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.
An elevated blood lactate on admission is common in AHF patients without overt clinical evidence of peripheral hypoperfusion and is associated with markers of organ dysfunction/damage and a worse prognosis.
Aims
The clinical significance of the measurement of urine sodium concentration (UNa+) in response to loop diuretic administration in patients with acute heart failure (AHF) is still unsettled. We studied the association of serial measurements of spot UNa+ during the first 48 h of AHF treatment with the indices of decongestion, renal function, and prognosis.
Methods and results
We enrolled 111 AHF patients, all of whom received intravenous furosemide on admission. The mean spot UNa+ significantly increased in the 6 h sample (P < 0.05 vs. baseline) and returned to baseline values in the 24 and 48 h samples. Based on the increase or decrease/no change of UNa+ in the 6 and 48 h samples vs. baseline, patients were divided into two groups at each time point, respectively. Patients did not differ in baseline clinical and laboratory characteristics. Patients with a decrease/no change of UNa+ in the 6 and 48 h samples had a lower weight loss during hospitalization. Patients with a decrease/no change of UNa+ in the 48 h sample had a poorer diuretic response and a significant increase in the urinary levels of the tubular biomarkers: kidney injury molecule‐1 and neutrophil gelatinase‐associated lipocalin. Low UNa+ and decrease/no change in UNa+ in the 6 and 48 h samples were independent predictors of higher risk of all‐cause mortality during 1‐year follow‐up (all P < 0.05).
Conclusion
In AHF, low spot UNa+ and lack to increase UNa+ in response to intravenous diuretics are associated with poor diuretic response, markers of tubular injury and high risk of 1‐year mortality.
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