Ulmann A, Chkoff N, Lacour B
Adv Nephrol Necker Hosp. 1983;12:331-40.
Systematic study undertaken of 44 transplant patients with plasma creatinine below 0.11 mmol/L indicated renal phosphorus leak in approximately two-thirds of them and increased plasma PTH in all but one. Plasma 1,25(OH)2D was elevated in half the patients in whom it was measured. The lack of correlation found between plasma 1,25(OH)2D and plasma PTH or phosphorus probably indicates tubular lesions resulting in decreased production of 1,25(OH)2D. A phosphorus restriction test in 12 hypophosphatemic patients demonstrated that the reduced renal phosphorus reabsorption probably was due to both persisting hyperparathyroidism and a PTH-independent phosphorus leak.
对44例血浆肌酐低于0.11 mmol/L的移植患者进行的系统研究表明,其中约三分之二存在肾磷泄漏,除1例患者外,其余患者的血浆甲状旁腺激素(PTH)均升高。在半数接受检测的患者中,血浆1,25(OH)₂D升高。血浆1,25(OH)₂D与血浆PTH或磷之间缺乏相关性,这可能表明肾小管病变导致1,25(OH)₂D生成减少。对12例低磷血症患者进行的磷限制试验表明,肾磷重吸收减少可能是由于持续性甲状旁腺功能亢进和一种不依赖PTH的磷泄漏共同所致。