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The L-cystine crystal surface is the pathological site of stone formation in patients with cystinuria, an autosomal recessive disorder affecting the transport of dibasic amino acids in the kidneys [1][2]. Due to the low solubility of L-cystine at physiological urinary pH, it precipitates into hexagonal crystals that aggregate into large, painful, and obstructive kidney stones [2][3]. Therapeutic targeting of the crystal surface involves the use of specific inhibitors that mimic the structure of L-cystine, such as L-cystine dimethyl ester (CDME) [1]. These inhibitors bind to the growth sites on the crystal faces, effectively poisoning the surface and preventing further molecular attachment [1]. This mechanism reduces the rate of crystal growth and alters crystal morphology, making stones easier to pass or preventing their formation entirely [1]. Unlike traditional treatments that focus on chemical modification of the cystine molecule itself, surface-targeted therapies aim to control the physical process of crystallization [1][2].
Inhibition of crystal growth through surface adsorption and lattice strain induction.
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