Noncalcium stones are also associated with specific metabolic, genetic, and infectious disorders. Uric acid stones primarily occur in the setting of overly acidic urine, in which uric acid crystallizes. These stones are more common among patients with insulin resistance and type II diabetes mellitus, in whom production and excretion of ammonia in the renal proximal tubule is impaired, leading to insufficient buffering of protons in urine. Magnesium ammonium phosphate (struvite) stones, in contrast, occur in the setting of overly alkaline urine, in which struvite and calcium carbonate precipitate. These stones primarily occur in patients who have urinary tract infections with urea-splitting bacteria, such as Proteus, Pseudomonas, Klebsiella, and Staphylococcus. The hydrolysis of urea produces high concentrations of ammonia, which buffers protons. Incorporation of bacteria into these stones may cause chronic infections. Finally, cystine stones occur because of an inherited disorder of amino acid transport in which proximal tubular reabsorption of dibasic amino acids (cystine, lysine, ornithine, arginine) is impaired, leading to high urinary concentrations. Because cystine is poorly soluble in urine, it crystallizes and forms stones at relatively low urinary concentrations.