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We studied the effects of spironolactone treatment on CTD development in the Dark Agouti-to-Wistar-Furth renal allograft transplant model, by treatment with 20 mg\/kg spironolactone or vehicle daily by oral gavage from 2 days before transplantation (donors and recipients) throughout the experiment (12 wk, recipients). Dark Agouti-to-Dark Agouti isografts served as negative controls. Spironolactone significantly ameliorated the development of transplant vasculopathy in allografts by reducing the number of affected intrarenal arteries. In addition, spironolactone treatment showed a trend toward reduced proteinuria and focal glomerulosclerosis, and significantly reduced glomerular macrophage influx. However, spironolactone treatment did not affect interstitial fibrosis, interstitial macrophage influx, creatinine clearance, and systolic blood pressure. We conclude that spironolactone selectively ameliorates transplant vasculopathy and glomerular lesions in renal CTD in rats. These results suggest that spironolactone may have renoprotective potential as an adjunct treatment in renal transplantation to ameliorate CTD.<\/jats:p>","DOI":"10.1152\/ajprenal.90643.2008","type":"journal-article","created":{"date-parts":[[2009,2,26]],"date-time":"2009-02-26T02:27:58Z","timestamp":1235615278000},"page":"F1072-F1079","source":"Crossref","is-referenced-by-count":33,"title":["Spironolactone ameliorates transplant vasculopathy in renal chronic transplant dysfunction in rats"],"prefix":"10.1152","volume":"296","author":[{"given":"Femke","family":"Waanders","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heleen","family":"Rienstra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark Walther","family":"Boer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9","family":"Zandvoort","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Rozing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerjan","family":"Navis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harry","family":"van Goor","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan-Luuk","family":"Hillebrands","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090804"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Amuchastegui SC, Azzollini N, Mister M, Pezzotta A, Perico N, Remuzzi G.Chronic allograft nephropathy in the rat is improved by angiotensin II receptor blockade but not by calcium channel antagonism.J Am Soc Nephrol9: 1948\u20131955, 1998.","DOI":"10.1681\/ASN.V9101948"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/12.8.1672"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.108.174235"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2005.12.025"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2005.00368.x"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050463"},{"key":"R8","unstructured":"Colvin RB, Nickeleit V.Renal transplant pathology. 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