{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T22:34:44Z","timestamp":1790634884571,"version":"4.1.0"},"reference-count":55,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2012,5,1]]},"abstract":"<jats:p>Progressive decline in renal function coexists with myocardial infarction (MI); however, little is known about its pathophysiology. This study aimed to systematically identify post-MI renal changes (functional, histological, and molecular) over time in a rat MI model and examine potential mechanisms that may underlie these changes. Rats were randomized into three groups: nonoperated, sham, and MI. Cardiac and renal function was assessed before death at 1, 4, 8, 12, and 16 wk with tissues collected for histological, protein, and gene studies. Tail-cuff blood pressure was lower in MI than sham and nonoperated animals only at 1 wk ( P &lt; 0.05). Systolic function was reduced ( P &lt; 0.0001) while heart\/body weight and left ventricle\/body weight were significantly greater in MI animals at all time points. Glomerular filtration rate decreased following MI at 1 and 4 wk ( P &lt; 0.05) but not at 8 and 12 wk and then deteriorated further at 16 wk ( P = 0.052). Increased IL-6 gene and transforming growth factor (TGF)-\u03b2 protein expression as well as macrophage infiltration in kidney cortex was detected at 1 wk ( P &lt; 0.05). Renal cortical interstitial fibrosis was significantly greater in MI animals from 4 wk, while TGF-\u03b2 bioactivity (phospho-Smad2) was upregulated at all time points. The degree of fibrosis increased and was maximal at 16 wk. In addition, kidney injury molecule-1-positive staining in the tubules was more prominent in MI animals, maximal at 1 wk. In conclusion, renal impairment occurs early post-MI and is associated with hemodynamic and structural changes in the kidney possibly via activation of the Smad2 signaling pathway.<\/jats:p>","DOI":"10.1152\/ajpheart.00967.2011","type":"journal-article","created":{"date-parts":[[2012,2,24]],"date-time":"2012-02-24T23:56:41Z","timestamp":1330127801000},"page":"H1884-H1893","source":"Crossref","is-referenced-by-count":79,"title":["Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome"],"prefix":"10.1152","volume":"302","author":[{"given":"Suree","family":"Lekawanvijit","sequence":"first","affiliation":[{"name":"Centre of Cardiovascular Research and Education in Therapeutics, Department of Epidemiology and Preventive Medicine, Monash University; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew 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