Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure.

AIM: Acute heart failure (AHF) critically deranges haemodynamic and metabolic homoeostasis. Iron is a key micronutrient for homoeostasis maintenance. We hypothesized that iron deficiency (ID) defined as depleted iron stores accompanied by unmet cellular iron requirements would in this setting predict the poor outcome. METHODS AND RESULTS: Among 165 AHF patients (age 65 ± 12 years, 81% men, 31% de novo HF), for ID diagnosis we prospectively applied: low serum hepcidin reflecting depleted iron stores (<14.5 ng/mL, the 5th percentile in healthy peers), and high-serum soluble transferrin receptor (sTfR) reflecting unmet cellular iron requirements (≥1.59 mg/L, the 95th percentile in healthy peers). Concomitance of low hepcidin and high sTfR (the most profound ID) was found in 37%, isolated either high sTfR or low hepcidin was found in 29 and 9% of patients, and 25% of subjects demonstrated preserved iron status. Patients with low hepcidin and high sTfR had peripheral oedema, high NT-proBNP, high uric acid, low haemoglobin (P < 0.05), and 5% in-hospital mortality (0% in remaining patients). During the 12-month follow-up, 33 (20%) patients died. Those with low hepcidin and high sTfR had the highest 12-month mortality [(41% (95% CI: 29-53%)] when compared with those with isolated high sTfR [15% (5-25%)], isolated low hepcidin [7% (0-19%)] and preserved iron status (0%) (P < 0.001). Analogous mortality patterns were seen separately in anaemics and non-anaemics. CONCLUSION: Iron deficiency defined as depleted body iron stores and unmet cellular iron requirements is common in AHF, and identifies those with the poor outcome. Its correction may be an attractive therapeutic approach.

Hemodialysis-induced changes in the blood composition affect function of the endothelium.

Hemodialysis induces oxidative stress causing intravascular inflammation, which may cause endothelial dysfunction. We evaluated how hemodialysis-induced changes in blood affect the function of endothelial cells in in vitro culture. Serum samples were collected from 42 uremic patients treated with hemodialysis, one before the start of dialysis and the other one at the end of session. All patients were dialysed with polysulfone dialyzer. Concentrations of the inflammatory molecules carbonyl protein and metabolites of NO synthesis were measured in blood. Additionally, the effect of the serum obtained before and after dialysis on the function of endothelial cells in in vitro culture was studied. Hemodialysis caused increase of monocyte chemoattractant protein (MCP)-1 (+17%), hepatocyte growth factor (+91%), and pentraxin-3 (+30%) concentration in serum. Concentration of carbonyl protein was decreased by 30%. Decrease of blood level of asymmetric dimethylarginine (-25%) and nitrate/nitrites (-62%) was observed. Serum obtained after hemodialysis stimulated proliferation of endothelial cells (+10%) and synthesis of MCP-1(+11%) in these cells. Hemodialysis-induced intravascular inflammation changes the function of endothelial cells, which may lead to acceleration of atherosclerosis.