Diastolic Dysfunction and Renal Disease: Analysis, Mechanisms, and Different Perspectives

Over the past few decades, heart failure with preserved ejection fraction has established itself as an individual clinical entity. Although it is associated with a better prognosis, it offers high resistance to classic treatment techniques, and the frequency of hospitalizations and mortality rates are comparable to cases of heart failure with reduced ejection fraction. Heart failure often leads to death and morbidity, and there has recently been a growing interest in studying the relationship between cardiac and renal function due to epidemiological evidence indicating that even a modest deterioration in renal function is a considerable risk factor in patients with heart failure, myocardial infarction or in the context of cardiovascular surgery. In fact, studies have proven that patients with chronic kidney disease have a cardiovascular risk about 10 times higher than a population of the same age, sex, and race without it. Before writing this review, research literature on heart failure with preserved ejection fraction and chronic kidney disease was reviewed. Studies have shown that in patients with chronic kidney disease, heart failure is mostly caused by the presence of left ventricular diastolic dysfunction, with aggravating comorbidities such as high blood pressure and coronary heart disease. A possible underlying mechanism may be the excessive activation of the renin-angiotensin-aldosterone system, which is known to be a determinant in the onset of profibrotic factors. In fact, it is known that, in patients with chronic heart failure, the renin-angiotensin-aldosterone system is activated, and it has even been shown that the activity of increased plasma renin levels directly contributes to mortality. Angiotensin II promotes cardiac remodeling, and aldosterone may increase myocardial fibrosis, which is a marker of diastolic dysfunction and cardiac necrosis, acting as an endogenous bioactive factor involved in the process of vascular calcification. On the other hand, the development of diastolic dysfunction in patients with chronic kidney disease may result from disorders of metabolism. Besides, evidence indicates that individuals with 25-hydroxyvitamin D deficiency have an increased risk of developing various cardiovascular conditions, such as hypertension, peripheral vascular disease, myocardial infarction, diabetes mellitus, heart failure, and even death. In recent studies, it has been described that the direct effect of vitamin D on cardiomyocytes consists essentially in the acceleration of myocardial relaxation, leading to the hypothesis that it causes a determining effect on diastolic function. Currently, both heart failure with preserved ejection fraction and chronic kidney disease are very prevalent and are closely linked to several other factors, including disturbances in phospho-calcium metabolism and variations in serum vitamin D levels. Although the concept of heart failure began to be explored a few decades ago, further studies are required in order to explain the factors that created the controversy behind the concept of diastolic dysfunction. This review aims precisely to identify the areas that lack further investigation, which can be essential to the development of more effective treatments and subsequently obtain better outcomes.