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Abstract: FR-OR47

Cytokines of Kidney Origin Are Retained in the Heart and Induce Cardiac Injury in CKD: A Renal-Cardio Axis

Session Information

Category: Pathology and Lab Medicine

  • 1600 Pathology and Lab Medicine


  • Chade, Alejandro R., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Mohamed, Tamer, University of Louisville, Louisville, Kentucky, United States
  • Eirin, Alfonso, Mayo Clinic Minnesota, Rochester, Minnesota, United States

Chronic kidney disease (CKD) is a major contributor to heart failure (HF), but the mechanisms underpinning CKD-induced HF remain to be fully elucidated. We hypothesize that inflammatory signaling from the kidney drives the development of cardiac injury in CKD.


CKD was induced in 4 pigs (bilateral renovascular disease and dyslipidemia) and observed for 14 weeks. Normal pigs served as controls. Renal hemodynamics (RBF, GFR) were quantified by multi-detector CT, and cardiac morphology and function by echocardiography. Renal vein, coronary sinus, and systemic blood was collected to quantify renal and cardiac gradients of TNF-α and IL-6. In a biomimetic heart culture system, pig heart slices were exposed to plasma from CKD or normal pigs and contractile/relaxation kinetics and sarcoplasmic-reticulum Ca+2 dynamics were investigated.


Loss of renal function in CKD was accompanied by positive renal (renal release) and negative cardiac (cardiac retention) cytokine gradients, left ventricular (LV) hypertrophy, diastolic dysfunction (E/A, E/e’ ratio) and abnormal LV strain. Cardiomyocytes exposed to CKD plasma showed impaired contractility and speed of relaxation, and altered Ca+2 cycling, which improved after TNF-α and IL-6 neutralization (Figure).


This study supports a link between TNF-α/IL-6 inflammatory signaling from the kidney in causing cardiac dysfunction in CKD. Cardiac impairment in vivo was mirrored by altered cardiomyocytes kinetics and Ca+2 cycling after exposure to CKD plasma in vitro, supporting an inflammatory renal-cardio axis in CKD-to-HF pathophysiology.


  • Other NIH Support