{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T19:40:07Z","timestamp":1790710807550,"version":"4.1.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,3,1]]},"abstract":"<jats:p>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 \u03bcmol\/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 &lt; 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 (<jats:sup>1<\/jats:sup>H-NMR) studies of urine demonstrated that soy diet was associated with increased losses of citric acid cycle organic anions.<jats:sup>1<\/jats:sup>H-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 &lt; 0.001), with reduced taurine and cholines, compared with casein-fed animals ( P &lt; 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.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.3.f541","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T16:00:40Z","timestamp":1514044840000},"page":"F541-F549","source":"Crossref","is-referenced-by-count":19,"title":["Soy protein modification of rat polycystic kidney disease"],"prefix":"10.1152","volume":"274","author":[{"given":"Malcolm R.","family":"Ogborn","sequence":"first","affiliation":[{"name":"Department of Pediatrics and Child Health,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neda","family":"Bankovic-Calic","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Child Health,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christen","family":"Shoesmith","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Child Health,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Buist","sequence":"additional","affiliation":[{"name":"Department of Radiology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Peeling","sequence":"additional","affiliation":[{"name":"Department of Radiology, and"},{"name":"Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0160-5402(87)90019-2"},{"key":"B2","doi-asserted-by":"crossref","first-page":"581S","DOI":"10.1093\/jn\/125.3_Suppl.581S","volume":"125","author":"Anderson R. 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