Khanna A, Kurtzman N A
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA.
J Nephrol. 2006 Mar-Apr;19 Suppl 9:S86-96.
Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation mainly in the proximal tubule and bicarbonate generation predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na-H antiporter and to a smaller extent by the H-ATPase. The principal factors affecting HCO 3 reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na delivery and reabsorption, aldosterone, arterial pH, and arterial pCO2. To generate metabolic alkalosis, either a gain of base or a loss of acid, must occur. The loss of acid may be via the GI tract or by the kidney. Excess base may be gained by oral or parenteral HCO 3 administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate (GFR), volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelma's Syndromes. The effects of metabolic alkalosis on the body are varied and include effects on the central nervous system, myocardium, skeletal muscle, and the liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors promoting alkalosis and in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
代谢性碱中毒是一种主要的病理生理事件，其特征是细胞外液中碳酸氢盐增加或非挥发性酸丢失。肾脏通过两种机制维持正常的酸碱平衡：主要在近端小管进行碳酸氢盐重吸收，主要在远端肾单位进行碳酸氢盐生成。碳酸氢盐重吸收主要由钠-氢反向转运体介导，在较小程度上由氢-ATP酶介导。影响HCO₃重吸收的主要因素包括有效动脉血容量、肾小球滤过率、氯和钾。碳酸氢盐生成主要受远端钠的输送和重吸收、醛固酮、动脉pH值和动脉pCO₂的影响。要发生代谢性碱中毒，必须出现碱的增加或酸的丢失。酸的丢失可能通过胃肠道或肾脏。过量的碱可通过口服或胃肠外给予HCO₃或给予乳酸盐、醋酸盐或柠檬酸盐获得。有助于维持代谢性碱中毒的因素包括肾小球滤过率（GFR）降低、容量收缩、低钾血症、低氯血症和醛固酮过多。与代谢性碱中毒相关的临床状态有呕吐、盐皮质激素过多、肾上腺生殖器综合征、摄入甘草、使用利尿剂以及巴特综合征和吉特曼综合征。代谢性碱中毒对身体的影响是多方面的，包括对中枢神经系统、心肌、骨骼肌和肝脏的影响。一旦明确病因的病理生理学，这种疾病的治疗很简单。治疗包括逆转促进碱中毒的相关因素，在严重情况下，给予碳酸酐酶抑制剂、输注酸和进行低碳酸氢盐透析。
