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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incidence of chronic renal failure has a worldwide tendency to growth. Hypertension occupies an important place among causes of this upward trend. That is why in patients with hypertension and incipient changes of the kidneys it seems most appropriate to use antihypertensive drugs with renoprotective properties. Early treatment with these drugs enables most effective lowering of risk of renal failure development and thus has a potential to prolong life of a patient. Selective microproteinuria is considered to be a marker of incipient renal impairement. Among groups of antihypertensive agents angiotensin converting enzyme inhibitors, angiotensin receptor blockers, calcium antagonists, beta-blockers, and diuretics have proven renoprotective properties.
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PMID:[Selective microproteinuria as a marker of incipient renal impairment in patients with hypertension]. 1547 95

Blockade of the renin-angiotensin system improves morbidity and mortality of patients with cardiovascular diseases, e.g. arterial hypertension, renal failure, following myocardial infarction and in congestive heart failure. The angiotensin II type 1 (AT(1)) receptor antagonists (angiotensin receptor blockers; ARBs), i.e. losartan, eprosartan, irbesartan and valsartan were developed by computer-based molecule design. Early observations already indicate that the ARBs elicit pleiotropic effects developing anti-aggregatory, anti-inflammatory and anti-mitogenic effects independent from their actions at the AT(1) receptor. Losartan metabolism indicates a number of known active intermediates and pointed to further interactions of these derivatives with other receptors and cellular signaling systems. Here we discuss a compilation of detailed pharmacokinetic and pharmacodynamic data of active metabolites of ARBs indicating their mode of action and suggest novel therapeutic implications. The clinical observations that ARBs elicit potencies in patients with cardiovascular diseases via the regulation of inflammatory, growth and homeostatic factors lead us to focus on specific, reactive metabolites, which hold potential for future indications and possible drug interactions in cardiovascular diseases.
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PMID:Therapeutic effects of angiotensin (AT1) receptor antagonists: potential contribution of mechanisms other than AT1 receptor blockade. 1555 21

Through an integrative understanding of cardiovascular pathophysiologic characteristics at the multiorgan level, significant achievements in cardiovascular therapeutics have been achieved and enabled the rationale design and development of drugs such as the angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). In this article, we present a detailed review of the physiologic features of the renin-angiotensin-aldosterone system (RAAS), ACE inhibitors and ARB clinical pharmacologic characteristics, and specific diseases in which they are considered to be the standard of the care as supported by important clinical trial data. It is envisioned that an updated and detailed understanding of ACE inhibitors and ARBs will facilitate their successful use in the treatment of heart failure, myocardial infarction, hypertension, renal failure, and diabetic nephropathy.
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PMID:The clinical use of angiotensin-converting enzyme inhibitors. 1558 52

Poorly controlled hypertension is a major risk for cardiovascular morbidity and mortality, strokes, heart failure and renal failure. Despite these devastating complications, blood pressure control of </=140/90 mmHg, which is above the current standard, is very poor worldwide, accounting for 34% of hypertensive patients in the United States, and 6% in other countries. The reasons for this poor control of blood pressure include lack of aggressive treatment by physicians, especially for the systolic blood pressure, drug selection and patient compliance. The blood pressure follows a circadian rhythm and is the highest between 0600 to 1200 h, when most complications occur. Long-acting drugs that extend their action to cover this vulnerable period are preferable, especially those that block the renin-angiotensin-aldosterone system, such as ACE inhibitors and angiotensin receptor blockers, and are the most effective in controlling blood pressure and preventing or reducing its cardiovascular and renal complications. With respect to the angiotensin receptor blockers, telmisartan has been demonstrated by several studies to be the longest acting among its class of drugs and to effectively prevent the early morning rise of blood pressure.
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PMID:Current status of angiotensin receptor blockers for the treatment of cardiovascular diseases: focus on telmisartan. 1566 Jan 22

High blood pressure plays a key role in the progression of renal failure. Hypertension is a common presentation of kidney disease and an almost invariable accompaniment of renal failure. Hypertension is also a major contributor to cardiovascular disease, the major cause of morbidity and mortality in renal failure. Hypertension is both cause and consequence of renal failure, but the precise nature and prevalence of hypertensive nephrosclerosis as a cause of renal failure remains controversial. There is strong evidence that hypertension accelerates the progression of experimental renal disease and that control of blood pressure is effective in preventing this progression. Hypertension, both accelerated and "benign" (a misnomer), has long been recognised as a poor prognostic feature in human renal disease and more recently in renal allograft survival. Blood pressure control is very effective in retarding renal disease progression. There are compelling indications for angiotensin-converting enzyme inhibitors in both non-diabetic and type 1 diabetic nephropathies, and for angiotensin receptor blockers in type 2 diabetic nephropathy. Most patients will require combination drug therapy to control blood pressure and reduce both progression of renal failure and the associated cardiovascular morbidity and mortality.
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PMID:Progression of renal failure -- the role of hypertension. 1572 14

Since recent studies demonstrated an impaired outcome after percutaneous coronary interventions (PCI) in patients with chronic renal failure but did not address the aetiology of renal failure, we now analysed the outcome of patients with diabetic nephropathy in 721 consecutive patients undergoing PCI. Diabetic nephropathy was present in 37 patients (5.1%), and diabetes alone in 126 patients (17.5%); 178 patients (24.7%) suffered from renal insufficiency of other causes; the other 380 patients (52.7%) were used as controls. Although angiographic success rates were similar in the subgroups (94-97%), 30-day and long-term mortality after 4 years was significantly higher in patients with diabetic nephropathy (8.1 and 27%, respectively) than in diabetics (1.6 and 8.7%, respectively), patients with renal insufficiency (3.9 and 16.8%, respectively), or controls (2.4 and 5.0%, respectively, each p<0.001, log-rank test). Treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with a marked decrease in 2-year mortality in patients with diabetic nephropathy (19.4 vs. 33.3%, respectively, p=0.02, log-rank test).
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PMID:Diabetic nephropathy, percutaneous coronary interventions, and blockade of the renin-angiotensin system. 1594 80

Increasing number of diabetic patients develop different stages of renal failure. However, often an inappropriate parameter, the serum creatinine is measured as a marker of glomerular function. Calculated glomerular filtration rate or endogenous creatinine clearance are suggested to be used for the estimation of the glomerular function. Important structures preventing proteinuria in the kidney are glomerular basement membrane, podocytes and proximal tubular cells. In diabetes mellitus loss of nephrin of podocytes can play a role in the development of microalbuminuria, and podocyte desquamation may result in the progression to proteinuria. In diabetes mellitus there is an increased formation of advanced glycation endproducts (AGE), of which the only elimination organ is the kidney. The AGE induce proteinuria and atherosclerosis. Therefore, in diabetes mellitus a vicious circle develops due to proteinuria, nephron loss and accumulation of AGE, which play a role in the initiation and progression of diabetic nephropathy and atherosclerosis. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers having antiproteinuric effect may decrease the risk of diabetic nephropathy and atherosclerosis. Improvement of carbohydrate metabolism with a consequential decrease in the formation of AGE is an important contributor to the prevention and treatment of diabetic nephropathy and atherosclerosis.
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PMID:Prevention and treatment of diabetic nephropathy. 1595 73

Diabetic nephropathy, or diabetic kidney disease, affects 20 to 30 percent of patients with diabetes. It is a common cause of kidney failure. Diabetic nephropathy presents in its earliest stage with low levels of albumin (microalbuminuria) in the urine. The most practical method of screening for microalbuminuria is to assess the albumin-to-creatinine ratio with a spot urine test. Results of two of three tests for microalbuminuria should be more than 30 mg per day or 20 mcg per minute in a three- to six-month period to diagnose a patient with diabetic nephropathy. Slowing the progression of diabetic nephropathy can be achieved by optimizing blood pressure (130/80 mm Hg or less) and glycemic control, and by prescribing an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Patients with diabetes and isolated microalbuminuria or hypertension benefit from angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. In the event that these medications cannot be prescribed, a nondihydropyridine calcium channel blocker may be considered. Serum creatinine and potassium levels should be monitored carefully for patients receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. These medications should be stopped if hyperkalemia is pronounced.
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PMID:Diabetic nephropathy: common questions. 1603 88

Renal artery stenosis is a common problem, particularly for patients with other manifestations of atherosclerosis. Wide practice variations are apparent regarding how best to manage this disorder. Part of this variation is based on a broad range of clinical presentation, from incidentally identified disease of no clinical importance to rapidly progressive hypertension, renal failure, and refractory congestive heart failure. Advances in antihypertensive therapy, particularly as a result of angiotensin-converting enzyme inhibition and angiotensin receptor blockade, have led to improved blood pressure control and delayed recognition of renal artery disease. As a result, patients now sent for revascularization are older than before and have high comorbid disease risk, primarily related to cardiovascular events. Clinicians need to be vigilant for evidence of unsuspected renal artery stenosis as a cause of treatment-resistant hypertension and/or renal failure. Renal revascularization should be considered in viable individuals before the development of advanced renal insufficiency.
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PMID:Atherosclerotic renal artery stenosis: how big is the problem, and what happens if nothing is done? 1625 47

(1) Some angiotensin-converting-enzyme inhibitors (ACE inhibitors) reduce mortality in patients with heart failure (captopril, enalapril, ramipril and trandolapril), and in patients with recent myocardial infarction and heart failure or marked left ventricular dysfunction (captopril, ramipril and trandolapril). (2) Angiotensin II receptor antagonists, otherwise known as angiotensin receptor blockers, have haemodynamic effects similar to ACE inhibitors, but differ in their mechanism of action and certain adverse effects. (3) Five clinical trials have evaluated angiotensin II receptor antagonists (candesartan, losartan and valsartan) in terms of their effect on mortality and on the risk of clinical deterioration in patients with symptomatic heart failure, but without severe renal failure, hyperkalemia or hypotension. In these trials, candesartan and valsartan were used at much higher doses than those recommended for the treatment of arterial hypertension. (4) In patients with heart failure who were not taking an angiotensin II receptor antagonist or an ACE inhibitor at enrollment, no significant difference was found between losartan and captopril in terms of mortality or the risk of clinical deterioration. (5) In patients with heart failure who had stopped taking an ACE inhibitor because of adverse effects, candesartan had no effect on mortality as compared with placebo, but it did reduce the risk of clinical deterioration (3 fewer hospitalisations per year per 100 patients). However, candesartan was associated with adverse effects such as renal failure and hyperkalemia, especially in patients who had experienced these same adverse effects while taking an ACE inhibitor. (6) In patients with heart failure who were already taking an ACE inhibitor, adjunctive candesartan or valsartan treatment did not influence mortality in comparison to the addition of a placebo. Adding candesartan or valsartan reduced the risk of hospitalisation (between 1 and 3 fewer hospitalisations per year per 100 patients), but increased the risk of renal failure and hyperkalemia. (7) In patients with heart failure and incapacitating dyspnea despite ACE inhibitor + diuretic combination therapy, there are no trials comparing the addition of an angiotensin II receptor antagonist versus spironolactone. Adjunctive spironolactone therapy prevents 5 to 6 deaths per year per 100 patients in this setting. (8) In patients with heart failure who do not have markedly altered cardiac contractility, candesartan appears to have no clinical advantages over placebo. (9) In some of these trials, mortality was higher with angiotensin II receptor antagonist therapy than with placebo among patients who were already taking a betablocker. (10) Two trials have compared an angiotensin II receptor antagonist with an ACE inhibitor in patients with recent myocardial infarction who had heart failure or an altered left ventricular ejection fraction, but who did not have hypotension or severe renal failure. However, there are no placebo-controlled randomised trials assessing the effects of angiotensin II receptor antagonists on mortality. (11) In patients with recent myocardial infarction, these trials showed no difference in mortality between angiotensin II receptor antagonist treatment (losartan or valsartan) and captopril. They did not rule out the possibility that these angiotensin II receptor antagonists are moderately less effective than captopril. Adding valsartan to ongoing captopril therapy did not reduce mortality or morbidity as compared with placebo, but did increase the risk of adverse effects. (12) Overall, these trials confirm the advantage of angiotensin II receptor antagonists over ACE inhibitors with respect to some adverse effects (cough, skin rash, etc.). However, the two drug classes share certain serious adverse effects such as hyperkalemia, renal failure and hypotension. In one trial, angioedema was less frequent with angiotensin II receptor antagonist therapy (one less case per 500 patients).
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PMID:Angiotensin II receptor antagonists and heart failure: angiotensin-converting-enzyme inhibitors remain the first-line option. 1628 75


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