Research conducted over the past four decades has resulted in a better understanding of the various factors involved in kidney stone formation. In addition, there is a better appreciation of the molecular and genetic basis of various stone-related disorders, including hyperoxaluria, hypercalciuria (not discussed here), and hypocitraturia (not discussed here). It has become obvious that stone formation is not simply the result of changes in the concentrations of individual urinary components, e.g., Ca, Ox, Mg, or citrate, but a consequence of their collective interactions and behavior. Ions such as Ca,Ox, citrate, or Mg affect stone formation not only by participating in crystallization, but also by interacting with renal cells. Both Ox ions and CaOx crystals cause injury and induce inflammation in kidneys. Injury to the renal epithelium can promote crystal attachment. In addition, membranes of dead cells promote crystallization in the renal tubules. The activities of so-called crystallization inhibitors are not limited to just modulating crystallization, but also to crystal attachment to the renal epithelium.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Endourology|
|State||Published - Aug 2002|
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