RESUMO
BACKGROUND: Haemofiltrate reinfusion (HFR) is a form of haemodiafiltration (HDF) in which replacement fluid is constituted by ultrafiltrate from the patient 'regenerated' through a cartridge containing hydrophobic styrene resin. Bicarbonate-based dialysis solutions (DS) used in routine haemodialysis and HDF contain small quantities of acetate (3-5 mMol/L) as stabilizing agent, one of the major causes of intradialytic hypotension. Acetate-free (AF) DS have recently been made available, substituting acetate with hydrochloric acid. Cardiac troponin (cTnT) constitutes an appreciable marker of myocardial damage and cardiac hypertrophy, and correlates with left ventricular mass. METHODS: The aim of this study was to assess the impact of the presence or lack of acetate in DS on cTnT levels in patients treated with HFR and to evaluate outcome of intra-session cardiovascular stability. Twenty-five patients devoid of major cardiovascular comorbidity were randomized and treated with AF HFR for 3 months. The same patients were subsequently treated by means of HFR with DS containing 3 mMol/L acetate for 3 months and finally with AF HFR for a further 3 months. Prior and subsequent to each treatment period, samples were collected for cTnT measurement. RESULTS: A significant decrease was observed in cTnT levels throughout the first session of AF HFR (1.32 ± 0.35-1.12 ± 0.31 ng/mL, P < 0.05) with a subsequent rise being registered during HFR with acetate-containing DS (1.12 ± 0.31-1.28 ± 0.37 ng/mL, P < 0.05) and a further drop from 1.28 ± 0.37 to 1.21 ± 0.35 ng/mL in the last AF HFR period. During HFR with acetate-containing DS, a significant drop in systolic and diastolic arterial pressure was observed in conjunction with a higher heart rate at the end of the session. CONCLUSION: We observed an increase in cTnT during HFR with acetate and drops manifested during HFR without acetate; it may therefore be concluded that the drop in cTnT level, significantly correlated with lack of acetate, is indicative of improvement of cardiac microvascular function.