Usberti M, Gazzotti R M, Poiesi C, D'Avanzo L, Ghielmi S
Servizio di Nefrologia e Dialisi, Ospedale di Leno (BS), Italia.
Am J Nephrol. 1995;15(1):38-47. doi: 10.1159/000168800.
Renin-angiotensin-aldosterone system, plasma atrial natriuretic peptide (PANP), and blood volume (BV) have been investigated in 20 nephrotic patients with normal renal function and with (group 1; n = 12) or without (group 2; n = 8) sodium retention. Patients of group 1 had a plasma albumin (PALB) concentration < 1.7 g/dl, low BV and PANP levels, a reduced fractional excretion of lithium (FELi), and high plasma angiotensin II levels. Patients of group 2 had PALB > 1.7 g/dl, and the other parameters were normal. The spontaneous intake of dietary sodium was lower in group 1 than in group 2. In all patients the BV was directly correlated with PALB, and the plasma renin activity (PRA) was inversely correlated with both BV and PALB. A nonlinear inverse relationship was present between plasma aldosterone (PALD) levels and fractional excretion of sodium (FENa). The acute expansion of the BV in patients of group 1 normalized PRA, PALD, PAII, FENa, and FELi and increased PANP. The administration of spironolactone to the patients of both groups had variable effects on FENa, did not modify PRA and PALD, and reduced body weight, PANP, and FELi, thus suggesting that the reduction of BV induced by the drug increased the proximal reabsorption of sodium. Three additional patients who had sodium retention, PALB of 2.3-2.4 g/dl, normal PRA and PALD, elevated urinary excretion of aldosterone, and a slightly low PANP showed a spontaneous normalization of urinary aldosterone and PANP associated with natriuresis and weight loss, but thereafter urinary aldosterone increased, PANP decreased, and the sodium retention began again. Our data suggest that in nephrotic patients with severe hypoalbuminemia, contraction of BV plays a major role in promoting the sodium retention through the activation of compensatory hormonal mechanisms. On the other hand, when PALB is not severely reduced, the patients have normal BV, but they are very sensitive to small changes of BV which are better evidenced by modifications of the urinary excretion of aldosterone and PANP rather than by the profiles of PRA and PALD.
对20例肾功能正常且有（第1组；n = 12）或无（第2组；n = 8）钠潴留的肾病患者的肾素 - 血管紧张素 - 醛固酮系统、血浆心钠素（PANP）和血容量（BV）进行了研究。第1组患者的血浆白蛋白（PALB）浓度<1.7 g/dl，血容量和PANP水平低，锂的分数排泄（FELi）降低，血浆血管紧张素II水平高。第2组患者的PALB>1.7 g/dl，其他参数正常。第1组患者的饮食钠自发摄入量低于第2组。在所有患者中，血容量与PALB直接相关，血浆肾素活性（PRA）与血容量和PALB均呈负相关。血浆醛固酮（PALD）水平与钠的分数排泄（FENa）之间存在非线性负相关。第1组患者血容量的急性增加使PRA、PALD、PAII、FENa和FELi恢复正常，并增加了PANP。对两组患者给予螺内酯对FENa有不同影响，未改变PRA和PALD，并降低了体重、PANP和FELi，因此表明该药物诱导的血容量减少增加了近端钠重吸收。另外3例有钠潴留、PALB为2.3 - 2.4 g/dl、PRA和PALD正常、醛固酮尿排泄增加且PANP略低的患者，其醛固酮尿和PANP自发恢复正常，伴有利钠和体重减轻，但此后醛固酮尿增加，PANP降低，钠潴留再次开始。我们的数据表明，在严重低白蛋白血症的肾病患者中，血容量收缩通过激活代偿性激素机制在促进钠潴留中起主要作用。另一方面，当PALB未严重降低时，患者血容量正常，但他们对血容量的微小变化非常敏感，这通过醛固酮尿排泄和PANP的改变比通过PRA和PALD的变化更能得到证明。
