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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progressive renal failure occurs in a large number of patients even in the absence of the original cause of injury. It is suggested that the initial reduction in nephron number progressively damages the remaining ones. Various mechanisms underlie the pathogenesis of progressive glomerular injury. Several studies have extensively shown that both dietary protein restriction and pharmacologic intervention with ACE-inhibitiors and angiotensin receptor antagonists effectively slow the progression of chronic renal diseases. This article will present treatment recommendations designed to delay the progression of chronic renal disease, to optimize its medical management and to reduce complications induced by renal insufficiency including hypertension, renal osteodystrophy and anemia. Ten steps in the management of patients with chronic renal failure recommended by an international panel of experts based on existing guidelines are presented.
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PMID:[Supportive medical management of patients with chronic renal failure]. 1197 99

Combination therapy with angiotensin receptor antagonist(ARB) plus angiotensin converting enzyme inhibitor(ACE-I) (ARB/ACE-I) was efficacious in reducing proteinuria in patients with progressive renal disease. However, this therapy may be associated with the worsening of anemia and hyperkalemia. The present study addressed whether or not triple therapy with low-dose ARB, low-dose diuretic (D) and calcium channel blocker(CCB) (ARB/D/CCB) is as effective as therapy with low-dose ARB/ACE-I in retarding the progression of overt diabetic nephropathy. In the triple therapy, the patients were initially subjected to monotherapy with CCB for 24 weeks. Low-dose ARB and low-dose D were added to the treatment for an additional 24-week period. In parallel, patients undergoing double therapy were initially treated with low-dose ACE-I alone for 24 weeks, and then low-dose ARB was added for an additional 24-week period. The results were as follows: 1) In the triple therapy, blood pressure was reduced by 9 mmHg in systole and 5 mmHg in diastole (not significant) compared to monotherapy with CCB. There was a significant decline in proteinuria (3.3 +/- 1.2 g/day in the CCB-treated period vs. 2.1 +/- 1.0 g/day in the ARB/D/CCB-treated period, n = 12, p = 0.0143). Furthermore, a significant improvement in the slope of reciprocal serum creatinine concentration(1/Cr) was found in response to triple therapy(1/Cr: -0.0118 +/- 0.0009 in the CCB-treated vs. -0.0035 +/- 0.0028(I/mg/dl/month) in the ARB/D/CCB-treated period, n = 12, p < 0.001). There was neither a worsening of anemia nor an increase in the serum potassium(K) concentration. 2) In the double therapy, blood pressure was reduced by 12 mmHg in systole(p = 0.0079, n = 11) and 6 mmHg in diastole(n = 11, p = 0.0037) compared to the monotherapy with ACE-I. A significant improvement in the slope of 1/Cr was found in the double therapy(1/Cr: -0.0095 +/- 0.0052 in the ACE-I treated period vs. -0.0029 +/- 0.0028(I/mg/dl/month) in the ARB/ACE-I, n = 11, p < 0.001). In addition, there was a substantial reduction in hematocrit and increase in serum K concentration. The present result suggests that triple therapy consisting of ARB/D/CCB is as efficacious as double therapy with ARB/ACE-I in protecting the kidney from the progression in patients with diabetic overt nephropathy. The former may be expected to have less adverse effects.
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PMID:[Renoprotective effect of triple therapy with low-dose angiotensin receptor blocker, low-dose diuretic and Ca-antagonist in hypertensive type 2 diabetic patients with overt nephropathy]. 1280 73

Early renal insufficiency (ERI), defined as a calculated or measured glomerular filtration rate (GFR) between 30 and 60 mL/min per 1.73 m2, is present in more than 10% of the adult Australian population. This pernicious condition is frequently unrecognised, progressive and accompanied by multiple associated comorbidities, including hypertension, renal osteodystrophy, anaemia, sleep apnoea, cardiovascular disease, hyperparathyroidism and malnutrition. Several treatments have been suggested to retard GFR decline in ERI, including blood pressure reduction, angiotensin-converting enzyme inhibition, angiotensin receptor antagonism, calcium channel blockade, cholesterol reduction, smoking cessation, erythropoietin therapy, dietary protein restriction, intensive glycaemic control and early intensive multidisciplinary patient education within a renal unit. In addition, specific interventions have been reported to be renoprotective in atherosclerotic renal artery stenosis, diabetic nephropathy, lupus nephritis and certain forms of primary glomerulonephritis. The present paper reviews the available published randomised controlled clinical trials and meta-analyses supporting (or refuting) a role for each of these therapeutic manoeuvres.
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PMID:Evidence-based guide to slowing the progression of early renal insufficiency. 1474 14

Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes.
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PMID:Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers. 1496 14

Diabetic nephropathy has become the most prevalent cause of end-stage renal disease (ESRD) in many countries. ESRD patients with diabetes have a particularly poor prognosis compared with patients without diabetes. The course of diabetic nephropathy can be modified with early management of the condition and it is important that diabetes patients are screened regularly for early signs of kidney damage. Blood pressure control and use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers have been shown to slow the progression of chronic kidney disease. Patients with diabetes are at considerable risk of cardiovascular complications, and modifiable cardiovascular risk factors, such as anaemia and dyslipidaemia, should be treated at an early stage. Correction of anaemia with recombinant human erythropoietin is associated with improvements in quality of life, functional status, and cardiovascular morbidity and mortality, and may slow the progression of renal disease. Abnormalities in calcium and phosphate metabolism and acidosis may also occur in patients with diabetes and nephropathy and these should be monitored regularly. It is important that patients with kidney disease are detected promptly to allow intervention to slow renal disease progression and to treat modifiable cardiovascular risk factors. Improved collaboration between diabetologists and nephrologists will also ensure that patients receive optimal care.
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PMID:Screening and management of patients with early chronic kidney disease. 1510 42

Dialysis patients show a high prevalence of cardiovascular complications among which left ventricular hypertrophy is one of the most frequent and is independently predictive of mortality. A recent study indicates that partial regression of left ventricular hypertrophy improves mortality and reduces cardiovascular events in end-stage renal disease (ESRD) patients, suggesting the importance of targeting therapeutic strategies to reduce cardiac hypertrophy and improve the outcome in these patients. The pathogenesis of left ventricular hypertrophy in ESRD patients is multifactorial and includes hypertension, activation of the renin-angiotensin system, increased sympathetic activity, chronic volume overload, chronic anaemia and hyperparathyroidism. In this paper, we review the available experimental and clinical evidence showing the important contribution of the renin-angiotensin system as well as its interaction with the sympathetic nervous system in the pathogenesis of left ventricular hypertrophy in ESRD patients. Furthermore, we summarize the results of currently available clinical studies that examined the effects of angiotensin-converting enzyme inhibition or angiotensin receptor antagonism on left ventricular hypertrophy in ESRD patients, and review evidences that support the use of angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists in the ESRD population.
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PMID:Angiotensin converting enzyme inhibition for cardiac hypertrophy in patients with end-stage renal disease: what is the evidence? 1536 49

The dose-response relationship between pharmacological blockade of the renin-angiotensin system (RAS) and angiotensin II concentration in the circulation, on the one hand, and decrease of blood pressure, on the other hand, has been well established. In contrast it is currently unclear which dose of ACE inhibitors and/or angiotensin receptor blockers is optimal for nephroprotection. Clinical studies are rendered quite complex by an early decrease of glomerular filtration after RAS blockade and by side effects at higher doses such as renal sodium loss, hyperkalemia, anemia, etc. Animal experiments and recent clinical studies suggest that the doses of ACE inhibitors or angiotensin receptor blockers required for maximal reduction of proteinuria (as a surrogate marker) and for optimal nephroprotection (retardation of the loss of glomerular filtration) exceed those required for maximal lowering of blood pressure. Ongoing studies try to define the relative merits of high dose monotherapy (ACE inhibitors or angiotensin receptor blockers) versus a combination therapy of the two.
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PMID:Renal failure and ACE inhibition: how much is too much? 1567 37

Heart failure affects 5 million persons in the United States, with 400,000 new cases occurring every year. Paradoxically, although advances in coronary angioplasty and effective drugs have increased survival post infarction, the myocardial damage and subsequent neurohormonal activation-induced remodeling causes significant morbidity years later in the form of heart failure. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) together with beta blockers modify the neurohormonal activation associated with heart failure and are key treatments for improving cardiac function and survival. Anemia is a significant risk factor predicting morbidity and mortality in heart failure. This article describes the various etiologies of anemia in heart failure. Of particular importance is the fact that recent stem cell studies have shown that the drugs acting on the renin-angiotensin system inhibit erythropoiesis in vivo and may cause anemia in patients with both normal renal function and end-stage renal disease (ESRD). The role of angiotensin-II as an erythropoietic growth factor and ACE in facilitating erythropoiesis is described in this article. Anemia has been shown to be a modifiable risk factor and its treatment correlates with improvement in clinical outcomes. Thus, anemia, its etiology (especially the contribution of ACEIs and ARBs), physiologic and prognostic impact, and treatment in the setting of heart failure are critical areas for investigation.
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PMID:Anemia in heart failure--a concise review. 1627 92

The rising incidence of type 2 diabetes mellitus and of its complications will make it the most important health care challenge in the first quarter of the 21st Century. Diabetic nephropathy left unchecked will overwhelm the renal resources. Simple methods (proper diet and exercise, prevention of obesity) are successful in preventing type 2 diabetes in the great majority of the persons at risk. In patients with established type 2 diabetes, nephropathy can be prevented or greatly delayed by strict metabolic control, strict control of blood pressure using angiotensin-converting enzyme inhibitors and angiotensin receptor blockers as the first line of drugs, tight control of serum lipids using statins as indicated, low protein diet, avoidance of smoking and other nephrotoxic influences, prevention of abnormalities in calcium/phosphorus metabolism, and prevention of renal anemia by the early use of erythropoietin. Current research offers the promise of definitive prevention of both type 2 diabetes and diabetic nephropathy.
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PMID:Prevention of nephropathy in patients with type 2 diabetes mellitus. 1630 58

Anemia has been described as an independent predictor of death in patients with chronic heart failure. Little is known, however, about the significance of anemia in heart failure patients with severely depressed socioeconomic backgrounds who receive comprehensive care in a heart failure management program. The impact of anemia on mortality was investigated in 410 indigent chronic heart failure patients, the majority of whom were in New York Heart Association functional class I-III and were treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and beta blockers at maximally tolerated doses. Anemia was present in 28% of patients. In an adjusted Cox analysis, anemia was strongly associated with mortality, but only in men: hazard ratio, 2.54; 95% confidence interval, 1.31-4.93; p = 0.006. The investigators conclude that anemia in this population is common and that, for men, the relative risk increase associated with anemia is high.
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PMID:The effect of anemia on mortality in indigent patients with mild-to-moderate chronic heart failure. 1659 40


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