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

Background. Previous studies have demonstrated that soy protein can slow pr ogression of renal injury in the Han: SPRD-cy rat. We undertook a study to establish whether this benefit was independent of any nutritional deprivati on, and whether or not it was associated with changes in polyunsaturated fa tty acid status that have been previously linked to the anti-inflammatory o r antineoplastic potential of soy diets. Methods. Male Han:SPRD-cy rats were pair fed a 20% casein or 20% soy protei n diet for six weeks from weaning. Tissue was harvested for analysis of cys tic change, cell proliferation, macrophage infiltration, and fibrosis. Rena l and hepatic tissues were also harvested for lipid analysis using gas chro matography. 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 fibros is (0.6 vs. 1.07 mL/kg, P < 0.0001). The soy diet prevented a significant e levation in serum creatinine in diseased versus normal animals. Soy feeding was associated with higher renal and hepatic linoleic acid content and hig her hepatic alpha-linolenic acid, but lower hepatic arachidonic acid conten t. Conclusions. Isocaloric soy protein feeding ameliorates both epithelial and interstitial changes in the Han:SPRD-cy rat independent of a hypocholester olemic effect. The histologic benefit is associated with changes in polyuns aturated fatty acid metabolism that may influence both inflammatory and pro liferative pathways.