Renal Expression of an Ammonia Transporter in Rats with a Unilateral Ureteral Obstruction / 대한내과학회지

ABSTRACT

BACKGROUND/AIMS: Urinary tract obstruction induces a form of renal tubular acidosis with a urinary acidification defect caused by decreasing net acid excretion, which is predominantly due to a decrease in urinary ammonia excretion. The present study examined whether this decrease is associated with changes in the renal expression of an ammonia transporter family member, Rh C glycoprotein (Rhcg), in rats with a unilateral ureteral obstruction. METHODS: Male Sprague-Dawley rats underwent a 24-h unilateral ureteral obstruction. Rhcg expression was then evaluated by immunoblotting and immunohistochemistry. Cell height, total cellular expression, expression in the apical 25% of the cell, and % of total expression in the apical region were quantified by immunohistochemistry with quantitative morphometric analysis. RESULTS: After 24 h of unilateral ureteral obstruction, the serum bicarbonate level and total urinary ammonia excretion were decreased. Both light microscopy and immunohistochemistry with quantitative morphometric analysis demonstrated that the total intensity of Rhcg expression was decreased in the obstructed kidneys, whereas Rhcg expression did not change in the cortical collecting duct (CCD) and outer medullary collecting duct (OMCD) of nonobstructed kidneys in rats with a 24-h unilateral ureteral obstruction. CONCLUSIONS: The rats with a unilateral ureteral obstruction showed decreased urinary ammonia excretion associated with decreased Rhcg expression in the CCD and OMCD. These changes suggest that the ammonia transporter Rhcg mediates a urinary acidification defect associated with unilateral ureteral obstruction.