group taking valsartan, however, demonstrated a smaller rise in serum potassium; this represents a 43 percent lower value when compared with the change in those who received lisinopril. The authors conclude that, in the presence of renal insufficiency, the ARB valsartan did not raise serum potassium to the same degree as the ACE inhibitor lisinopril. 4 figures. 3 tables. 29 references.
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Angiotensin-Converting Enzyme Inhibitor-Associated Elevations in Serum Creatinine: Is This a Cause for Concern?. Archives of Internal Medicine. 160(5): 685-693. March 13, 2000.
Reducing the actions of the renin angiotensin aldosterone system with angiotensin converting enzyme (ACE) inhibitors slows nephropathy (kidney disease) progression in patients with or without diabetes. This article reports on a study undertaken to determine whether limited initial reduction in either glomerular filtration rate (GFR) or elevation in serum creatinine levels, associated with ACE inhibitor or angiotensin receptor blocker use, results in long term protection against decline in renal (kidney) function in patients with renal insufficiency. The authors reviewed 12 randomized clinical trials that evaluated renal disease progression among patients with preexisting renal insufficiency. Six of these studies were multicenter, double blinded, and placebo controlled, with the remainder being smaller randomized studies with a minimum 2 year followup on renal function. These investigations evaluated patients with and without diabetes or systolic heart failure. Most trials demonstrated that patients with preexisting renal insufficiency manifested an acute fall in GFR, a rise in serum creatinine, or both. Those randomized to an ACE inhibitor with a serum creatinine level of 124 or greater demonstrated a 55 to 75 percent risk reduction in renal disease progression, compared with those with normal renal function randomized to an ACE inhibitor. An inverse correlation was observed between the amount of renal function loss at baseline and the subsequent rate of annual decline in renal function following randomization to an antihypertensive regimen that contained an ACE inhibitor. The authors conclude that in both diabetic and nondiabetic renal disease, if an elevation in serum creatinine occurs within the first 2 months of ACE inhibitor therapy, it stabilizes quickly, does not progressively worsen, and is strongly associated with long term preservation of renal function. Withdrawal of ACE inhibitor use in these patients should occur only when the rise of creatinine exceeds 30 percent above baseline within the first 2 months of ACE inhibitor use, or if hyperkalemia (excessive potassium in the blood) develops. 7 figures. 1 table. 53 references.
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Hypertension in Dialysis Patients. In: Lameire, N. and Mehta, R.L., eds. Complications of Dialysis. New York, NY: Marcel Dekker, Inc. 2000. p. 471-484.
Arterial hypertension (high blood pressure) remains one of the major public health problems of industrialized nations, resulting in a great burden of morbidity (illness), mortality (death), and cost. For patients with end stage renal disease (ESRD), hypertension poses a particular problem, notably contribution to the high rates of cardiovascular disease and mortality experienced by dialysis patients. This chapter on hypertension in hemodialysis (HD) and peritoneal dialysis (PD) patients is from a book that offers a comprehensive, multidisciplinary resource for the nephrologist and caregiver providing dialysis, covering all aspects of dialysis therapies and their complications. In this chapter, the authors review the complicated subject of hypertension management for patients treated with HD or PD. The authors cover the measurement of blood pressure in dialysis patients; target blood pressure values; pathogenesis; the role of sodium and volume excess and the renin angiotensin axis; sympathetic activity; the role of erythropoietin; the role of divalent ions and parathyroid hormone; the vascular endothelium; and outcomes and treatment of hypertension in dialysis patients. Nonmedicinal treatments of hypertension can include aerobic exercise, control of salt and fluid intake, cessation of smoking, weight reduction, and avoidance of alcohol. The authors stress that the approach to the control of hypertension in dialysis patients should be multidisciplinary (medical, nursing, social work, and dietary). The mainstay of therapy for the control of hypertension in dialysis patients is adequate fluid removal. The use of antihypertensive medications is summarized in table format. 7 tables. 127 references.
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Nocturnal Polyuria in Older People: Pathophysiology and Clinical Implications. JAGS. Journal of the American Geriatrics Society. 48(10): 1321-1329. October 2000.
This article reports on a literature review that covered the physiological changes of aging that affect the systems involved in urine formation and that considered how these changes interact with changes in bladder function, thereby leading to the onset of nocturnal polyuria (excessive urination) with associated urinary frequency, nocturia (urinating at night), and incontinence (involuntary loss of urine). Based on this information, the author presents data on the effectiveness of pharmacological interventions (drug therapy) which reduce the rate of urine formation and, thus, can be of benefit in reducing symptoms, especially during the nighttime. Peer reviewed journal articles were identified by MEDLINE search and by review of the literature. As a consequence of age associated diminished renal (kidney) concentrating capacity, diminished sodium conserving ability, loss of the circadian rhythm of antidiuretic hormone secretion, decreased secretion of renin angiotensin aldosterone, and increased secretion of atrial natriuretic hormone, there is an age related alteration in the circadian rhythm of water excretion, leading to increased nighttime urine production in older people. The interaction of nocturnal polyuria with age related diminution in functional bladder volume and detrusor instability results in the symptoms of urinary frequency, nocturia, and, in some persons, incontinence. The additional impact of Alzheimer's disease on these physiological and aging changes, as well as on a diminished perception of bladder fullness, leads to an even greater risk of urinary incontinence in these patients. Treatment of nocturnal polyuria with the antidiuretic hormone analog, DDAVP (desmopressin), can result in decreased nocturnal urine production with improvement in symptoms of frequency, nocturia, and incontinence. 4 tables. 104 references.
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Vascular Effects of Erythropoietin and Anemia Correction. Seminars in Nephrology. 20(4): 356-363. July 2000.
Since its introduction for clinical use a decade ago, recombinant human erythropoietin (rHuEPO) has revolutionized the management of the anemia of end stage renal disease (ESRD). Soon after its release, it became evident that the biological targets of rHuEPO were not limited to the erythroid progenitor cells. Instead, numerous clinical and laboratory studies have shown the modulatory action of rHuEPO on a wide array of cell types and organ systems. This article provides an overview of the modulatory actions of rHuEPO on the production and action of vasoregulatory factors and its direct and indirect effects on vascular function and structure. Chronic rHuEPO administration can result in a hematocrit (red blood cell) independent rise in arterial blood pressure in humans and in experimental animals with CRF (chronic renal failure). This is associated with and, in part, mediated by up regulation of the tissue renin angiotensin system, increased ET 1 production, enhanced generation of vasoconstrictive and depressed production of vasodilatory prostaglandins, elevation of cytosolic and induction of NO resistance. In addition, in vitro studies point to stimulation of vascular cell growth by rHuEPO. Thus, rHuEPO exerts a broad modulatory action on various vasoregulatory factors in a manner favoring a rise in arterial blood pressure. 59 references.
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