Siddiqui A A, Wilson D R
Can Med Assoc J. 1972 Mar 18;106(6):654-9.
Two cases of primary hyperparathyroidism due to single parathyroid adenomas presented with the additional feature of hyperchloremic acidosis. The defect in urinary acidification responsible was not of the distal or gradient-limited type since both patients could lower urine pH adequately. However, there was a defect of bicarbonate reabsorption, an abnormality referred to as the proximal or rate-limited type of renal tubular acidosis. It is suggested that this defect represents an exaggeration of the physiological effect of parathormone on bicarbonate reabsorption and may be responsible for the frequent finding of hyperchloremia in association with primary hyperparathyroidism as well as for the urinary bicarbonate-wasting associated with a variety of causes of secondary hyperparathyroidism.
两例因单发甲状旁腺腺瘤导致的原发性甲状旁腺功能亢进患者出现了高氯性酸中毒这一额外特征。导致尿酸化缺陷的原因并非远端或梯度受限型，因为两名患者均可充分降低尿液pH值。然而，存在碳酸氢盐重吸收缺陷，这种异常被称为近端或速率受限型肾小管酸中毒。有人提出，这种缺陷代表了甲状旁腺激素对碳酸氢盐重吸收的生理作用的过度增强，可能是原发性甲状旁腺功能亢进症中频繁出现高氯血症的原因，也可能是与各种继发性甲状旁腺功能亢进症病因相关的尿碳酸氢盐流失的原因。
