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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension. Since then, they have been shown to reduce morbidity or mortality in congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal 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, and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. (Am Fam Physician 2002;66:473.)
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PMID:Using ACE inhibitors appropriately. 1248 85

Secondary hyperparathyroidism (SHPT) is an important complication of end-stage renal disease. However, SHPT begins during earlier stages of chronic renal insufficiency (CRI), and little is known about risk factors for SHPT in this population. This study evaluated 218 patients in an ethnically diverse ambulatory nephrology practice at the University of California San Francisco during calendar years 1999 and 2000. Demographic data, comorbid diseases, medications, and laboratory parameters were collected, and independent correlates of intact parathyroid hormone (PTH) were identified by using multiple linear regression. The mean estimated GFR was 34 ml/min per 1.73 m(2) (10%-90% range, 13 to 61 ml/min per 1.73 m(2)); PTH was inversely related to GFR (P < 0.0001). The adjusted mean PTH was higher among African Americans and lower among Asian/Pacific Islanders compared with white patients (233 versus 95 versus 139 pg/ml; P < 0.0001). Moreover, among the 196 patients with GFR <60 ml/min per 1.73 m(2), the slope of GFR versus PTH was significantly steeper among African Americans than among white patients (10.6 versus 3.9 pg/ml per ml per min per 1.73 m(2); P = 0.01). After adjusting for age and diabetes, PTH was associated with a history of myocardial infarction (OR, 1.6; 95% CI, 1.1 to 2.3 per unit natural log PTH) and congestive heart failure (OR, 2.0; 95% CI, 1.3 to 2.9 per unit natural log PTH) and not associated with other co-morbid conditions. These factors should be considered when screening and managing SHPT in CRI.
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PMID:The severity of secondary hyperparathyroidism in chronic renal insufficiency is GFR-dependent, race-dependent, and associated with cardiovascular disease. 1239 47

Radiocontrast-induced nephropathy develops in approximately 10% to 20% of patients following administration of iodine-based dye and is one of the most prognostically detrimental complications that invasive cardiologists and radiologists encounter. Preexisting renal dysfunction and diabetes mellitus are two of the most powerful predictors of the likelihood of developing acute renal insufficiency after contrast delivery. To date, only adequate preprocedural hydration and postprocedural hydration to offset dehydration from contrast-induced diuresis have been shown to be effective in preventing this condition. Fenoldopam mesylate, a systemic vasodilator currently FDA-approved for short-term, in-hospital management of severe hypertension, has been shown to increase renal plasma flow in patients with and without chronic renal insufficiency. As a selective agonist of the dopamine-1 receptor, fenoldopam may preserve outer medullary renal blood flow and thereby attenuate radiocontrast-induced nephropathy. Small studies with fenoldopam prior to iodine-based dye administration have demonstrated low rates of radiocontrast nephropathy, and a larger, randomized trial has found that renal blood flow 1 hour after angiography rose in the fenoldopam group compared to a decline in the placebo group. The CONTRAST study has been designed to determine whether fenoldopam is indeed effective in diminishing the occurrence of radiocontrast-induced nephropathy.
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PMID:Design and rationale of CONTRAST--a prospective, randomized, placebo-controlled trial of fenoldopam mesylate for the prevention of radiocontrast nephropathy. 1243 66

A case of acquired reactive perforating collagenosis is reported in a 57-year-old Thai woman, with a history of diabetes mellitus, chronic renal insufficiency needing hemodialysis, and dry gangrene of the right fourth toe. Physical examination revealed multiple scattered erythematous hyperkeratotic nodules and plaques and some showed ulceration. Histopathology showed vertical strands of collagen perforating from the ulcerated lesions. The authors also reviewed the literature on this subject.
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PMID:Acquired reactive perforating collagenosis: report of a case and review of the literature. 1245 82

The coexistence of hypertension increases cardiovascular risks and the rate of deterioration of renal function for diabetic patients. For patients with left ventricular hypertrophy (LVH), the use of an angiotensin converting enzyme (ACE) inhibitor is known to be effective and well tolerated and to be protective against chronic renal insufficiency (CRI). However, serious adverse reactions to ACE inhibitors, such as the rapid deterioration of renal function, have been reported, making physicians hesitant to use these agents. To resolve this dilemma, we compared changes in renal function and left ventricular function and the safety and effectiveness of benazepril, an ACE inhibitor, in patients with diabetic nephropathy, with or without LVH. The age, sex, duration of diabetes, levels of blood pressure and blood glucose and rates of creatinine clearance (CrCl) were compared between 36 diabetic patients with LVH and 36 matched diabetic patients without LVH. The rates of CrCl in all patients were between 14 and 35 ml/min, and all patients received an ACE inhibitor before enrollment. The group comprised 43 men and 29 women, with a mean age of 56 +/- 4 years. These patients were divided into three groups, each of which was subdivided into a group with and a group without LVH. Group I (without LVH) or I-L (with LVH) received a half dose of benazepril (2.5 mg daily), Group II (without LVH) or II-L (with LVH) received a normal daily dose of 5 mg benazepril, and Group III (without LVH) or III-L (with LVH) discontinued the administration of the ACE inhibitor. The follow-up period was 1 year and, during the study, blood pressure was maintained at less than 140/90 mmHg. If the blood pressure control was not satisfactory, benidipine, a calcium antagonist, and/or furosemide, a loop diuretic, and/or guanabenz, a central acting antihypertensive agent, were administered. In the diabetic patients with LVH, the administration of a normal dose of benazepril inhibited the decline of renal function and cardiac function (CrCl: 24.2 +/- 1.5 to 22.0 +/- 2.5 ml/min; EF (ejection fraction): 56 +/- 3 to 54 +/- 6%) compared to the other two groups. In patients without LVH, a half dose of benazepril preserved renal function (23.4 +/- 2.6 to 22.0 +/- 3.1 ml/min; EF: 54 +/- 3 to 56 +/- 3%). Discontinuation of the administration of ACE inhibitor led to the further progression of renal dysfunction and decreases in EF in patients with or without LVH. Our results provide some indications for the use of ACE inhibitors in diabetic patients when renal dysfunction and/or cardiac hypertrophy are present.
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PMID:Selection of the dose of angiotensin converting enzyme inhibitor for patients with diabetic nephropathy depends on the presence or absence of left ventricular hypertrophy. 1248 10

Traditionally, the term complex hypertension has been applied to patients who have clinical evidence of target organ damage. However, this definition can be expanded to include many hypertensive patients who either present without manifest disease but harbor silent concomitant organ damage, or belong to a high-risk group and are likely to develop such damage. Thus, the number of patients who deserve special consideration as complex patients is considerable. Various factors may contribute toward classifying a patient as having complex hypertension. These include severe hypertension, concomitant conditions such as diabetes, chronic renal insufficiency, coronary artery disease, orcongestive heart failure; and high-risk populations such as the elderly and African Americans. Recent evidence demonstrates that aggressive goal blood pressure (BP)-lowering therapy is the key toward halting the progression of vascular disease. Although the choice of initial therapy seems less important than achieving goal BP, the drug selected must impart efficacy, organ protection, and tolerability. Combination therapy consisting of calcium-channel blockers and angiotensin-converting enzyme inhibitors seems to achieve these desirable effects. Several clinical trials have demonstrated these agents to have favorable effects on BP and organ protection even in complex hypertension, particularly when used in combination.
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PMID:Getting to goal in complex patients. 1262 19

The clinical-and-biochemical signs of the dialysis amyloidosis syndrome were studied in two groups of patients with chronic renal insufficiency (CRI), who have been undergoing a multi-year renal-substitutive therapy (program-type hemodialysis). The first group comprised 77 adult patients (aged 18-40), the second group comprised 49 "elderly" patients (aged 55-73). Apart from the standard analyses, the dynamics of beta 2-microglobulin (beta 2-M) was studied in the blood of patients. Specific features in the development of the syndrome of dialysis amyloidosis were described; they correlated with the level of beta 2-M, with a duration of program-type hemodialysis, with the elderly age of patients, with variants of renal pathologies, and with an concomitant diabetes mellitus.
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PMID:[Dialysis amyloidosis syndrome in patients aged over 55 years and undergoing a hemodialysis program]. 1268 13

Cardiovascular (CV) disease in uremic patients is a major concern to the nephrologist because it represents the main cause of morbidity and mortality in chronic renal failure patients, both predialysis and while on dialysis therapy. CV mortality is 3 to 20 times higher in dialysis patients than in the general population at similar age. Of note, a high prevalence of CV comorbidity is already present at start of maintenance dialysis, and is predictive of subsequent mortality on dialysis. CV disease progresses over years prior to the onset of ESRD, because risk factors develop from the early stage of chronic renal insufficiency. However, CV disease may be prevented or attenuated in patients who benefit from early, regular care of CV risk factors. Mechanisms of uremic cardiopathy, the major cause of mortality in uremic patients, are multifactorial and their effects are cumulative. Risk factors for left ventricular hypertrophy are hypertension, anemia, fluid overload and arteriosclosis, all of which are amendable by therapy. Risk factors for accelerated atherosclerosis, responsible for ischemic cardiopathy and myocardial infarction, are both common factors (e.g., hypertension, tobacco smoking and diabetes) and factors more specific for the uremic state (e.g., dyslipidemia, hyperhomocysteinemia and oxidative stress), all of which also are amendable by proper therapy. As a result, mixed hypertensive and ischemic cardiomyopathy develops, ultimately leading to cardiac failure, together with accidents resulting from valvular and arterial calcifications (favored by calcium-phosphate disorders), and from occlusion of coronary, cerebral and peripheral arteries. Cardioprotective therapy thus has become a cornerstone in the management of chronic renal failure patients, in conjunction with renoprotective therapy. Cardioprotective strategy involves optimal treatment of hypertension, anemia, fluid overload, dyslipidemia, hyperhomocysteinemia and calcium-phosphate disorders, and smoking cessation. To achieve a maximal efficacy, such treatment has to be initiated as early as possible in the course of renal failure. Because of its complexity, the integrated combined nephrotective and cardioprotective therapy requires early and sustained guidance by a nephrologist throughout the whole predialysis period.
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PMID:[Cardioprotection: an essential component for predialysis chronic renal failure treatment]. 1272 13

Contrast-induced nephropathy is one of the adverse events of diagnostic and therapeutic intravascular application of contrast agent. In general, the condition was defined as an increase in the serum creatinine concentration of more than 44 mmol/l or of more than 25% within 48 hours after the contrast agent administration. Other cause of creatinine increase should be excluded. Contrast-induced nephropathy has been reported to be the third leading cause of acute nephropathy in hospitalized patients, occurring at a rate of 1-6% in unselected population and of 30-50% in high-risk patients. One year mortality can be as high as 45% in high-risk patient population. The most important risk factors are chronic renal insufficiency, diabetes mellitus and high volume of contrast agent. Clinical presentation is mostly asymptomatic, but in some patients acute renal failure with necessity of hemodialysis can occur. Prevention is underlying tool in reducing of contrast-induced nephropathy incidence. It is based on the identification of risk patients, stop of medication which can increase risk of contrast-induced nephropathy and proper hydratation of patients before, during and after the contrast agent administration. In high-risk patients, non-ionic and low-osmolarity contrast agent should be used. Several clinical studies testing different drugs to prevent contrast-induced nephropathy were performed, but no convincing result has been found. Promising substancies are N-acetylcysteine and fenoldopam.
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PMID:[Contrast nephropathy and its prevention]. 1272 80

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.
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PMID:[Atherosclerosis and uremia: signifance of non-traditional risk factors]. 1277 74


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