Pathophysiology and therapy of hypercalciuria in patients who form recurrent stones.
There are two alternative mechanisms that might be responsible for idiopathic hypercalciuria in recurrent stone formers: increased intestinal absorption of calcium with parathyroid suppression and overflow hypercalciuria (primary intestinal hyperabsorption) or renal calcium leak with compensatory hyperparathyroidism and intestinal hyperabsorption (primary renal-tubular hypercalciuria). In this study, urinary excretion of cAMP, the intracellular effector substance synthetised under parathyroid hormone stimulation, was found to be in the normal range. This finding would argue against intestinal hyperabsorption of calcium as the primary cause of hypercalciuria.
D001581:Benzothiadiazines; D002118:Calcium / Q000097:blood / Q000652:urine*; D000242:Cyclic AMP / Q000652:urine; D004232:Diuretics; D006801:Humans; D007408:Intestinal Absorption; D007684:Kidney Tubules / Q000378:metabolism; D010280:Parathyroid Glands / Q000503:physiopathology; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000378:metabolism; D012008:Recurrence; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use; D014545:Urinary Calculi / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*
D001581:Benzothiadiazines; D004232:Diuretics; D010281:Parathyroid Hormone; D049993:Sodium Chloride Symporter Inhibitors; D010758:Phosphorus; D000242:Cyclic AMP; D002118:Calcium