My research focuses on evaluating for the possible role of dysfunctional iron metabolism and its associated insulin resistance in the development of cardiac fibrosis in pre-dialysis chronic kidney disease (CKD) patients.
Patients with CKD develop disproportionately increased risk for cardiac mortality, specifically from heart failure, arrhythmia, and sudden cardiac death rather than from myocardial infarction. In contrast to the general population, the relative importance of atherosclerotic coronary disease is diminished in the CKD, and non-atherosclerotic processes such as arterial stiffening, cardiac fibrosis, and left ventricular remodeling predominate. The pathomechanism and risk factors for the development of uremic cardiomyopathy remain incompletely understood without effectives strategies for risk stratification or treatment. Delineating mediators critically involved in the development of uremic cardiomyopathy, therefore, is pivotal for identifying modifiable risk factors and potential targets for intervention. In the recent years, the knowledge regarding dysfunctional iron metabolism and its effect on metabolic and glucose regulation has rapidly expanded. Disturbed iron homeostasis, a frequent comorbidity in chronic illnesses such as CKD and chronic heart failure (CHF), has far greater implications than anemia and may represent a significant therapeutic opportunity for the CKD population.
