Graber M, Corish D
Department of Medicine, Veterans Administration Medical Center, Northport, NY.
Am J Kidney Dis. 1991 Nov;18(5):527-45. doi: 10.1016/s0272-6386(12)80647-0.
It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).
通常认为，自由水潴留是低钠血症时降低血清钠浓度的主要因素。为了确定其他电解质的浓度是否也会被类似地稀释，我们纳入了51例低钠血症患者（血钠 = 121±1 mmol/L [mEq/L]），并将低钠血症时的电解质和实验室检查值与血钠在正常范围时（138±1 mmol/L）的值进行了比较。这两次测量之间的平均间隔时间为12天。在低钠血症时，血清钠和氯显著降低了12%至15%。虽然许多低钠血症患者其他被测电解质的浓度明显升高或降低，但在低钠血症时这些电解质的平均浓度均无显著变化。碳酸氢盐（正常时血浆浓度为26.1±0.6，低钠血症时为25.2±0.8 mmol/L）、钾（4.31±0.10 vs 4.33±0.15 mmol/L）、白蛋白、磷酸盐和肌酐的平均值均未改变。在细胞外液（ECF）容量临床正常的患者以及存在真性或有效ECF减少的患者中，均观察到了这些实验室检查值的稳定性。尿钠（UNa）浓度被发现是ECF容量状态的可靠预测指标，而钠排泄分数（FENa）则不是。电解质紊乱在低钠血症患者中很常见，但通常仅限于使用利尿剂的患者或ECF容量异常的患者。在没有这些复杂情况时，血浆电解质通常是正常的，不会像钠和氯那样因稀释而降低。基于对低钠血症时电解质调节的经典知识和最新知识的综述，我们提出两个因素可以解释这些观察结果。首先，由于尿中钠的丢失以及可能存在的钠向细胞内转移，稀释程度被高估了。其次，低钠血症激活了肾脏和肾外的适应性机制，从而稳定了其他离子的浓度。其中一种机制是细胞肿胀，它触发了一种容量调节反应，导致离子和水释放到ECF中。其他适应性机制由抗利尿激素（ADH）本身以及心房利钠肽（ANP）介导。
