Blazheevich N V, Fernándes R, Isaeva V A, Pereverzeva O G, Alekseeva I A
Vopr Med Khim. 1980 Jan-Feb;26(1):13-23.
Experimental chronic kidney insufficiency caused in rats the impairments of phosphoerus-calcium turnover (hyperphosphatemia and hypocalcemia), osteoporotic alterations in bones (decreas in specific gravity, in content of Ca, P and hydroxyproline) as well as calcinosis of internal tissues, particularly in the impaired kidney tissue. Decrease in phosphorus content of food down to 0.3% inhibited distinctly the development of these impairments and modulated their severity, lowering mortality of the animals with chronic kidney insufficienty. Administration of physiologic doses (0.025 mg) of 1 alpha-hydroxy vitamin D3/(1 alpha OHD3) which is a synthetic analogue of 1,25-dihydroxycholecalciferol (hormonal form of vitamin D synthesized in kidney) into rats with chronic kidney insufficiency (with limited content of phosphorus in the food) did not exhibit any additional curative effect on the patterns of bone metabolism studied; in this case calcinosis was slightly increased and mortality of the animals also increased. After administration of 1 alpha OHD3 into rats with chronic kidney insufficiency, maintained on food containing 1.2% of phosphorus, impairments in phosphorus-calcium turnover were distinctly increased. Osteoporosis and calcinosis were elevated in the impared kidney; this led to death of all the animals within first 2 months of the experiments.
实验性慢性肾功能不全在大鼠中引发了磷钙代谢紊乱（高磷血症和低钙血症）、骨骼的骨质疏松性改变（比重、钙、磷和羟脯氨酸含量降低）以及内脏组织的钙质沉着，尤其是受损的肾脏组织。将食物中的磷含量降至0.3%可显著抑制这些损伤的发展并调节其严重程度，降低慢性肾功能不全动物的死亡率。给慢性肾功能不全的大鼠（食物中磷含量有限）给予生理剂量（0.025毫克）的1α-羟基维生素D3（1α-OHD3），这是1,25-二羟胆钙化醇（在肾脏中合成的维生素D的激素形式）的合成类似物，对所研究的骨代谢模式未显示出任何额外的治疗效果；在这种情况下，钙质沉着略有增加，动物死亡率也有所上升。给以含1.2%磷的食物维持的慢性肾功能不全大鼠给予1α-OHD3后，磷钙代谢紊乱明显加剧。受损肾脏中的骨质疏松和钙质沉着加剧；这导致所有动物在实验的前两个月内死亡。
