Plasma concentration and urinary excretion of N-terminal proatrial natriuretic peptides in patients with kidney diseases

Background Biologically active N-terminal fragments such as proANP(1-30), p roANP(31-67), and proATP(1-98) derive from the prohor mone of alpha -human atrial natriuretic peptide [Fro4NP(99-126) or alpha -ANP]. No systematic da ta are available for patients with different kidney diseases. Methods. Specific immunoassays were developed to determine plasma and urine concentrations of these fragments in 121 patients with different degrees o f kidney function and urinary protein excretion, respectively. Results. In patients with kidney disease and normal renal function without proteinuria, circulating proANP(1-30) and proANP(31-67) increased 2.8-fold and 6.5-fold, respectively. Urinary excretion of proANP(31-67) increased by a factor of 7.7 in these patients, whereas proANP(1-30) was not affected. Patients with impaired renal function had a dramatic increase of urinary pr oANP(31-67) excretion even before serum creatinine levels starred to rise. The progression of renal failure caused a significant rise of circulating p roANP(1-30) (1.3-fold) and proANP(31-67) (3.0-fold) compared with patients with normal renal function. Urinary; excretion of proANP peptides significa ntly increased, particularly when the serum creatinine level was >5.0 mg/dL [proANP(1-30) 26-fold, proANP(31-67) 8.4-fold]. Urinary excretion of proAN P(130) increased up to 4.4-fold and urinary excretion of proANP(31-67) incr eased up to 2.4-fold in patients with proteinuria in excess of 3 g/24 h. Conclusions. Plasma concentrations and urinary excretion of proANP(1-30) an d proANP(31-67) are affected by kidney disease and function, but not by pro teinuria per se. it is proposed that the diseased kidney increases early ur inary excretion of proANP fragments to participate in the regulation of ren al function as well as sodium and water excretion.