Chronic heart failure is a common disorder associated with unacceptably high mortality rates. Chronic renal disease and anemia are two important comorbidities that significantly influence morbidity and mortality in patients with chronic heart failure (CHF). Progress in CHF again may cause worsening of kidney function and anemia. To describe this vicious cycle, the term cardio-renal anemia syndrome has been suggested. Iron deficiency is part of the pathophysiology of anemia in both CHF and chronic kidney disease, which makes it an interesting target for treatment of anemia in cardio-renal anemia syndrome. Recently, studies have highlighted the potential clinical benefits of treating iron deficiency in patients with CHF, even if these patients are nonanemic. This article summarizes studies investigating the influence of iron deficiency with or without anemia in chronic kidney disease and CHF and gives an overview of preparations of intravenous iron currently available.
[Show abstract][Hide abstract] ABSTRACT: Worsening renal function (WRF) during the treatment of acute decompensated heart failure (ADHF) occurs in up to a third of patients and is associated with worse survival. Venous congestion is increasingly being recognized as a key player associated with WRF in ADHF. Understanding the hemodynamic effects of venous congestion and the interplay between venous congestion and other pathophysiological factors such as raised abdominal pressure, endothelial cell activation, anemia/ iron deficiency, sympathetic overactivity, and stimulation of the renin-angiotensin-aldosterone system will help in devising effective management strategies. Early recognition of venous congestion through novel techniques such as bioimpedance measurements and remote monitoring of volume status combined with customized diuretic regimens may prevent venous congestion and perhaps avoid significant WRF.Kidney International advance online publication, 19 December 2012; doi:10.1038/ki.2012.406.
Kidney International 12/2012; 83(3). DOI:10.1038/ki.2012.406 · 8.56 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background:
Impaired renal function and anaemia are common among patients with acute myocardial infarction (AMI). While both conditions are known independent risk factors for increased mortality, their interaction as risk factors for increased mortality in AMI is unclear.
We studied 5395 subjects hospitalized for AMI between January 2000 and December 2005. An estimated glomerular filtration rate (GFR) <60 mL/min/1.73 m(2) was defined as impaired GFR and GFR ≥ 60 mL/min/1.73 m(2) was defined as preserved GFR. Anaemia was defined as <13 g/dL (males) and <12 g/dL (females). The odds ratio (OR) for one-year mortality and its 95% confidence interval (CI) were calculated by logistic regression.
We identified 758 (14%) patients with impaired GFR and anaemia, 1105 (20.5%) patients with impaired GFR without anaemia, 465 (8.6%) patients with preserved GFR and anaemia, and 3012 (55.8%) patients with preserved GFR without anaemia; one-year mortality rates were 56.5%, 41.8%, 31.8% and 10.3% respectively in these 4 groups. Among patients with impaired GFR, anaemia was associated with an adjusted OR of 1.47 (95% CI=1.17-1.85) for one-year mortality, while among patients with preserved GFR, anaemia was associated with a higher adjusted OR of 2.07 (95% CI=1.54-2.76) for one-year mortality, interaction P<0.001.
The combination of impaired GFR and anaemia confers greater than five-fold increased risk of mortality after AMI. The differential effect of anaemia among patients with impaired and preserved GFR on mortality suggests that in patients with preserved GFR anaemia confers a greater relative hazard than in patients with impaired renal function.
International journal of cardiology 01/2013; 168(2). DOI:10.1016/j.ijcard.2012.12.017 · 4.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background:
Anemia is a major complication of end stage renal disease. The anemia is mainly the result of impaired formation of erythrocytes due to lack of erythropoietin and iron deficiency. Compelling evidence, however, points to the contribution of accelerated erythrocyte death, which decreases the life span of circulating erythrocytes. Erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine-exposure at the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). Erythrocytes could be sensitized to cytosolic Ca(2+) by ceramide. In end stage renal disease, eryptosis may possibly be stimulated by uremic toxins. The present study explored, whether the uremic toxin acrolein could trigger eryptosis.
Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin-V-binding, hemolysis from hemoglobin release, [Ca(2+)]i from Fluo3-fluorescence, and ceramide from fluorescent antibodies.
A 48 h exposure to acrolein (30 － 50 µM) did not significantly modify [Ca(2+)]i but significantly decreased forward scatter and increased annexin-V-binding. Acrolein further triggered slight, but significant hemolysis and increased ceramide formation in erythrocytes. Acrolein (50 µM) induced annexin-V-binding was significantly blunted in the nominal absence of extracellular Ca(2+). Acrolein augmented the annexin-V-binding following treatment with Ca(2+) ionophore ionomycin (1 µM).
Acrolein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of ceramide formation with subsequent sensitisation of the erythrocytes to cytosolic Ca(2+).
Kidney and Blood Pressure Research 05/2013; 37(2-3):158-167. DOI:10.1159/000350141 · 2.12 Impact Factor
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