背景:肾结石形成化合物的结晶实验(草酸钙,磷酸钙,尿酸)通常是通过在类似于尿液在肾脏内滞留的时间段内监测这些过程来进行的。然而,胱氨酸结晶需要高的过饱和,大多数实验持续时间更长。必须考虑到,在高过饱和时,结晶发展的抑制剂效果较差。方法:通过比浊法测定在类似于胱氨酸肾结石形成的实验条件下,胱氨酸结晶的诱导时间(ti)以及不同的胱氨酸结合硫醇剂的作用。我们还通过立体显微镜和扫描电子显微镜研究了30个胱氨酸肾结石的宏观和微观结构。结果:在研究条件下,在没有结晶抑制剂的情况下,ti为15分钟,和9mM的青霉胺的存在,硫普罗宁,或N-乙酰半胱氨酸完全抑制结晶,因为它们的作用与胱氨酸复合物的形成有关,虽然N-乙酰半胱氨酸也延缓了胱氨酸晶体的发育和修饰的胱氨酸晶体形态。胱氨酸结石传统上被分类为光滑和粗糙。对它们结构的研究表明,它们都是从几个产生紧凑径向结构的晶体开始形成的。他们随后的成长,取决于它们所在的肾腔,以胱氨酸晶体的大块形式产生粗糙结构或具有小晶体的光滑结构。结论:预防胱氨酸肾结石的发生,必须通过减少尿胱氨酸过饱和来避免小晶体的形成,其中N-乙酰半胱氨酸是研究的胱氨酸结合硫醇剂中最有效的。此外,通过增加水的摄入量和身体活动来去除胱氨酸晶体可能是非常重要的预防措施。
Background: Crystallization experiments of renal-calculi-forming compounds (calcium oxalate, calcium phosphates, uric acid) are normally performed by monitoring these processes during periods of time similar to the residence of urine inside the kidney. Nevertheless,
cystine requires high supersaturation for its crystallization, and most experiments last for longer periods. It must be considered that at high supersaturation, the inhibitors of crystalline development have poor effects. Methods: The induction time of crystallization (ti) of cystine in experimental conditions similar to those of the formation of
cystine renal calculi and the effect of different
cystine-binding thiol agents was determined through turbidimetric measurements. We also studied the macro- and microstructure of 30 cystine kidney stones through stereoscopic microscopy and scanning electron microscopy. Results: Under the studied conditions, the ti in absence of crystallization inhibitors was 15 min, and the presence of 9 mM of penicillamine, tiopronin, or N-acetylcysteine totally inhibited crystallization, as their effects relate to the formation of complexes with cystine, although N-acetylcysteine also delayed
cystine crystalline development and modified
cystine crystal morphology.
Cystine stones have traditionally been classified as smooth and rough. The study of their structure shows that all of them begin their formation from a few crystals that generate a compact radial structure. Their subsequent growth, depending on the renal cavity where they are located, gives rise to the rough structure in the form of large blocks of cystine crystals or the smooth structure with small crystals. Conclusions: To prevent the development of cystine renal stones, the formation of small crystals must be avoided by reducing urinary cystine supersaturation, with N-acetylcysteine being the most effective among the studied
cystine-binding thiol agents. Also, the removal of cystine crystals through increased water intake and physical activity can be a very important preventive measure.