UMLS:C0011881 - FACTA Search

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Query: UMLS:C0011881 (diabetic nephropathy)
10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking has adverse effects on health causing ischemic heart disease, stroke, chronic obstructive lung disease and cancers of the respiratory and upper digestive tract, pancreas, kidney and urinary tract. Smoking causes an acute increase in mean arterial pressure and heart rate mediated by catecholamines and beta-adrenergic mechanisms. Chronic cigarette smoking reduces renal plasma flow, probably increasing synthesis of the vasoconstrictor endothelin and reducing generation of the vasodilatory endothelial nitric oxide. There is clinical evidence that cigarette smoking has important adverse effects on renal outcome in primary hypertension, diabetic nephropathy, primary glomerular diseases, systemic diseases involving the kidney and in patients on chronic hemodialysis, or after renal transplantation.
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PMID:Cigarette smoking and kidney involvement. 1128 41

The number of patients who needs for dialysis therapy is increasing rapidly among the older population. Although control of hypertension can delay or arrest the progression of renal failure, there are lacking of studies about antihypertensive treatment of chronic renal failure in the elderly. We have studied the effects of treating hypertension with a calcium antagonist, benidipine, on renal function and blood pressure in 58 patients (mean age: 71 +/- 9) with hypertension and chronic renal insufficiency (the levels of creatinine ranging from 1.5 to 4.0 mg/dl). The underlying disease included glomerulopathies (in 33), diabetic nephropathy (in 15), and other causes (in 10). Forty two patients who had been treated with other antihypertensive drugs other than angiotensin converting enzyme (ACE) inhibitors, antihypertensive drugs were withdrawn 2 weeks before the entry. At the entry, patients should have sitting systolic blood pressure (SBP) of above 160 mmHg and diastolic blood pressure (DBP) of above 90 mmHg. In total, both SBP and DBP decreased from 169/95+/-12.5/8.9 to 148/81+/-16.1/8.0 mmHg (p<0.001) with remaining the serum creatinine levels from 2.2+/-0.8 vs 2.4+/-1.3 mg/dl (P>0.05). Retrospective analysis revealed that in 4 of 4 patients treated with benidipine and 2 of 3 patients with benidipine and ACE inhibitors with systolic blood pressure more than 160 mmHg at the end of the study, the levels of serum creatinine increased from 2.5+/-0.3 to 2.8+/-0.4 with significance (P<0.05). If systolic blood pressure was reduced less than 159 mmHg, 38 of 48 patients did not show any deterioration of renal function. Compared to the significance of SBP in preserving renal function, DBP did not associate with the changes in renal function. No patients died during the study. One patient had transient ischemic attack and one patient had stroke in benidipine treated group. One patient had angina pectoris in benidipine-ACE inhibitors treated group. The results of our trial seem to give some support for the idea that long-acting calcium antagonists such as benidipine are renoprotective through reduction of SBP in the elderly people with hypertension and chronic renal insufficiency. However, if systolic blood pressure was not reduced below 160 mmHg throughout a year, the substantial declines in renal function would be expected.
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PMID:Effects of calcium antagonist, benidipine, on the progression of chronic renal failure in the elderly: a 1-year follow-up. 1133 86

Diabetic nephropathy is a leading cause of end-stage renal disease, and its prevalence and incidence vary greatly from country to country, being highest in the United States and Japan. In the United States, diabetic nephropathy accounts for approximately 40% of patients beginning renal replacement therapy. Type 2 diabetes is the largest and fastest-growing single disease that requires dialytic therapy. Most patients succumb to cardiovascular causes, including coronary artery disease and myocardial infarction, sudden death, cardiac failure, and stroke. The survival from cardiovascular complications is relatively better in East Asian countries and to a lesser extent in Mediterranean countries compared with countries that traditionally have higher cardiovascular death rates. Peripheral vascular disease and sepsis contribute to increased morbidity and mortality. Amputation of limbs secondary to peripheral vascular disease in particular has adverse effects on rehabilitation. Asymptomatic hypoglycemia may develop in hemodialysis patients. Such hypoglycemia is not associated with a hormonal balance but is postulated to be due to blunted hormonal response to hypoglycemia. Diabetic muscle infarction is another rare complication attributable to diabetic microangiopathy; magnetic resonance imaging may help in the diagnosis. Risk factors for increased mortality include advanced age, poor glycemic control before starting dialysis, smoking, left ventricular hypertrophy, hypoalbuminemia, and neuropathy, in particular, autonomic dysfunction. In addition to adequate dialysis, it is advisable to achieve tight blood pressure control (at least <140/90 mm Hg and preferably much lower), better blood glucose control (hemoglobin A(1c), <7%), correction of nutritional status, and appropriate foot care.
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PMID:Hemodialysis in diabetic patients. 1157 54

Diabetes is a major risk factor for cardiovascular events. Indeed, people with diabetes are 2-4 times more likely to die from cardiovascular causes than individuals without diabetes. Despite evidence to suggest that the burden of cardiovascular disease may be decreasing in Western populations, this trend has not been repeated in diabetic populations. Diabetes is also the most common cause of new-onset end-stage renal disease, blindness and amputations. The growing incidence of diabetes throughout the world, particularly in developing nations, suggests that diabetes-related cardiovascular disease and other chronic cardiovascular diseases will constitute a serious global threat to health and well-being. The HOPE (Heart Outcomes Prevention Evaluation) study was designed to determine if the angiotensin converting enzyme (ACE) inhibitor, ramipril, prevents cardiovascular events in high risk patients. As people with diabetes have a high risk of such events, this group was specified for inclusion and analysis in the HOPE study. The HOPE study was designed to include up to 4,000 people with diabetes and was designed with high power to detect an 18% risk reduction in the diabetic sub group alone. A total of 3,577 individuals with diabetes were randomised to receive either 10 mg of ramipril or placebo. After a period of 4.5 years of follow-up, the group of patients receiving ramipril had a statistically and clinically significant risk reduction of 25% in the primary outcome of myocardial infarction (MI), stroke or cardiovascular (CV) death. This comprises a 37% risk reduction in CV death, a 22% risk reduction in MI, a 33% reduction in stroke and a 24% reduction in all-cause mortality. The MICRO-HOPE (Microalbuminuria, Cardiovascular, and Renal Outcomes) sub study assessed the effect of ramipril on diabetic nephropathy. This was detected by a centrally measured urine albumin:creatinine ratio and confirmed by timed urine collection. Ramipril significantly reduced the risk of overt nephropathy by 22% (P = 0.045), and overt nephropathy, laser therapy or dialysis by 15% (P = 0.05). ACE inhibition with ramipril represents a new macrovascular and microvascular preventive therapy for people with diabetes.
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PMID:Diabetes and the HOPE study: implications for macrovascular and microvascular disease. 1171 57

Platelet glycoprotein receptors play a role in the pathogenesis of chronic diabetic complications. Genetic polymorphisms of the alpha2beta1 integrin and glycoprotein IIIa (GPIIIa) have been associated with myocardial infarction, stroke, and diabetic retinopathy. To identify risk factors for their development in a cohort of patients with type 2 diabetes, we evaluated clinical variables and genetic polymorphisms in the alpha2beta1 integrin and GPIIIa genes. Two hundred thirty-four subjects with type 2 diabetes (126 patients with and 108 patients without diabetic nephropathy), as well as 217 nondiabetic healthy subjects, were recruited for this study. Clinical factors for investigation included sex, age at diagnosis, duration of diabetes, body mass index (BMI), and fasting plasma glucose, hemoglobin A(1c) (HbA(1c)), total cholesterol, and triglyceride levels. Genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism analyses. No difference in the Bgl II polymorphism of the alpha2beta1 integrin gene was found between patients with type 2 diabetes with or without nephropathy (11 [8.7%], 47 [37.3%], and 68 patients [54.0%] versus 10 [9.3%], 32 [29.6%], and 66 patients [61.1%] for Bgl II+/+, Bgl II+/-, and Bgl II-/-, respectively; P = 0.271). Multiple logistic regression analyses showed that duration of diabetes, BMI, hypertension, and poor glycemic control were four independent predictors for the development of diabetic nephropathy. No contribution of the Bgl II+ allele of the alpha2beta1 integrin was found for the risk for nephropathy (odds ratio, 1.258; 95% confidence interval, 0.655 to 2.418; P = 0.490). The Pl(A2) allele genotype was not found among our studied subjects. In conclusion, age, duration of diabetes, BMI, and HbA(1c) level are strong predictors for nephropathy in patients with type 2 diabetes. However, the Bgl II polymorphism of the alpha2beta1 integrin gene and the Apa I polymorphism of the platelet GPIIIa gene do not have a major role in the development of diabetic nephropathy in our population.
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PMID:Platelet collagen receptor alpha2beta1 integrin and glycoprotein IIIa Pl(A1/A2) polymorphisms are not associated with nephropathy in type 2 diabetes. 1172 49

The rising incidence of stroke, congestive heart failure (CHF) and end stage renal disease (ESRD) has signalled a need to increase awareness, treatment and control of hypertension. There continues to be a need for effective antihypertensive medications since hypertension is a major precursor to various forms of cardiovascular disease. The renin-angiotensin (AT) aldosterone system (RAAS) is a key component to the development of hypertension and can be one target of drug therapy. Angotensin II (ATII) receptor blockers (ARBs) are the most recent class of agents available to treat hypertension, which work by by inhibiting ATII at the receptor level. Currently, national consensus guidelines recommend that ARBs should be reserved for hypertensive patients who cannot tolerate angiotensin converting enzyme (ACE) inhibitors (ACEIs). ARBs, however, are moving to the forefront of therapy with a promising role in the area of renoprotection and CHF. Recent trials such as the The Renoprotective Effect of the Angiotensin-Receptor Antagonist Irbesartan in Patients with Nephropathy Due to Type 2 Diabetes Trial (IDNT), the Effect of Irbesartan on the Development of Diabetic Nephropathy in Patients with Type 2 Diabetes (IRMA2), and The Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy (RENAAL) study have demonstrated the renoprotective effects of ARBs in patients with Type 2 diabetes. The Valsartan Heart Failure Trial (Val-HeFT) adds to the growing body of evidence that ARBs may improve morbidity and mortality in CHF patients. As a class, ARBs are well tolerated and have a lower incidence of cough and angioedema compared to ACEIs. This article reviews the differences among the ARBs, existing efficacy data in hypertension, and explores the role of ARBs in CHF and renal disease.
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PMID:Angiotensin II receptor blockers for the treatment of hypertension. 1182 17

Last year, in 2001, the results of several major clinical trials have been published, concerning hypertensive patients with type 2 diabetes (IRMA, RENAAL and IDNT studies) and patients with previous strokes. Angiotensin II antagonists (irbesartan and losartan) are able to reduce the rate of progression of diabetic nephropathy in hypertensive patients with type 2 diabetes. This preventive effect occurs independently of the stage of renal dysfunction (early stage in IRMA, patent nephropathy in RENAAL and advanced nephropathy in IDNT). The PROGRESS study shows that the decrease in blood pressure, in response to an ACE inhibitor/diuretic bitherapy (perindopril/indapamide), in patients with previous minor stroke or transient ischaemic attack, reduces significantly the risk of recurrent stroke.
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PMID:[The best of 2001. Arterial hypertension]. 1190 4

Imidapril hydrochloride (imidapril) is a long-acting, non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, which has been used clinically in the treatment of hypertension, chronic congestive heart failure (CHF), acute myocardial infarction (AMI), and diabetic nephropathy. It has the unique advantage over other ACE inhibitors in causing a lower incidence of dry cough. After oral administration, imidapril is rapidly converted in the liver to its active metabolite imidaprilat. The plasma levels of imidaprilat gradually increase in proportion to the dose, and decline slowly. The time to reach the maximum plasma concentration (T(max)) is 2.0 h for imidapril and 9.3 h for imidaprilat. The elimination half-lives (t(1/2)) of imidapril and imidaprilat is 1.7 and 14.8 h, respectively. Imidapril and its metabolites are excreted chiefly in the urine. As an ACE inhibitor, imidaprilat is as potent as enalaprilat, an active metabolite of enalapril, and about twice as potent as captopril. In patients with hypertension, blood pressure was still decreased at 24 h after imidapril administration. The antihypertensive effect of imidapril was dose-dependent. The maximal reduction of blood pressure and plasma ACE was achieved with imidapril, 10 mg once daily, and the additional effect was not prominent with higher doses. When administered to patients with AMI, imidapril improved left ventricular ejection fraction and reduced plasma brain natriuretic peptide (BNP) levels. In patients with mild-to-moderate CHF [New York Heart Association (NYHA) functional class II-III], imidapril increased exercise time and physical working capacity and decreased plasma atrial natriuretic peptide (ANP) and BNP levels in a dose-related manner. In patients with diabetic nephropathy, imidapril decreased urinary albumin excretion. Interestingly, imidapril improved asymptomatic dysphagia in patients with a history of stroke. In the same patients it increased serum substance P levels, while the angiotensin II receptor antagonist losartan was ineffective. These studies indicate that imidapril is a versatile ACE inhibitor. In addition to its effectiveness in the treatment of hypertension, CHF, and AMI, imidapril has beneficial effects in the treatment of diabetic nephropathy and asymptomatic dysphagia. Good tissue penetration and inhibition of tissue ACE by imidapril contributes to its effectiveness in preventing cardiovascular complications of hypertension. The major advantages of imidapril are its activity in the treatment of various cardiovascular diseases and lower incidence of cough compared with some of the older ACE inhibitors.
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PMID:Protection of the cardiovascular system by imidapril, a versatile angiotensin-converting enzyme inhibitor. 1217 88

Angiotensin II not only is a vasoconstrictor, but it also affects cell growth and apoptosis, inflammation, fibrosis, and coagulation. Blockade of the renin-angiotensin system, either with inhibitors of the generation of angiotensin (angiotensin-converting enzyme [ACE] inhibitors) or with blockers of angiotensin receptors, reduces blood pressure and inhibits other pathophysiological actions. These other effects provide benefits in coronary heart disease, heart failure, diabetic nephropathy, and stroke beyond blood pressure reduction. These benefits were first demonstrated with ACE inhibitors. However, the mechanism of action of angiotensin receptor blockers, which block angiotensin II stimulation at the angiotensin type 1 receptor but not at the type 2 receptor, may have advantages, particularly for endothelial dysfunction and vascular remodeling, as well as cardiac and renal protection. Recent multicenter trials suggest that ACE inhibitors and angiotensin receptor blockers may reduce morbidity and mortality associated with cardiovascular and renal disease beyond blood pressure reduction. Several studies with different angiotensin receptor blockers, including comparisons with ACE inhibitors, are under way, and should provide further guidance for their clinical use.
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PMID:Vascular and cardiac benefits of angiotensin receptor blockers. 1240 36

Albuminuria has long been recognized as a harbinger for the progression of diabetic nephropathy. Recently, it has become increasingly recognized that albuminuria is a powerful risk factor for cardiovascular disease and stroke. In this article we explore evidence for albuminuria being an integral component of the cardiometabolic syndrome and a risk factor for cardiovascular disease and stroke.
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PMID:Microalbuminuria in diabetes: focus on cardiovascular and renal risk reduction. 1264 82

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