Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure

1994 ◽  
Vol 72 (6) ◽  
Author(s):  
C. Haug ◽  
A. Metzele ◽  
J. Steffgen ◽  
M. Kochs ◽  
V. Hombach ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Ventricular Filling Pressure ◽  
Ventricular Filling

Elevated Plasma C-Type Natriuretic Peptide Concentrations in Patients with Chronic Renal Failure

1994 ◽  
Vol 87 (3) ◽  
pp. 319-322 ◽  
Author(s):  
Kazuhito Totsune ◽  
Kazuhiro Takahashi ◽  
Osamu Murakami ◽  
Fumitoshi Satoh ◽  
Masahiko Sone ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Heart Association ◽  
Normal Subjects ◽  
Atrial Natriuretic

1. C-type natriuretic peptide is a neuropeptide, which is also produced by the vascular endothelial cells. Plasma immunoreactive C-type natriuretic peptide concentrations in patients with various diseases have not yet been studied. 2. Plasma immunoreactive C-type natriuretic peptide concentrations were studied by radioimmunoassay in normal subjects, patients with congestive heart failure, non-dialysed patients with chronic renal failure and haemodialysis patients with chronic renal failure. The C-type natriuretic peptide levels were compared with the levels of atrial natriuretic peptide and brain natriuretic peptide. 3. Plasma immunoreactive C-type natriuretic peptide concentrations were greatly elevated in patients with chronic renal failure [non-dialysed, 13.0 ± 4.2 pmol/l (mean ± SEM), n = 9, P < 0.01) compared with normal subjects (4.4 ± 0.4 pmol/l, n = 26); haemodialysis, 16.1 ± 2.1 pmol/l, n = 13, P < 0.01], but not in patients with congestive heart failure (New York Heart Association Class II-IV, 3.0 ± 0.7 pmol/l, n = 11, P > 0.05). Plasma immunoreactive atrial natriuretic peptide and brain natriuretic peptide concentrations were elevated both in patients with congestive heart failure and in haemodialysis patients with chronic renal failure. 4. Reverse-phase high performance liquid chromatography showed that immunoreactive C-type natriuretic peptide in plasma from normal subjects and haemodialysis patients was eluted in the positions of C-type natriuretic peptide −22 and −53. 5. These findings suggest that C-type natriuretic peptide is a non-cardiac circulating hormone and participates in the cardiovascular regulation in a different manner from atrial natriuretic peptide and brain natriuretic peptide.

Effect of haemodialysis on plasma concentrations of atrial natriuretic peptide in adult patients with chronic renal failure

1986 ◽  
Vol 110 (2) ◽  
pp. 193-196 ◽  
Author(s):  
J. V. Anderson ◽  
A. E. G. Raine ◽  
A. Proudler ◽  
S. R. Bloom
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Molecular Form ◽  
Plasma Concentrations ◽  
Before And After ◽  
Healthy Control ◽  
Water Accumulation ◽  
Atrial Natriuretic

ABSTRACT Twenty patients with chronic renal failure were studied before and after haemodialysis. Plasma atrial natriuretic peptide (ANP) concentrations were markedly elevated (P < 0·01) before dialysis in comparison with healthy control subjects. After haemodialysis the plasma ANP concentration was lower in 19 patients (P < 0·01) but remained above the normal range in all but three cases. Systolic and diastolic blood pressure and body weight fell during dialysis but none of these changes correlated with the reduction of the plasma ANP concentration. Chromatographic analysis of plasma extracts indicated that α-ANP is the predominant circulating molecular form. The increase in concentration of ANP in plasma between dialyses, at a time when many patients are susceptible to sodium and water overload, and its return towards normal after dialysis supports the putative role of ANP as a circulating factor released in response to sodium and water accumulation. J. Endocr. (1986) 110, 193–196

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