The prevalence of chronic heart failure (HF) increases fast due to a population of increasing age and an increasing prevalence of diabetes, resulting in a prevalence of HF of 10–20% in 70–80 year old people [
1,
2]. Chronic HF may occur in the presence of a preserved (diastolic HF) or depressed (systolic HF) left ventricular ejection fraction (LVEF), both having a similar (poor) prognosis [
1,
3‐
5]. The prevalence of diabetes in systolic HF is estimated at 23% [
6,
7] and in diastolic HF at 25–33% [
8‐
11]. A possible mechanism underlying diastolic HF may be an increase in advanced glycation end-products (AGEs). AGEs are formed during a non-enzymatic reaction between proteins and sugar residues [
12,
13]. AGEs accumulate in the body with age and are increased in patients with chronic systolic and diastolic HF, diabetic complications and renal dysfunction [
12,
14]. In diabetic HF patients tissue AGEs are more increased compared with HF patients without diabetes [
14]. Whether a difference in accumulation of AGEs in diabetic patients between systolic and diastolic HF is present, remains to be established. AGEs can also activate the receptor for AGE (RAGE) and thereby induce cardiovascular dysfunction [
12]. In cardiovascular disease, renal dysfunction often exists and is frequently referred to as the cardiorenal syndrome [
15]. The cardiorenal syndrome is a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other and vice versa [
16]. Interestingly, patients with renal dysfunction often have diastolic dysfunction, and have an increased prevalence of HF, in particular diastolic HF [
17‐
20]. In addition, the risk factors for developing renal dysfunction have an overlap with the risk factors for the accumulation of AGEs.