Coburn J W, Massry S G
J Clin Invest. 1970 Jun;49(6):1073-87. doi: 10.1172/JCI106323.
The changes in serum calcium and the renal handling of this ion were evaluated during phosphate depletion. 96 renal clearance studies were carried out in 10 dogs before and after prolonged phosphate depletion (30-160 days) and after repletion. Depletion was produced by reducing phosphate intake and administering aluminum hydroxide gel while intakes of sodium, calcium, and magnesium were constant. With phosphate depletion, serum phosphorus fell to less than 1.0 mg/100 ml and diffusible serum calcium either remained unchanged or rose transiently. Glomerular filtration rate (GFR) fell by 15 to 53%. Despite the reduced filtered load of calcium, its fractional excretion increased in most experiments. This hypercalciuria was not dependent upon changes in sodium or magnesium excretion, or the urinary concentration of complexing anions, and persisted after sodium restriction. Phosphate repletion reversed the effects on GFR and calcium excretion. The intravenous infusion of small quantities of phosphate (0.04 mmole/min) into either intact or thyroparathyroidectomized (T-PTX), phosphate-depleted animals caused a significant reduction in fractional excretion of calcium, but the intrarenal infusion of 0.02 mmole/min of phosphate into one kidney failed to produce an ipsilateral effect. The administration of parathyroid extract reduced fractional calcium excretion, but the latter remained significantly elevated. After T-PTX, fractional calcium excretion did not increase in the phosphate-depleted animals. Furthermore, serum calcium was normal after T-PTX until serum phosphorus increased slightly, and only then did hypocalcemia develop. These observations indicate that (a) phosphate depletion produces hypercalciuria through a reduction in tubular reabsorption of calcium which is not due to changes in the tubular reabsorption of other ions; this effect is not reversed by the direct intrarenal infusion of phosphate; (b) a state of functional hypoparathyroidsm occurs during phosphate depletion which may, in part, cause reduced tubular reabsorption of calcium; (c) other extra renal mechanism(s), possibly related to events occurring in bone as a result of phosphate depletion, may have an effect on urinary calcium excretion; and (d) in the phosphatedepleted state, parathyroid hormone is not required for the maintenance of a normal level of serum calcium.
在磷酸盐缺乏期间，对血清钙的变化以及该离子在肾脏中的处理情况进行了评估。在10只狗身上进行了96次肾脏清除率研究，研究时间为长期磷酸盐缺乏（30 - 160天）之前、之后以及补充之后。通过减少磷酸盐摄入并给予氢氧化铝凝胶来造成缺乏，同时钠、钙和镁的摄入量保持恒定。随着磷酸盐缺乏，血清磷降至低于1.0mg/100ml，可扩散血清钙要么保持不变，要么短暂升高。肾小球滤过率（GFR）下降了15%至53%。尽管钙的滤过负荷降低，但在大多数实验中其分数排泄增加。这种高钙尿症不依赖于钠或镁排泄的变化，也不依赖于络合阴离子的尿浓度，并且在限钠后仍然存在。补充磷酸盐可逆转对GFR和钙排泄的影响。向完整或甲状旁腺切除（T - PTX）的磷酸盐缺乏动物静脉内输注少量磷酸盐（0.04毫摩尔/分钟）会导致钙的分数排泄显著降低，但向一侧肾脏肾内输注0.02毫摩尔/分钟的磷酸盐未能产生同侧效应。给予甲状旁腺提取物可降低钙的分数排泄，但后者仍显著升高。T - PTX后，磷酸盐缺乏动物的钙分数排泄并未增加。此外，T - PTX后血清钙正常，直到血清磷略有升高，此时才出现低钙血症。这些观察结果表明：（a）磷酸盐缺乏通过降低钙的肾小管重吸收产生高钙尿症，这并非由于其他离子的肾小管重吸收变化所致；直接肾内输注磷酸盐并不能逆转这种效应；（b）在磷酸盐缺乏期间会出现功能性甲状旁腺功能减退状态，这可能部分导致钙的肾小管重吸收减少；（c）其他肾外机制，可能与磷酸盐缺乏导致的骨骼中发生的事件有关，可能会对尿钙排泄产生影响；（d）在磷酸盐缺乏状态下，维持正常血清钙水平不需要甲状旁腺激素。
