Diabetes converts from a metabolic disorder into a predominantly vascular disease, once its duration extends over several years or/and when additional cardiovascular risk factors such as hypertension coexist. In a large cross-sectional analysis we analyzed various vascular parameters in the renal, retinal and systemic circulation, with the goal to identify which vascular parameter of early organ damage is the earliest that can be clinically detected.
In 111 patients with type 2 diabetes (T2DM) (off any anti-diabetic medication for at least 4 weeks) and 54 subjects without T2DM we assessed urinary albumin creatinine ratio (urinary albumin creatinine ratio [UACR], early morning spot urine) and estimated glomerular filtration rate (eGFR), retinal capillary flow (RCF), intercapillary distance (ICD) as parameters of capillary rarefaction, wall-to-lumen ratio (WLR) of the retinal arterioles [all assessed by Scanning Laser Doppler Flowmetry], and central systolic pressure (cSBP) and central pulse pressure (cPP) [measured by pulse wave analysis, Syphygmocor] both reflecting vascular stiffness of large arteries.
Compared to subjects without T2DM, patients with T2DM (duration: mean 63.9 ± 56.4, range 1–271 months) were older (59.8 ± 7.3 vs. 43.4 ± 12.9 years, p < 0.001), more females (33.3 vs 20.4 %, p < 0.001) but 24-hour systolic and diastolic blood pressure did not differ between the two groups (129.3 ± 11.4 / 78.9 ± 8.3 vs. 130.4 ± 10.8 / 77.4 ± 5.6 mmHg). The analysis adjusted for age, gender and cardiovascular risk factors showed that ICD, cPP were significantly higher and eGFR was significantly lower in patients with T2DM than in subjects without T2DM.
These data suggest that at similar blood pressure capillary rarefication in the retinal circulation (ICD), eGFR in the renal circulation and central pulse pressure (cPP) of large arteries are earlier detectable than vascular remodeling of the micro- (WLR, RCF, UACR) and macrocirculation (cSPB) in patients with T2DM.
1Department of Nephrology and Hypertension, University Hospital of the University of Erlangen-Nuremberg, Erlangen, Germany
2Department of Pathophysiology, University of Warmia and Mazury, Olsztyn, Poland