Renal tubular cell protein breakdown in uninephrectomized and ammonium chloride-loaded rats.

Abstract

Kidney enlargement after unilateral nephrectomy or the induction of a systemic acidosis with ammonium chloride is associated with an increase in kidney protein content. This reflects an imbalance between protein breakdown and protein synthesis. Because it has been shown in diabetic nephromegaly that depressed protein breakdown contributes to the increase in kidney protein content, this study examined whether altered protein breakdown is common to all forms of renal hypertrophy. Accordingly, protein turnover was measured in isolated proximal tubules from kidney in rats undergoing renal enlargement after uninephrectomy or chronic ammonium chloride-induced acidosis. In both conditions, kidney protein content and protein synthesis ([14C]valine incorporation) increased significantly. Fractional protein degradation was depressed in renal tubules isolated from the acidotic rats and was accompanied by a decrease in proximal tubule cathepsin B and combined B and L activities. These changes are comparable to earlier observations with the diabetic kidney. In contrast, after unilateral nephrectomy, protein breakdown is not reduced, and it can reasonably be concluded that, in this condition, protein gain reflects increased protein synthesis alone. It was concluded that the pattern of protein turnover leading to protein accretion in renal hypertrophy varies according to the initial stimulus for renal growth.