INCREASED BRAIN NATRIURETIC PEPTIDE AND ATRIAL-NATRIURETIC-PEPTIDE PLASMA-CONCENTRATIONS IN DIALYSIS-DEPENDENT CHRONIC-RENAL-FAILURE AND INPATIENTS WITH ELEVATED LEFT-VENTRICULAR FILLING PRESSURE
C. Haug et al., INCREASED BRAIN NATRIURETIC PEPTIDE AND ATRIAL-NATRIURETIC-PEPTIDE PLASMA-CONCENTRATIONS IN DIALYSIS-DEPENDENT CHRONIC-RENAL-FAILURE AND INPATIENTS WITH ELEVATED LEFT-VENTRICULAR FILLING PRESSURE, The Clinical investigator, 72(6), 1994, pp. 430-434
Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) p
lasma concentrations were measured in patients with dialysis-dependent
chronic renal failure and in patients with coronary artery disease ex
hibiting normal or elevated left ventricular end-diastolic pressure (L
VEDP) (n = 30 each). Blood samples were obtained from the arterial lin
e of the arteriovenous shunt before, 2 h after the beginning of, and a
t the end of hemodialysis in patients with chronic renal failure. In p
atients with coronary artery disease arterial blood samples were colle
cted during cardiac catheterization. BNP and ANP concentrations were d
etermined by radioimmunoassay after Sep Pak C,, extraction. BNP and AN
P concentrations decreased significantly (P < 0.001) during hemodialys
is (BNP: 192.1 +/- 24.9, 178.6 +/- 23.0, 167.2 +/- 21.8 pg/ml; ANP: 24
0.2 +/- 28.7, 166.7 +/- 21.3, 133.0 +/- 15.5 pg/ml). The decrease in B
NP plasma concentrations, however, was less marked than that in ANP pl
asma levels (BNP 13.5 +/- 1.8%, ANP 40.2 +/- 3.5%; P < 0.001). Plasma
BNP and ANP concentrations were 10.7 +/- 1.0 and 60.3 +/- 4.0 pg/ml in
patients with normal LVEDP and 31.7 +/- 3.6 and 118.3 +/- 9.4 pg/ml i
n patients with elevated LVEDP. These data demonstrate that BNP and AN
P levels are strongly elevated in patients with dialysis-dependent chr
onic renal failure compared to patients with normal LVEDP (BNP 15.6-fo
ld, ANP 2.2-fold, after hemodialysis; P < 0.001) or elevated LVEDP (BN
P 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that th
e elevation in BNP concentrations was more pronounced than that in ANP
plasma concentrations. The present results provide support that other
factors than volume overload, for example, decreased renal clearance,
are also involved in the elevation in BNP and ANP plasma levels in ch
ronic renal failure. The stronger elevation in BNP concentrations in p
atients with chronic renal failure and in patients with elevated LVEDP
and the less pronounced decrease during hemodialysis suggest a differ
ent regulation of BNP and ANP plasma concentrations.