| Popis: |
There is now considerable evidence suggesting that tubular dysfunction may contribute to renal stone formation. In certain normocalcernic patients with recurrent calcium-containing kidney stones, this defect is manifest as an impairment of calcium or phosphate reabsorption (1). Other patients exhibit more generalized defects in tubular function, exhibiting impaired reabsorption of water, sodium, bicarbonate, calcium, and magnesium (2, 3). These findings led us to examine an animal model of nephrolithiasis that combines proximal tubular dysfunction with renal stone formation: gentamycin-treated rats fed ammonium oxalate diets. The studies presented here reflect our preliminary assessment of renal structure and function in this animal model. |
