Graf H, Kovarik J, Stummvoll H K, Wolf A, Pinggera W F
Proc Eur Dial Transplant Assoc. 1979;16:624-9.
Maximal tubular phosphate reabsorption capacity corrected for changes in glomerular filtration rate (TmP/GFR) was taken as a measure of renal phosphate handling in patients with good and stable functioning kidney allografts. TmP/GFR values were within the normal range in only one-fifth of the patients. Eighty per cent had an abnormally low renal phosphate threshold concentration. Persistent hyperparathyroidism was the causative factor of this diminished tubular reabsorption in less than half of these patients, the majority of them showing an iPTH independent phosphate leak. Although glucocorticoids, azathioprine and tubular damage of the graft in the perioperative phase may contribute to this iPTH independent phosphate wasting, no single causative factor could be identified. Cases with hypophosphataemia should be treated in order to avoid symptoms of phosphate depletion. Active Vitamin D metabolites would be the therapy of choice by suppressing the parathyroid glands ("chemical PTX") and by directly enhancing tubular phosphate reabsorption. In persistent hyperpathyroidism with hypercalcaemia, surgical parathyroidectomy must be considered. Therapy with phosphate salts is only symptomatic and should be used only as an adjunct.
用肾小球滤过率变化校正的最大肾小管磷重吸收能力（TmP/GFR）作为衡量功能良好且稳定的同种异体肾移植患者肾脏磷处理情况的指标。仅五分之一的患者TmP/GFR值在正常范围内。80%的患者肾磷阈值浓度异常低。在不到一半的此类患者中，持续性甲状旁腺功能亢进是肾小管重吸收减少的致病因素，其中大多数患者表现为独立于甲状旁腺激素的磷泄漏。尽管糖皮质激素、硫唑嘌呤和围手术期移植物的肾小管损伤可能导致这种独立于甲状旁腺激素的磷消耗，但无法确定单一的致病因素。低磷血症患者应接受治疗，以避免磷耗竭症状。活性维生素D代谢产物将是首选治疗方法，通过抑制甲状旁腺（“化学性甲状旁腺切除”）并直接增强肾小管对磷的重吸收。对于伴有高钙血症的持续性甲状旁腺功能亢进，必须考虑进行手术甲状旁腺切除术。磷酸盐治疗仅为对症治疗，应仅作为辅助手段使用。
