Kurtz I, Dass P D, Cramer S
Division of Nephrology, UCLA School of Medicine.
Miner Electrolyte Metab. 1990;16(5):331-40.
Traditionally, the renal collecting duct has been assigned the dual role of (1) secreting protons derived from dietary metabolism to form luminal NH4+ and titratable acid and (2) generating new HCO3-. This view has recently been challenged. According to current concepts, whole body proton balance is maintained predominantly by the lungs which excrete protons derived from dietary metabolism as the acid anhydride CO2. In the process of excreting CO2, HCO3- is also lost from the body. It is the function of the kidney to generate new HCO3- to replenish this loss. The major site of new HCO3- generation is the proximal tubule rather than the collecting duct. New HCO3- is generated predominantly via the metabolism of organic anions, i.e. alpha-ketoglutarate, citrate, lactate, fatty acids. In the process of generating alpha-ketoglutarate from glutamine, NH4+ is formed. Under normal acid-base conditions, 50% of the NH4+ produced is excreted in the urine, and the remaining 50% is delivered to the renal veins. NH4+ delivered to the renal veins consumes HCO3- during ureagenesis. In the discussion which follows, these new concepts are reviewed and applied to an analysis of the pathophysiology of renal tubular acidosis.
传统上，肾集合管被赋予双重作用：（1）分泌源自饮食代谢的质子，以形成管腔NH4+和可滴定酸；（2）生成新的HCO3-。最近这一观点受到了挑战。根据当前的概念，全身质子平衡主要由肺维持，肺将源自饮食代谢的质子以酸酐CO2的形式排出。在排出CO2的过程中，HCO3-也从体内丢失。肾脏的功能是生成新的HCO3-以补充这种损失。新HCO3-生成的主要部位是近端小管而非集合管。新HCO3-主要通过有机阴离子（即α-酮戊二酸、柠檬酸、乳酸、脂肪酸）的代谢产生。在由谷氨酰胺生成α-酮戊二酸的过程中，会形成NH4+。在正常酸碱条件下，产生的NH4+有50%经尿液排出，其余50%则输送至肾静脉。输送至肾静脉的NH4+在尿素生成过程中消耗HCO3-。在接下来的讨论中，将对这些新概念进行回顾，并应用于肾小管酸中毒病理生理学的分析。
