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Your search term(s) "Renin Angiotensin" returned 34 results.

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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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