Modification of polycystic kidney disease and fatty acid status by soy protein diet.

UNLABELLED

Modification of polycystic kidney disease and fatty acid status by soy protein diet.

BACKGROUND

Previous studies have demonstrated that soy protein can slow progression of renal injury in the Han:SPRD-cy rat. We undertook a study to establish whether this benefit was independent of any nutritional deprivation, and whether or not it was associated with changes in polyunsaturated fatty acid status that have been previously linked to the anti-inflammatory or antineoplastic potential of soy diets.

METHODS

Male Han:SPRD-cy rats were pair fed a 20% casein or 20% soy protein diet for six weeks from weaning. Tissue was harvested for analysis of cystic change, cell proliferation, macrophage infiltration, and fibrosis. Renal and hepatic tissues were also harvested for lipid analysis using gas chromatography.

RESULTS

Animals thrived on both diets. Soy protein feeding was associated with reduced cystic change (4.3 vs. 7.0 mL/kg, P < 0.0001), epithelial cell proliferation (15.7 vs. 21.0 cells/mm epithelium, P < 0.0001), macrophage infiltration (25.3 vs. 43.5 cells/high-power field, P < 0.0001), and fibrosis (0.6 vs. 1.07 mL/kg, P < 0.0001). The soy diet prevented a significant elevation in serum creatinine in diseased versus normal animals. Soy feeding was associated with higher renal and hepatic linoleic acid content and higher hepatic alpha-linolenic acid, but lower hepatic arachidonic acid content.

CONCLUSIONS

Isocaloric soy protein feeding ameliorates both epithelial and interstitial changes in the Han:SPRD-cy rat independent of a hypocholesterolemic effect. The histologic benefit is associated with changes in polyunsaturated fatty acid metabolism that may influence both inflammatory and proliferative pathways.