Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anemia is one of the most serious complications in patients on dialysis. Erythropoietin improves the anemia. However, erythropoietin resistance is sometimes encountered from causes such as functional iron deficiency, secondary hyperparathyroidism, blood loss, or interaction with other drugs. To clarify the interaction between erythropoietin and the renin-angiotensin system, we studied the maintenance dose of recombinant human erythropoietin (rHuEPO) in patients on continuous ambulatory peritoneal dialysis (CAPD) with and without angiotensin converting enzyme inhibitor (ACEIs), angiotensin II type I receptor blockers (ARBs), and calcium channel blockers. We divided 36 hypertensive patients on CAPD into three groups--an ACEI group (n = 12), an ARB group (n = 12), and a Ca channel blocker group (n = 12)--and then we compared the doses of rHuEPO required to maintain the patients' hematocrit (Hct) above 30%. In the Ca channel blocker group, the weekly dose of erythropoietin had not changed significantly at the end of the study (74 +/- 7 U/kg at the end vs. 76 +/- 8 U/kg at the start). The (oral) ACEI group needed a significantly higher weekly dose of erythropoietin at the end of the study (89 -/+ 9 U/kg at the end vs. 74 -/+ 8 U/kg at the start, p < 0.01). The (oral) ARB group also needed a significantly higher weekly dose of erythropoietin at the end of the study (82 -/+ 10 U/kg at the end vs. 76 +/- 8 U/kg at the start, p < 0.05). Furthermore, the weekly dose of erythropoietin required in the ACEI group was significantly larger than that required in the ARB group. We conclude that treatment with ACEIs and ARBs induces erythropoietin resistance in patients on CAPD. The inhibitory effect of ARBs on erythropoiesis is less than that of ACEIs.
 ...
PMID:Erythropoietin resistance in patients on continuous ambulatory peritoneal dialysis. 1538 8

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.
 ...
PMID:Renal failure and ACE inhibition: how much is too much? 1567 37

Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.
 ...
PMID:A case of insulin edema with inappropriate hyperaldosteronism. 1576 45

Cardiovascular risk is dramatically increased in patients with end-stage renal disease (ESRD). However, even minor dys-functions such as microalbuminuria or a mild increase in serum creatinine (Cr) have a major impact on cardiovascular risk. Increased cardiovascular risk is present in multiple populations, including general populations, patients with moderate risk such as hypertensives, and high-risk patients including patients with heart failure and myocardial necrosis. There are many mechanisms underpinning the increased cardiovascular risk. Regarding atherosclerosis, the kidney can be victim or villain. On the one hand, both kidney disease per se and renal insufficiency can induce vascular damage, thereby increasing cardiovascular risk. Kidney disease without renal insufficiency can cause an increased prevalence in hypertension, dyslipidemia (nephrotic syndrome), sympathetic system hyperactivity, and in renin angiotensin system hyperactivity. A moderate-severe renal insufficiency can induce an increase in many vasculotoxic substances such as ADMA, lipoprotein(a), homocysteine, disturbances in calcium and phosphate metabolism, anemia and left ventricular hypertrophy. A more severe renal insufficiency can induce the ominous malnutrition-inflammation-atherosclerosis (MIA) syndrome. On the other hand, the kidney can be the victim of atherosclerosis. Ischemic nephropathy, caused by atherosclerotic renal artery disease and atheroembolism from abdominal aorta are two examples. Finally, it is important to consider that the kidney, being an organ with a wide vasculature, could be a sophisticated sensor of subclinical cardiovascular damage.
 ...
PMID:[Hypertension, atherosclerosis and kidney]. 1578 9

End-stage renal disease (ESRD) is a social and economical threat worldwide. Much has been done in previous decades to develop new treatments, but we remain a long way from being satisfied. Recently, growing attention has been paid to polytherapeutic approaches to chronic kidney disease (CKD) to control different causal factors involved in progression and in the meantime, and reduce them as much as possible. Starting from a paper published in the British Medical Journal, which suggested the use of a polypill to prevent cardiovascular events in the general population, I tried to apply a similar approach in the nephrology setting, focusing my attention on therapeutic strategies to slow down CKD progression, which could possibly be included in a 'anti-dialysis polypill'. Among these strategies, I selected the effect of the inhibition of the renin-angiotensin system, the use of statins and anemia correction. Unfortunately, this approach is not applicable theoretically, due to the lack of a sufficient number of randomized clinical trials calculating the relative risk, in particular concerning the use of statins and the treatment of anemia. However, while awaiting new therapeutical approaches to be more selective and efficacious, a treatment combination seems to be, together with better implementation of single therapies, the only possible strategy to apply.
 ...
PMID:[Polypharmacological approach to progressive chronic kidney disease: the new scenery]. 1587 75

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.
 ...
PMID:Anemia in heart failure--a concise review. 1627 92

Recent studies emphasize the role of chronic hypoxia in the tubulointerstitium as a final common pathway to end-stage renal failure. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries. Associated interstitial fibrosis impairs oxygen diffusion and supply to tubular and interstitial cells. Hypoxia of tubular cells leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. A number of mechanisms that induce tubulointerstitial hypoxia at an early stage have been identified. Glomerular injury and vasoconstriction of efferent arterioles as a result of imbalances in vasoactive substances decrease postglomerular peritubular capillary blood flow. Angiotensin II not only constricts efferent arterioles but, via its induction of oxidative stress, also hampers the efficient utilization of oxygen in tubular cells. Relative hypoxia in the kidney also results from increased metabolic demand in tubular cells. Furthermore, renal anemia hinders oxygen delivery. These factors can affect the kidney before the appearance of significant pathologic changes in the vasculature and predispose the kidney to tubulointerstitial injury. Therapeutic approaches that target the chronic hypoxia should prove effective against a broad range of renal diseases. Current modalities include the improvement of anemia with erythropoietin, the preservation of peritubular capillary blood flow by blockade of the renin-angiotensin system, and the use of antioxidants. Recent studies have elucidated the mechanism of hypoxia-induced transcription, namely that prolyl hydroxylase regulates hypoxia-inducible factor. This has given hope for the development of novel therapeutic approaches against this final common pathway.
 ...
PMID:Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure. 1629 37

Cardiac artery disease and heart failure are major causes for morbidity and mortality in diabetes in general and in those with chronic kidney disease (CKD) in particular. Hypertension and dyslipidemia are more common in diabetes and the prevalence of coronary artery disease in diabetics is two-fold to four-fold higher than in nondiabetics. In those with CKD the incidence of cardiovascular complications is nearly two-fold higher than those without CKD. Recent studies suggest that the pathophysiology of cardiac disease is complex process involving both microvascular and macrovascular disease. In addition, myocardial lipotoxicity may be a novel contributing factor particularly in type 2 diabetics. Compelling evidence from cardiovascular outcomes trials indicates that treatment with drugs that block the renin-angiotensin system are cardioprotective in diabetics with microalbuminuria and early stages of kidney disease. Multiple risk factor intervention aimed at optimal blood pressure control (BP <130/<80 mmHG), lowering LDL cholesterol below 100 mg/dl, lowering triglyceride level to 150 mg/dl, A1C <6.5%, treatment with an ACE inhibitor or an angiotensin II receptor blocker, administration of once daily low-dose aspirin and smoking cessation together reduce cardiovascular morbidity and mortality in type 2 diabetics. Novel studies including diabetics with nephropathy aimed at improving outcomes in diabetics by treatment of anemia and optimal control of dyslipidemia are now underway. These and other clinical trials should provide important new insights into improving the quality of life in diabetics and ultimately preventing cardiac disease.
 ...
PMID:Heart disease in diabetic patients. 1629 58

Chronic kidney disease constitutes a highly prevalent health problem worldwide. Left untreated, it progresses inexorably to greater levels of severity at variable rates. The morbid impact of chronic kidney disease is heightened by its role as risk factor for cardiovascular disease. In the past two decades, considerable gains have been realized in retarding progression of chronic kidney disease by emphasizing blood pressure control and blockade of the renin-angiotensin system. Notwithstanding, the therapeutic goal of preventing or arresting chronic kidney disease progression remains unfulfilled. Currently attainable rates of decrease in glomerular filtration rate remain at 2 to 8 mL/min/y depending on the underlying disease. It is now believed that to achieve optimal therapeutic targets (proteinuria of <500 mg/day and decrease in glomerular filtration rate of 1 mL/min/y, the average age-related decline) we must introduce novel strategies and a multifaceted approach to treatment that interrupts multiple mechanisms of progression. To this end, and wherever relevant, new approaches to cause-specific treatment must be applied, such as targeted immunosuppression, intensive glycemic control, gene therapy, and enzyme replacement therapy. Furthermore, in all chronic kidney disease, we must interfere more effectively with the multitude of common mechanisms of progression. Established or putative, such approaches include aggressive blood pressure control; advanced renin-angiotensin system blockade; cytokine modulation and antifibrotic therapy; aldosterone blockade; endothelin blockade, nitric oxide modulation and vasopeptidase inhibition; antioxidant therapy; statin therapy; glycosaminoglycan therapy; anemia therapy; dietary restrictions; lifestyle changes; and pharmacogenomic profiling. Such a concerted, multifaceted approach to management might indeed prevent or arrest progression of chronic kidney disease, or even achieve regression of chronic kidney disease.
 ...
PMID:Progression of chronic kidney disease: can it be prevented or arrested? 1734 29

The use of mycophenolate mofetil (MMF) and renin-angiotensin system blockers (RAB) to prevent and treat chronic graft nephropathy may affect the incidence of anemia in renal transplant recipients. We compared 2 sets of cadaver-donor recipients, namely those followed at the end of 1995 (group 1; n = 252) versus 2003 (group 2; n = 530) in terms of general characteristics, incidence of anemia (hemoglobin [Hb] < or =13 g/L males, 12 g/L females) or severe anemia (Hb < or =11 g/L males, 10 g/L females) and use cost of treatment with erythropoietin (EPO). Group 2 was significantly older, heavier and longer since grafting. Fifty-seven percent received MMF, 21% received azathioprine, and 5% received rapamycin. In group 1, 83% were given azathioprine. RAB were administered to 35.1% in group 2 versus 14.7% in group 1 (P < .001). Mean blood pressure was identical in the 2 groups, but graft function was worse in group 2 (Cockroft, 62 vs 74 mL/min; P < .001). Mean Hb levels (13.66 + - 3.1 vs 13.82 + - 1.7 g/L) and prevalence of anemia (36.9% vs 34.5%) for groups 1 and 2, respectively, were similar. The rate of severe anemia, however, was lower in group 2 (2.3% vs 8.7%; P < .001). The use of EPO increased from 2.8% (group 1) to 8.7% (group 2; P < .01). In 2003, the cost of EPO was calculated at 1982 Euros/patient-year and 91,150 Euros per year for the whole patient group. Despite accumulation of predisposing factors, the control of anemia in our patients has improved due to the expanded use of EPO. Along with its high cost, EPO therapy has potential positive repercussions on the quality of life and patient prognosis. Therefore, we need to precisely define the optimal use of EPO in renal transplant recipients.
 ...
PMID:Influence of the current management of renal transplant recipients on the prevalence of anemia and related costs. 1638 51


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>