{"id":11520,"date":"2020-05-26T16:08:24","date_gmt":"2020-05-26T20:08:24","guid":{"rendered":"https:\/\/www.bumc.bu.edu\/im-residency\/?page_id=11520"},"modified":"2020-05-26T16:08:24","modified_gmt":"2020-05-26T20:08:24","slug":"pathogenic-insights-into-the-cardiorenal-syndrome-in-heart-failure-hf-with-preserved-ejection-fraction-hfpef","status":"publish","type":"page","link":"https:\/\/www.bumc.bu.edu\/im-residency\/pathogenic-insights-into-the-cardiorenal-syndrome-in-heart-failure-hf-with-preserved-ejection-fraction-hfpef\/","title":{"rendered":"Pathogenic Insights into the Cardiorenal Syndrome in Heart Failure (HF) with Preserved Ejection Fraction (HFpEF)"},"content":{"rendered":"

\"\"<\/p>\n

Albin Oh, MD<\/h3>\n

Albin Oh MD, Maria Valero-Munoz PhD, Flora Sam MD<\/p>\n

Background:<\/strong> The lack of therapies for heart failure with preserved ejection fraction (HFpEF) suggests that identifying novel pathways is a priority. Clinical management of HF, particularly HFpEF, is challenged by concurrent renal dysfunction, known as the cardiorenal syndrome (CRS). In a murine HFpEF model, we previously demonstrated cardiac hypertrophy, fibrosis & lung congestion. We next investigated the effect of HFpEF induction in the renal phenotype.<\/p>\n

Methods:<\/strong>\u00a0 <\/span>Uninephrectomized mice received 1% NaCl drinking water \u00b1 d-aldosterone for 4 weeks. The kidneys were collected and histology and qPCR performed.<\/p>\n

Results:<\/strong> Renal hypertrophy & fibrosis were evident as shown by a 46% increase of kidney to body weight mass (P<0.0001) & a 15% increase in fibrosis in HFpEF vs. Sham (P<0.03). In parallel, mRNA fibrotic markers were also increased in the kidneys of HFpEF mice (tgf-\u03b2: 1.7-fold; col-I: 4.0-fold; col-III: 3.0-fold vs. Sham, P<0.005). These results were associated with activation of the endothelial-mesenchymal transition (endo-MT) process, showed by 1.4-, 1.7-, 1.8-, 2.6- and 2.0-fold increases in ve-cadherin, snail, fibronectin, fibroblast-specific protein 1 and vimentin renal transcripts in HFpEF vs. Sham (P<0.05).<\/p>\n

Conclusion:<\/strong> This HFpEF model aptly mirrors the hallmarks of human HFpEF. Evidence of renal hypertrophy and fibrosis mimics the cardiac phenotype and activation of markers associated with Endo-MT suggests this may be a major mechanism of CRS in HFpEF. Further studies are warranted.<\/p>\n","protected":false},"excerpt":{"rendered":"

Albin Oh, MD Albin Oh MD, Maria Valero-Munoz PhD, Flora Sam MD Background: The lack of therapies for heart failure with preserved ejection fraction (HFpEF) suggests that identifying novel pathways is a priority. Clinical management of HF, particularly HFpEF, is challenged by concurrent renal dysfunction, known as the cardiorenal syndrome (CRS). In a murine HFpEF […]<\/p>\n","protected":false},"author":15816,"featured_media":0,"parent":0,"menu_order":93,"comment_status":"open","ping_status":"closed","template":"page-templates\/no-sidebars.php","meta":[],"_links":{"self":[{"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/pages\/11520"}],"collection":[{"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/users\/15816"}],"replies":[{"embeddable":true,"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/comments?post=11520"}],"version-history":[{"count":1,"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/pages\/11520\/revisions"}],"predecessor-version":[{"id":11521,"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/pages\/11520\/revisions\/11521"}],"wp:attachment":[{"href":"https:\/\/www.bumc.bu.edu\/im-residency\/wp-json\/wp\/v2\/media?parent=11520"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}