Vaziri N D, Nellans R E, Brueggemann R M, Barton C H, Martin D C
South Med J. 1979 May;72(5):530-4, 536. doi: 10.1097/00007611-197905000-00009.
We studied 15 renal transplant recipients for evidence of tubular dysfunction. Eight patients were hypophosphatemic, and two had systemic acidosis with a urinary acidification defect. Mild aminoaciduria and bicarbonaturia were present in four and 14 patients, respectively. Elevated parathyroid hormone level was found in only one patient. Tubular reabsorption of phosphorus was depressed in all eight hypophosphatemic patients, while no such abnormalities were observed in 14 control subjects. Defective tubular reabsorption of phosphorus was the most striking abnormality. None of the parameters studied, including immunosuppressant therapy, parathyroid hormone levels, creatinine clearance, or acid-base balance, clearly account for the pathogenesis of this abnormality.
我们研究了15例肾移植受者,以寻找肾小管功能障碍的证据。8例患者出现低磷血症,2例有系统性酸中毒伴尿酸化缺陷。分别有4例和14例患者存在轻度氨基酸尿和重碳酸盐尿。仅1例患者甲状旁腺激素水平升高。所有8例低磷血症患者的肾小管对磷的重吸收均降低,而14例对照受试者未观察到此类异常。肾小管对磷的重吸收缺陷是最显著的异常。所研究的参数,包括免疫抑制治疗、甲状旁腺激素水平、肌酐清除率或酸碱平衡,均不能明确解释这种异常的发病机制。