SERUM POTASSIUM CONCENTRATION IN ACIDEMIC STATES
SERUM POTASSIUM CONCENTRATION IN ACIDEMIC STATES
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DOI：
10.1159/000182061
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发表时间：
1981-01-01
期刊：
影响因子：
2.5
通讯作者：
VAAMONDE, CA
中科院分区：
文献类型：
--
作者：
PEREZ, GO;OSTER, JR;VAAMONDE, CA
人们普遍认为，酸中毒导致高钾血症是由于钾从细胞内转移到细胞外。有充分的临床和实验证据支持简单的有机酸中毒不会引起高钾血症的结论。在与无机酸相关的酸中毒（呼吸性酸中毒、终末期尿毒症酸中毒、NH 4Cl-或CaCl 2-诱导的酸中毒）中，酸血症可导致血清K浓度可预测的升高。在与非无机有机酸相关的酸中毒中（糖尿病和酒精性酸中毒、乳酸酸中毒、甲醇和继发于甲基丙二酸和异戊酸的不常见形式的有机酸中毒，以及乙二醇、三聚乙醛和水杨酸中毒），在无并发症的病例中，血清K浓度通常保持在正常范围内。除酸血症外，许多因素可能导致其中一些患者的高钾血症。这些包括脱水和肾灌注不足、既存肾脏疾病、高钙血症、糖尿病、醛固酮减少症、钾平衡状态和治疗。无机酸和有机酸对钾跨膜运动的不同影响的机制尚不清楚。普遍的假设，有利于自由的有机阴离子进入细胞，而不产生一个梯度的H+，并避免了细胞内的K外流。高钾血症在有机酸中毒临床状态中的重要性是显而易见的。由于有机酸中毒不应伴有血清钾浓度升高，因此应寻找上述并发因素。经典的教学，没有高钾血症在严重的酸中毒是指示严重的钾缺乏症，可能不是普遍有效的患者与简单的有机酸中毒。
It has been generally accepted that acidosis results in hyperkalemia because of shifts of K from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl- or CaCl2-induced acidosis), acidemia results in predictable increases in serum K concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methyl-malonica and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum K concentration usually remains within the normal range in uncomplicated cases. A number of factors may be responsible for hyperkalemia in some of these patients other than the acidemia. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of K balance and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of K remains undefined. The prevalent hypothesis, favors the free penetrance of the organic anion into cells without creating a gradient for the H+ and, obviating the efflux of intracellular K. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias should not be expected to be accompanied by elevations of serum K concentration. The classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe K deficiency, may not be universally valid in patients with uncomplicated organic acidemias.