Fiaschi E, Mioni G, Maschio G, D'Angelo A, Ossi E
Nephron. 1975;14(2):163-80. doi: 10.1159/000180446.
In chronic uremia, the clinical disorders o calcium and phosphorus metabolism are influenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in TmPO4 values; (3) physiochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO4], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme 'avidity' of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; (4) structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually observed.
在慢性尿毒症中，钙和磷代谢的临床紊乱受以下因素影响：（1）肠道对钙和磷的吸收，导致在正常饮食摄入情况下钙和磷呈负平衡；（2）肾脏对钙和磷的处理：钙的分数转运（近端小管中发生的等渗重吸收）不受肾小球滤过率（GFR）改变的影响，而Tm限制的重吸收严重受损；即使在肾单位数量减少的情况下，通过TmPO4值的成比例降低，仍可维持磷的外部平衡；（3）体内钙和磷的物理化学状态及周转：与对照组相比，尿毒症患者的分布空间、钙周转率和骨 accretion率增加；肾性骨软化症患者进行钙输注试验后，血浆[PO4]会有规律地升高，而肾性骨纤维炎患者则会出现显著下降，这是由于骨骼对磷酸钙的极度“亲和力”所致；高磷血症在使血浆[Ca]低于给定代谢状态预期值方面起关键作用；此外，细胞对磷摄取的增加可在一定程度上抵消肾脏对磷清除的减少；（4）骨组织的结构和生化改变：尿毒症骨营养不良主要由两个成分组成：（a）骨软化症，有类骨质过多、钙化前沿消失和弥漫性病理性矿化，以及（b）骨纤维炎，有正常矿化骨的严重吸收、轻微类骨质过多和几乎正常的钙化前沿；（5）激素因素：甲状旁腺的慢性刺激可能导致可抑制甚至自主性甲状旁腺功能亢进。至于维生素D，有人提出尿毒症肾无法合成维生素D的活性代谢产物1,25 - 二羟胆钙化醇：这导致肠道对钙的吸收受损。相反，降钙素在慢性尿毒症中的作用仍不确定，因为通常观察到血浆[Ca]值较低。
