Franz M, Woloszczuk W, Hörl W H
Division of Nephrology and Dialysis, Department of Internal Medicine, University of Vienna, Austria.
Kidney Int. 2001 May;59(5):1928-34. doi: 10.1046/j.1523-1755.2001.0590051928.x.
Biologically active N-terminal fragments such as proANP(1-30), proANP(31-67), and proANP(1-98) derive from the prohormone of alpha-human atrial natriuretic peptide [proANP(99-126) or alpha-ANP]. No systematic data are available for patients with different kidney diseases.
Specific immunoassays were developed to determine plasma and urine concentrations of these fragments in 121 patients with different degrees of kidney function and urinary protein excretion, respectively.
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 proANP(31-67) excretion even before serum creatinine levels started to rise. The progression of renal failure caused a significant rise of circulating proANP(1-30) (4.3-fold) and proANP(31-67) (3.0-fold) compared with patients with normal renal function. Urinary excretion of proANP peptides significantly 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 proANP(1-30) increased up to 4.4-fold and urinary excretion of proANP(31-67) increased up to 2.4-fold in patients with proteinuria in excess of 3 g/24 h.
Plasma concentrations and urinary excretion of proANP(1-30) and proANP(31-67) are affected by kidney disease and function, but not by proteinuria per se. It is proposed that the diseased kidney increases early urinary excretion of proANP fragments to participate in the regulation of renal function as well as sodium and water excretion.
生物活性N端片段，如proANP(1 - 30)、proANP(31 - 67)和proANP(1 - 98)，来源于α - 人心房利钠肽的前体激素[proANP(99 - 126)或α - ANP]。目前尚无针对不同肾脏疾病患者的系统性数据。
分别开发了特异性免疫测定法，以测定121例肾功能和尿蛋白排泄程度不同的患者血浆和尿液中这些片段的浓度。
在患有肾脏疾病且肾功能正常无蛋白尿的患者中，循环中的proANP(1 - 30)和proANP(31 - 67)分别增加了2.8倍和6.5倍。这些患者中proANP(31 - 67)的尿排泄量增加了7.7倍，而proANP(1 - 30)未受影响。肾功能受损的患者即使在血清肌酐水平开始升高之前，尿中proANP(31 - 67)的排泄量也会急剧增加。与肾功能正常的患者相比，肾衰竭的进展导致循环中的proANP(1 - 30)（4.3倍）和proANP(31 - 67)（3.0倍）显著升高。当血清肌酐水平>5.0 mg/dL时，proANP肽的尿排泄量显著增加[proANP(1 - 30)为26倍，proANP(31 - 67)为8.4倍]。蛋白尿超过3 g/24 h的患者中，proANP(1 - 30)的尿排泄量增加至4.4倍，proANP(31 - 67)的尿排泄量增加至2.4倍。
proANP(1 - 30)和proANP(31 - 67)的血浆浓度和尿排泄量受肾脏疾病和功能影响，但不受蛋白尿本身影响。研究表明，患病肾脏会增加proANP片段的早期尿排泄，以参与肾功能以及钠和水排泄的调节。
