Stinebaugh B J, Ghafary E, Goldstein M B, Halperin M L, Schloeder F X, Suki W N
Nephron. 1978;20(3):141-6. doi: 10.1159/000181212.
An augmented renal capacity to reabsorb bicarbonate (RHCO3) has been noted in patients with distal renal tubular acidosis (dRTA), and construed as evidence that the basic defect in dRTA is abnormal distal tubular permeability. According to this interpretation, the absence of a disequilibrium pH due to a back-leak of H2C03 permits increased distal H+ secretion and results in an increased RHCO3. To test this assumption, we have evaluated the effect of acute elimination of the disequilibrium pH by carbonic anhydrase infusion. The results establish that this maneuver doses not cause a rise in RHCO3. Thus, the elevated value of RHC3 described in dRTA cannot be the consequence of increased back-diffusion of H2CO3 and is more likely due to coexisting extracellular volume depletion and/or postassium deficiency.
在远端肾小管酸中毒（dRTA）患者中已观察到肾脏重吸收碳酸氢盐（RHCO3）的能力增强，这被解释为dRTA的基本缺陷是远端肾小管通透性异常的证据。根据这一解释，由于H2C03的反向弥散导致的pH失衡缺失，使得远端H+分泌增加，从而导致RHCO3增加。为了验证这一假设，我们评估了通过输注碳酸酐酶急性消除pH失衡的效果。结果表明，这一操作不会导致RHCO3升高。因此，dRTA中描述的RHC3升高值并非H2CO3反向弥散增加的结果，更可能是由于并存的细胞外液容量减少和/或钾缺乏。
