Abstract
Patients who form calcium kidney stones often have metabolic disorders such as idiopathic hypercalciuria (IH) that reflect abnormalities in mineral handling in the kidney. Renal handling of calcium is altered by ingestion of nutrients such as carbohydrates, protein, and sodium, and patients with IH appear to be more sensitive to these stimuli. Studies using probes such as diuretics or lithium clearance have the ability to clarify which nephron segments are involved in the altered renal calcium transport with nutrient seen in IH. Studies in the genetic hypercalciuric rat demonstrate alterations in both proximal tubule and thick ascending limb calcium reabsorption. Similar studies in humans have begun to provide evidence about the corresponding abnormalities in stone formers with IH. A pattern of altered renal tubule transport in calcium stone formers is suggested by the frequency of such findings as decreased tubular maximal reabsorption of phosphate and abnormal urine acidification as well as hypercalciuria in such patients, not explained by monogenic transport abnormalities.