The impact of crystal phase transition on the hardness and structure of kidney stones

Uta Michibata1, Mihoko Maruyama1,2, Yutaro Tanaka1,3, Masashi Yoshimura4, Hiroshi Y. Yoshikawa1, Kazufumi Takano2, Yoshihiro Furukawa5, Koichi Momma6, Rie Tajiri7, Kazumi Taguchi3, Shuzo Hamamoto3, Atsushi Okada3, Kenjiro Kohri3, Takahiro Yasui3, Shigeyoshi Usami1, Masayuki Imanishi1, Yusuke Mori1
1Graduate School of Engineering, Osaka University, Suita, Japan
2Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto, Japan
3Department of Nephro-urology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan
4Institute of Laser Engineering, Osaka University, Suita City, Japan
5Department of Earth Science, Tohoku University, Sendai, Japan
6National Museum of Nature and Science, Tsukuba, Japan
7Tajiri Thin Section Laboratory, Higashiosaka, Japan

Tóm tắt

Calcium oxalate kidney stones, the most prevalent type of kidney stones, undergo a multi-step process of crystal nucleation, growth, aggregation, and secondary transition. The secondary transition has been rather overlooked, and thus, the effects on the disease and the underlying mechanism remain unclear. Here, we show, by periodic micro-CT images of human kidney stones in an ex vivo incubation experiment, that the growth of porous aggregates of calcium oxalate dihydrate (COD) crystals triggers the hardening of the kidney stones that causes difficulty in lithotripsy of kidney stone disease in the secondary transition. This hardening was caused by the internal nucleation and growth of precise calcium oxalate monohydrate (COM) crystals from isolated urine in which the calcium oxalate concentrations decreased by the growth of COD in closed grain boundaries of COD aggregate kidney stones. Reducing the calcium oxalate concentrations in urine is regarded as a typical approach for avoiding the recurrence. However, our results revealed that the decrease of the concentrations in closed microenvironments conversely promotes the transition of the COD aggregates into hard COM aggregates. We anticipate that the suppression of the secondary transition has the potential to manage the deterioration of kidney stone disease.

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