A diagnosis of uric acid urolithiasis is supported by the presence of a radiolucent stone in the face of persistent urine acidity, in conjunction with the finding of uric acid crystals in fresh urine samples.As noted above (section on calcium oxalate stones), people with inflammatory bowel disease (Crohns disease, ulcerative colitis) tend to have hyperoxaluria and form oxalate stones. They also have a tendency to form urate stones. Urate stones are especially common after colon resection. Uric acid stones appear as pleomorphic crystals, usually diamond-shaped. They may also look like squares or rods which are polarizable. Other types
People with certain rare inborn errors of metabolism have a propensity to accumulate crystal-forming substances in their urine. For example, those with cystinuria, cystinosis, and Fanconi syndrome may form stones composed of cystine. Cystine stone formation can be treated with urine alkalinization and dietary protein restriction. People affected by xanthinuria often produce stones composed of xanthine. People affected by adenine phosphoribosyltransferase deficiency may produce 2,8-dihydroxyadenine stones, alkaptonurics produce homogentisic acid stones, and iminoglycinurics produce stones of glycine, proline, and hydroxyproline. Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of drug forming within the renal tract in some people currently being treated with agents such as indinavir, sulfadiazine, and triamterene. Location
Urolithiasis refers to stones originating anywhere in the urinary system, including the kidneys and bladder. Nephrolithiasis refers to the presence of such stones in the kidneys.
Hyperproinsulinemia is a disease where insulin is not sufficiently processed before secretion and immature forms of insulin make up the majority of circulating insulin immunoreactivity in both fasting and glucose-stimulated conditions (insulin immunoreactivity refers to all molecules detectable by an insulin antibody, i.e. insulin, proinsulin, and proinsulin-like material). The term is composed of hyper - high, proinsulin - immature insulin molecule, and -emia - blood condition.Hyperproinsulinemia is more frequent in type 2 diabetes. It has been attributed to either a direct β-cells defect or an indirect effect of cell dysregulation under sustained elevated blood glucose (hyperglycemia).Some alleles of insulin can cause hyperproinsulinemia (see table 2: monogenic forms of type 1 diabetes, INS (insulin). For a more detailed descriptions of the insulin gene variations leading to hyperproinsulinemia see NCBIs OMIM 176730

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