Fluid balance in patients with chronic renal failure assessed with N‐terminal proatrial natriuretic peptide, atrial natriuretic peptide and ultrasonography

Abstract

The N-terminal proatrial natriuretic peptide (proANP) has become an important parameter for assessing the prognosis of patients with cardiac disease. Its use for evaluating the hydration status in patients with chronic renal failure, however, is still under investigation. The present study comprised 12 haemodialysis (HD) and 17 pre-dialysis patients. In the HD patients, the inferior vena cava diameter during quiet expiration (IVCe) was estimated by ultrasonography and plasma concentrations of N-terminal proANP, atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) were measured before and 4 h after termination of HD. In the pre-dialysis patients venous blood samples were taken during rest to measure plasma N-terminal proANP and ANP and serum creatinine. Normal values for N-terminal proANP and ANP were obtained from 18 healthy volunteers. The plasma concentrations of N-terminal proANP and ANP in healthy volunteers were 328 +/- 92 and 11.4.0 +/- 3.1 pM L-1, respectively. In pre-dialysis patients, serum creatinine ranged from 110 to 447 microM L-1 and was significantly correlated to plasma N-terminal proANP (r = 0.60, P < 0.05) but not to ANP. This may indicate that N-terminal proANP is more dependent on renal function for its clearance than ANP, which is probably cleared by extrarenal mechanisms as well. In HD patients, IVCe was significantly correlated to the three hormones before HD, most strongly to N-terminal proANP. After dialysis, IVCe was significantly correlated to ANP and cGMP but was not correlated to N-terminal proANP. This may suggest that proANP takes a longer time than other hormones to reflect changes in intravascular volume. In conclusion, N-terminal proANP is a hormone closely related to degree of renal function. Furthermore, it is a sensitive marker reflecting the interdialytic hydration status in HD patients, as indicated by its high correlation to IVCe, a standard method which is used frequently nowadays to assess the body hydration. However N-terminal proANP could not reflect the acute changes in fluid volume induced by HD, probably because it is slowly metabolized.

Proatrial Natriuretic Peptide (1–98), but Not Cystatin C, Is Predictive for Occurrence of Acute Renal Insufficiency in Critically Ill Septic Patients

“…Among patients with chronic renal failure it has been found to be highly dependent on renal function for its clearance and a better marker of renal impairment than α-ANP, which is also cleared by extrarenal mechanisms [6]. In the same study, N-terminal proANP was closely related to the degree of renal function and better correlated with hydration status measured by inferior vena cava diameter than α-ANP.…”

“…It is associated with increased levels of N-terminal proANP, but not with left ventricular failure (LVEF) [1]. In patients with chronic renal failure, proANP(1–98) has been closely related to renal function and interdialytic hydration status [6]. The greatest difference among natriuretic peptides in patients with chronic renal failure and controls was with proANP(1–98).…”

N-terminal proBNP—Marker of Cardiac Dysfunction, Fluid Overload, or Malnutrition in Hemodialysis Patients?

“…Atrial natriuretic peptide (ANP) and its cleavage product N-terminal pro-ANP were the first natriuretic peptides to be studied, but more recently focus has shifted to brain natriuretic peptide (BNP), which is released by the ventricle rather than the atrium. In patients with ESRD on hemodialysis, ANP has been reported to be more responsive to changes in intravascular volume than BNP, whereas BNP appears more reflective of cardiac dysfunction (3). This may be due to the different sizes and half-lives of the peptides, because ANP is cleared during high-flux hemodialysis, with a post dialysis rebound taking some 80 to 100 minutes to re-equilibrate (Mathavakkannan, unpublished data).…”

Regulation of cell volume by glycosaminoglycans

“…Hyaluronan is synthesised at the inner side of plasma membranes [Prehm, 1984] and exported by the ABC transporters MRP5 from fibroblasts [Schulz et al, 2007] and CFTR from epithelial cells . Hyaluronan export from fibroblasts is inhibited by intracellular cGMP which also acts as a vasodilator [Carvajal et al, 2000], and mediator of tissue hydration [Metry et al, 2001]. …”