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Introduction: The aim of the study was to evaluate cerebral microangiopathy in type 2 non-insulin-dependent diabetes mellitus (NIDDM) patients and to establish potentially conducive factors. Materials and Methods: A group of 34 patients with NIDDM and 31 gender- and age-matched normal controls (NC) were assessed by extracranial Doppler ultrasound, in order to evaluate the pulsatility index (PI) and the resistance index (RI) in the internal carotid arteries (ICAs); transcranial Doppler was utilised to assess the same parameters in the middle cerebral arteries (MCAs). All patients underwent screening for favouring factors for cerebral vascular remodelling. Results: Of the 34 NIDDM patients, 21 patients (61.76%) (subgroup A) presented with microangiopathic complications [of these, 19 patients (90.46%) had diabetic nephropathy (DN)] versus 13 NIDDM patients (38.24%) (subgroup B) without complications. In subgroup A, 16 patients (76.19%) had PI >1 and RI >0.7 in the ICAs and MCAs (changes consistent with cerebral microangiopathy) versus 5 patients (35.46%) in subgroup B, and no modifications in NC. Of the 19 patients with DN, 14 patients (73.68 %) had impaired haemodynamic indices. Univariate regression analysis showed the following risk factors for the cerebral haemodynamics changes: fibrinogen (F) (OR = 3.11), C-reactive protein (CRP) (OR = 2.40), duration of DM (OR=2.40), proteinuria (OR = 1.80), serum creatinine (OR = 1.66). Multivariate regression analysis showed as predictors for impaired haemodynamic indices: duration of DM (HR =1.70), proteinuria (HR = 1.70). The haemodynamic indices in the ICAs correlated with duration of DM (r = 0.87, P

Background: Advanced glycation end-products have been involved in the pathogenesis of proximal tubule dysfunction which characterizes diabetic tubulopathy. Methods: A total of 76 Type 2 diabetes mellitus patients and 28 healthy controls were evaluated concerning a potential association of glycated peptides with proximal tubule dysfunction by assessing urine albumin:creatinine ratio, urinary alpha1-microglobulin, urinary neutrophil gelatinase-associated lipocalin, plasma and urinary advanced glycation end-products, plasma asymmetric dimethyl-arginine, serum cystatin C. Fully automated chip-nanoelectrospray ionization and high-capacity ion trap multistage mass spectrometry characterized the urinary proteomic profile. Results: The urinary glycated proteins displayed a molecular weight of 15,121.4 Da in normoalbuminuric patients and of 30,180.4 Da in microalbuminuric patients. Urinary alpha1-microglobulin and neutrophil gelatinase-associated lipocalin correlated with urinary advanced glycation end-products (R2=0.586; R2=0.415), urine albumin: creatinine ratio (R2=0.292; R2=0.116), estimated glomerular filtration rate (R2=0.172; R2=0.135), serum cystatin C (R2=0.146; R2=0.129), but not with asymmetric dimethyl-arginine. In multivariable regression analysis models, the correlations for urinary alpha1-microglobulin and neutrophil gelatinase-associated lipocalin remained significant with urine albumin: creatinine ratio, urinary advanced glycation end-products, estimated glomerular filtration rate (P