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. 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. 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.

Aim Multi‐organ dysfunction often complicates the natural course of acute heart failure (AHF) and identifies patients with poor prognosis. The MELD score (Model of End‐Stage Liver Dysfunction) combines data reflecting liver and kidney function, which makes it a potentially useful tool for the assessment of patients with AHF. The aim of this study was to assess the prognostic utility of the MELD score in patients with AHF. Methods and results The MELD score was calculated on admission and during hospital stay (days 2–3) using a formula that does not take into account the international normalized ratio (MELD XI). The study population consisted of 203 AHF patients (mean age 65 ± 12 years, 76% male). The mean MELD XI score was −14.8 ± 4.5 points on admission and 13.9 ± 4.3 points during hospitalization. Contributors of elevated MELD XI score at baseline and during hospital stay were isolated increase in creatinine in 22–25%, isolated increase in bilirubin in 17–19%, and abnormal values of both in 40–46% of patients. During 1‐year follow‐up, 67 (33%) patients died. After adjustment for well‐established prognosticators, MELD XI score at baseline and during hospital stay were significant predictors of poor outcome [hazard ratio (95% confidence interval): 1.11 (1.05–1.2) and 1.14 (1.09–1.2), respectively, P < 0.001]. An increase in the MELD XI score during hospital stay occurred in 31% of patients and was related to increased risk of death at 1 year [1.97 (1.2–3.2), P < 0.005]. Conclusions Impairment of hepato‐renal function defined by the MELD XI score is common and carries unfavourable prognosis in AHF patients.

Aims Recent studies indicate the need to redefine worsening renal function (WRF) in acute heart failure (AHF), linking a rise in creatinine with clinical status to identify patients who develop ‘true WRF’. We evaluated the usefulness of serial assessment of urinary levels of neutrophil gelatinase‐associated lipocalin (uNGAL), kidney injury molecule‐1 (uKIM‐1), and cystatin C (uCysC) for prediction of ‘true WRF’. Methods and results In 132 patients with AHF, uNGAL, uKIM‐1, and uCysC were measured using a highly sensitive immunoassay based on a single‐molecule counting technology (Singulex, Alameda, CA, USA) at baseline, day 2, and day 3. Patients who developed WRF (a ≥0.3 mg/dL increase in serum creatinine or a >25% decrease in the estimated glomerular filtration rate from the baseline value) were differentiated into those ‘true WRF’ (presence of deterioration/no improvement in clinical status during hospitalization) vs. ‘pseudo‐WRF’ (uneventful clinical course). ‘True WRF’ occurred in 13 (10%), ‘pseudo‐WRF’ in 15 (11%), whereas the remaining 104 (79%) patients did not develop WRF. Patients with ‘true WRF’ were more often females, had higher levels of NT‐proBNP, creatinine, and urea on admission, higher urine albumin to creatinine ratio at day 2, higher uNGAL at baseline, day 2, and day 3, and higher KIM‐1 at day 2 (vs. pseudo‐WRF vs. without WRF, all P < 0.05). Patients with pseudo‐WRF did not differ from those without WRF. In the multivariable model, elevated uNGAL at all time points and uKIM‐1 at day 2 remained independent predictors of ‘true WRF’. Conclusion Elevated levels of uNGAL and uKIM‐1 may predict development of ‘true WRF’ in AHF.