Kidney Stones: Various Forms and Treatment

Abstract

Calcium urolithiasis is not a homogeneous entity, but is a result of many etiologies, with different physicochemical and physiological backgrounds. This diversity of presentation requires an appreciation of specific diagnostic criteria, and a selection of an appropriate treatment regimen for each cause.

Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug

“…Several mechanisms and theories related to the calciumphosphorus metabolism have been suggested to explain the pathogenesis of the excessive calcium excretion in IHC. Actually, three different mechanisms are regarded as the main causes of hypercalciuria: a reduction in the tubular reabsorption of calcium, with the emergence of compensatory hyperparathyroidism [Coe et al 1988]; an increase in the intestinal reabsorption of calcium secondary to high levels or hypersensitivity to calcitriol [Pak, 1979]; and a renal loss of phosphates with secondary increased synthesis of calcitriol and intestinal hyperabsorption [Navarro et al 1994]. Studies on humans, however, suggest that whereas some patients have a single specific defect resulting in hypercalciuria, most subjects do not have a specific site of mineral ion transport dysregulation.…”

“…Bisphosphonates are potent inhibitors of bone resorption and are well established as the leading drugs for the treatment of osteoporosis [Russell et al 2008 [Coe et al 1988]; an increase in the intestinal reabsorption of calcium secondary to high levels or hypersensitivity to calcitriol [Pak, 1979]; and a renal loss of phosphates with secondary increased synthesis of calcitriol and intestinal hyperabsorption [Navarro et al 1994]. Studies on humans, however, suggest that whereas some patients have a single specific defect resulting in hypercalciuria, most subjects do not have a specific site of mineral ion transport dysregulation.…”

Pharmacological interventions for preventing complications in idiopathic hypercalciuria

“…1. reduction in the tubular reabsorption of calcium, with the emergence of compensatory hyperparathyroidism (Coe 1988); 2. an increase in, or hypersensitivity to, the intestinal reabsorption of calcium secondary to high levels of calcitriol (Pak 1979); and 3. renal loss of phosphates with secondary increased synthesis of calcitriol and intestinal hyperabsorption (Navarro 1994).…”