The diabetic cardiorenal nexus involves synergistic interactions between diabetes, kidney, and cardiac dysfunction, requiring novel pathophysiologic targets beyond current hemodynamic therapies.
This review emphasizes the need to explore novel pathophysiologic targets at the cellular and extracellular matrix levels to address the synergistic burden of diabetic cardiorenal syndrome.
The end-stage of the clinical combination of heart failure and kidney disease has become known as cardiorenal syndrome. Adverse consequences related to diabetes, hyperlipidemia, obesity, hypertension and renal impairment on cardiovascular function, morbidity and mortality are well known. Guidelines for the treatment of these risk factors have led to the improved prognosis of patients with coronary artery disease and reduced ejection fraction. Heart failure hospital admissions and readmission often occur, however, in the presence of metabolic, renal dysfunction and relatively preserved systolic function. In this domain, few advances have been described. Diabetes, kidney and cardiac dysfunction act synergistically to magnify healthcare costs. Current therapy relies on improving hemodynamic factors destructive to both the heart and kidney. We consider that additional hemodynamic solutions may be limited without the use of animal models focusing on the cardiomyocyte, nephron and extracellular matrices. We review herein potential common pathophysiologic targets for treatment to prevent and ameliorate this syndrome.
D’Elia et al. (Fri,) conducted a review in Cardiorenal syndrome. The diabetic cardiorenal nexus involves synergistic interactions between diabetes, kidney, and cardiac dysfunction, requiring novel pathophysiologic targets beyond current hemodynamic therapies.