Cianciaruso B, Bellizzi V, Minutolo R, Colucci G, Bisesti V, Russo D, Conte G, De Nicola L
Division of Nephrology, School of Medicine, First University, Naples, Italy.
J Am Soc Nephrol. 1996 Feb;7(2):306-13. doi: 10.1681/ASN.V72306.
The renal response to sodium restriction was evaluated, and the concurrent changes of the plasma levels of aldosterone (ALDO) and atrial natriuretic peptide (ANP), in healthy patients (NOR), in normotensive patients with non-nephrotic chronic glomerulonephritis and normal renal function (GN), and in patients with glomerulonephritis and moderate renal failure (GFR, 41 +/- 4 mL/min; CRF). The three groups were studied for 1 wk after changing from a normal-sodium diet (NSD, 235 mEq NaCl/day) to a low-sodium diet (LSD, 35 mEq NaCl/day). All patients reached a steady sodium balance within the 4th and 5th day of LSD with an analogous cumulative loss of sodium. After salt restriction, the fractional urinary sodium excretion diminished by the same extent in the three groups, whereas the fractional free-water generation, measured during water diuresis, did not vary in NOR and markedly decreased in GN and CRF. Plasma levels of ALDO were similar in all groups at NSD and similarly increased during LSD. In GN and CRF, as compared to NOR, ANP levels were higher at NSD and decreased by a minor extent during LSD. Notably, in GN and CRF, but not in NOR, the attainment of the new sodium balance after sodium restriction was preceded by a significant parallel reduction of blood pressure and GFR; the GFR decline was secondary to a major decrement of RPF so that filtration fraction (FF) increased. It was concluded that in NOR, distal tubular effects of ANP and ALDO account for the attainment of sodium balance during LSD. As a difference, both GN and CRF patients achieve the new sodium balance primarily through hemodynamic changes: the renal hypoperfusion secondary to a decrease in blood pressure that diminishes the filtered load of sodium, and the increase of FF that enhances the proximal tubular sodium reabsorption. This abnormal response seems related to both the minor suppression of ANP and the increased salt-sensitivity of blood pressure that are likely the result of the presence of volume expansion.
对健康患者（NOR组）、肾功能正常的非肾病性慢性肾小球肾炎的血压正常患者（GN组）以及患有肾小球肾炎和中度肾衰竭的患者（GFR为41±4 mL/min；CRF组），评估了肾脏对钠限制的反应以及醛固酮（ALDO）和心房利钠肽（ANP）血浆水平的同时变化。在从正常钠饮食（NSD，235 mEq氯化钠/天）改为低钠饮食（LSD，35 mEq氯化钠/天）后，对这三组进行了1周的研究。所有患者在LSD的第4天和第5天内达到稳定的钠平衡，钠的累积损失相似。限盐后，三组的尿钠排泄分数均以相同程度降低，而在水利尿期间测量的自由水生成分数在NOR组中没有变化，在GN组和CRF组中显著降低。在NSD时，所有组的ALDO血浆水平相似，在LSD期间同样升高。与NOR组相比，在NSD时，GN组和CRF组的ANP水平较高，在LSD期间下降幅度较小。值得注意的是，在GN组和CRF组而非NOR组中，钠限制后达到新的钠平衡之前，血压和GFR会出现显著的平行下降；GFR下降继发于肾血浆流量（RPF）的大幅减少，从而使滤过分数（FF）增加。得出的结论是，在NOR组中，ANP和ALDO的远端肾小管作用导致了LSD期间钠平衡的实现。不同的是，GN组和CRF组患者主要通过血流动力学变化实现新的钠平衡：血压下降继发的肾脏灌注不足减少了钠的滤过负荷，以及FF增加增强了近端肾小管钠重吸收。这种异常反应似乎与ANP的轻微抑制以及血压盐敏感性增加有关，这可能是容量扩张存在的结果。
