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镉中毒大鼠的肾功能及钙磷代谢紊乱

Disturbances in kidney functions and calcium and phosphate metabolism in cadmium-poisoned rats.

作者信息

Kawamura J, Yoshida O, Nishino K, Itokawa Y

出版信息

Nephron. 1978;20(2):101-10. doi: 10.1159/000181202.

Abstract

In an attempt to elucidate the etiology and pathogenesis of 'Itai-Itai' disease, the relationship between bone and kidney lesions in cadmium-poisoned rats was determined using the standard renal clearance technique. Calcium and cadmium contents in the femur and kidney were also estimated. The severity of renal lesions was histologically evident both in the tubule and glomerulus, and paralleled the decrease in GFR and the increase in FF. There was no significant change in fractional excretion of phosphate, but fractional excretion of calcium increased in the cadmium-poisoned rats. The secondary hyperparathyroidism followed by uremic renal osteodystrophy did not result in an osteomalacia. Thus, it is apparent that disturbance in calcium reabsorption in the tubules plays a role in the loss of calcium, and cadmium associated with low levels of calcium has a direct effect on the bone-causing osteomalacia.

摘要

为了阐明“痛痛病”的病因和发病机制,采用标准的肾脏清除技术测定了镉中毒大鼠骨与肾损伤之间的关系。同时还估算了股骨和肾脏中的钙和镉含量。肾脏病变的严重程度在肾小管和肾小球中在组织学上都很明显,并且与肾小球滤过率(GFR)的降低和滤过分数(FF)的增加平行。磷酸盐的分数排泄没有显著变化,但镉中毒大鼠的钙分数排泄增加。继发性甲状旁腺功能亢进继而导致尿毒症性肾性骨营养不良,但并未引起骨软化症。因此,显然肾小管中钙重吸收的紊乱在钙流失中起作用,并且与低钙水平相关的镉对骨骼有直接影响,导致骨软化症。

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