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lüll Recent advances in the pathophysiology of nephrolithiasis Sakhaee KKidney Int 2009[Mar]; 75 (6): 585-95Over the past 10 years, major progress has been made in the pathogenesis of uric acid and calcium stones. These advances have led to our further understanding of a pathogenetic link between uric acid nephrolithiasis and the metabolic syndrome, the role of Oxalobacter formigenes in calcium oxalate stone formation, oxalate transport in Slc26a6-null mice, the potential pathogenetic role of Randall's plaque as a precursor for calcium oxalate nephrolithiasis, and the role of renal tubular crystal retention. With these advances, we may target the development of novel drugs including (1) insulin sensitizers; (2) probiotic therapy with O. formigenes, recombinant enzymes, or engineered bacteria; (3) treatments that involve the upregulation of intestinal luminal oxalate secretion by increasing anion transporter activity (Slc26a6), luminally active nonabsorbed agents, or oxalate binders; and (4) drugs that prevent the formation of Randall's plaque and/or renal tubular crystal adhesions.|*Nephrolithiasis/drug therapy/etiology/physiopathology[MESH]|Animals[MESH]|Calcium Oxalate/metabolism[MESH]|Humans[MESH]|Kidney Calculi/etiology/microbiology[MESH]|Kidney Tubules/pathology[MESH]|Metabolic Syndrome[MESH]|Oxalobacter formigenes[MESH]|Uric Acid[MESH] |