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Am J Physiol Renal Physiol 274: F541-F549, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 3, F541-F549, March 1998

Soy protein modification of rat polycystic kidney disease

Malcolm R. Ogborn1, Neda Bankovic-Calic1, Christen Shoesmith1, Richard Buist2, and James Peeling2,3

1 Department of Pediatrics and Child Health, 2 Department of Radiology, and 3 Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada

We undertook a study to determine whether soy protein feeding would ameliorate renal injury in the Han:SPRD-cy rat model of polycystic kidney disease (PKD). Male offspring of Han:SPRD-cy heterozygotes received isocaloric diets based on 20% casein or 20% heat-treated soy protein at weaning ad libitum for 8 wk. Soy-fed animals demonstrated lower serum creatinine (66 vs. 125 µmol/l; P = 0.002), lower urinary ammonium excretion (0.080 vs. 0.173 mmol/kg; P = 0.01), reduced renal cysts (0.98 vs. 4.92 ml/kg body wt, P < 0.0001), renal fibrosis (0.79 vs. 1.4 ml/kg; P = 0.016), macrophage infiltration, renal tubular cell proliferation, and apoptosis. Proton nuclear magnetic resonance (1H-NMR) studies of urine demonstrated that soy diet was associated with increased losses of citric acid cycle organic anions. 1H-NMR of perchloric acid-extracted tissue found that levels of succinate were not depleted in soy-fed animals, despite increased urinary losses. Soy-fed animals had marked elevation of tissue betaine (P < 0.001), with reduced taurine and cholines, compared with casein-fed animals (P < 0.001). Soy feeding dramatically reduces both tubular and interstitial pathology in the Han:SPRD-cy rat model of PKD, through mechanisms that remain to be determined.

Han:SPRD-cy rat; proton nuclear magnetic resonance; casein; fibrosis; renal inflammation


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