Intermittent haemodiafiltration in refractory congestive heart failure: BNP and balance of inflammatory cytokines.
BACKGROUND
Elevated plasma levels of cytokines have been associated with an increased risk of congestive heart failure (CHF) even in people without history of myocardial infarction. Here we have tested the hypothesis that effective removal of pro-inflammatory cytokines in patients with advanced CHF unresponsive to diuretic treatment is associated with diuresis restoration and with a significant reduction of B-type natriuretic peptide (BNP) circulating levels.


METHODS
We prospectively enrolled 10 patients with decompensated CHF (NYHA classes III-IV). Five patients unresponsive to diuretic treatment underwent a short course of intermittent haemodiafiltration (iHDF), whereas five patients responsive to diuretics were treated with intravenous boluses of furosemide. Renal function was similar between the two groups.


RESULTS
Excess body fluids were removed in both groups always resulting in a reduction of pulmonary congestion and peripheral oedema. NYHA class improved in all patients, but one treated by intravenous boluses of furosemide. Only patients treated with iHDF showed a significant reduction of circulating interleukin-8 and monocyte chemoattractant protein-1. After the end of iHDF treatment, patients showed consistent restoration of diuretic responsiveness to significantly lower doses of oral furosemide up to one month of follow-up. Plasma levels of BNP before treatment were significantly higher in the iHDF group, lowering significantly in both groups after treatment.


CONCLUSIONS
Our results suggest that HDF is an effective treatment for patients with advanced CHF when cytokines have to be cleared and diuretic responsiveness needs to be restored. In our experience, iHDF is a cost-effective option when compared with continuous ultrafiltration methods because it can be performed in a routine dialysis unit without adjunctive costs for machinery or personnel training.
Libetta
Carmelo
C
Unit of Nephrology, Department of Respiratory Diseases, IRCCS Policlinico San Matteo and University of Pavia, Italy. carmelo.libetta@unipv.it
Sepe
Vincenzo
V
Zucchi
Manuela
M
Pisacco
Patrizia
P
Cosmai
Laura
L
Meloni
Federica
F
Campana
Carlo
C
Rampino
Teresa
T
Monti
Cristina
C
Tavazzi
Luigi
L
Dal Canton
Antonio
A
D000328:Adult; D001826:Body Fluids / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood; D016207:Cytokines / Q000097:blood*; D004232:Diuretics / Q000008:administration & dosage / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D005665:Furosemide / Q000008:administration & dosage / Q000627:therapeutic use; D006333:Heart Failure / Q000097:blood* / Q000378:metabolism / Q000628:therapy*; D017583:Hemodiafiltration / Q000379:methods*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016209:Interleukin-8 / Q000097:blood; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D011446:Prospective Studies; D019233:Retreatment; D017211:Treatment Failure; D016896:Treatment Outcome
D018932:Chemokine CCL2; D016207:Cytokines; D004232:Diuretics; D018836:Inflammation Mediators; D016209:Interleukin-8; D020097:Natriuretic Peptide, Brain; D005665:Furosemide