Molecular modifiers of kidney stonesAlamani, Bryan G.a,b; Rimer, Jeffrey D.aCurrent Opinion in Nephrology and Hypertension: July 2017 - Volume 26 - Issue 4 - p 256–265 doi: 10.1097/MNH.0000000000000330 MINERAL METABOLISM: Edited by Myles Wolf and David A. Bushinsky Abstract Author InformationAuthors Article MetricsMetrics Purpose of review This review discusses the role of molecular modifiers as inhibitors of kidney stone formation, drawing largely from in-vitro evidence while also citing relevant in-vivo studies. An emphasis is placed on physical observations of crystal growth inhibition, including mechanisms of action that focus predominantly on the literature of calcium oxalate and L-cystine. Recent findings The last decade has witnessed several breakthroughs in the identification of molecules with promise to curb kidney stone formation, as well as discoveries of the mechanisms by which these molecules (or combinations thereof) function as inhibitors of pathological crystal growth. Studies of L-cystine and calcium oxalate crystallization have uncovered inhibitors that are more effective than current therapies. In-vitro assays using advanced techniques such as atomic force microscopy have been able to characterize modifier–crystal interactions and the mechanisms of crystal growth inhibition. A recent study of calcium oxalate crystals uncovered a new inhibition pathway leading to crystal dissolution at relatively low modifier concentrations. Summary Advanced methods of identifying therapeutics for kidney stone disease have created a greater awareness of the potential impact of crystal modifiers in pathological crystallization. Many natural and synthetic species have the capacity to act as growth inhibitors; however, the challenge of bridging in-vitro and in-vivo evidence has proven to be difficult. Future effort to better integrate laboratory research, clinical trials and animal studies has the potential to broaden our understanding of crystal growth modification and its role in mitigating pathological crystallization. aDepartment of Chemical and Biomolecular Engineering, University of Houston, Houston, Texas, USA bDepartment of Chemical Engineering, University of the Philippines Diliman, Quezon City, Philippines Correspondence to Jeffrey D. Rimer, Department of Chemical and Biomolecular Engineering, University of Houston, TX 77204, USA. Tel: +1 713 743 4131; e-mail: firstname.lastname@example.org Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.