The mean age of this population was 66.1 +/- 11.5 years, 49.3% were males, mean glomerular filtration rate (GFR) 68.9 +/- 22.6 ml/min/1.73 m(2). The 30-day mortality rate was 17.2%. One hundred and fifty-eight patients presented with haemorrhagic stroke and 932 patients had ischaemic stroke. Stroke mortality was-14% for ischaemic stroke and almost twice as high for haemorrhagic stroke-36.3%. One hundred fifty-eight (14.5%) patients were classified as developing AKI. The AKI patients were older, had a higher baseline serum creatinine, lower GFR, higher serum glucose, higher prevalence of chronic heart failure and ischaemic heart disease, were more likely to have suffered a haemorrhagic stroke, and had a significantly higher 30-day mortality rate (43.1 vs 12.8%) (P < 0.05 for all). Independent predictors for AKI development in the logistic regression analysis were age, GFR, presence of comorbidities (ischaemic heart disease and chronic heart failure) and type of stroke (Cox and Snell R(2) 0.244; Nagelkerke R(2) 0.431; P < 0.05). In our study, we demonstrated that the occurrence of AKI is not a rare finding in stroke patients. This is the first study to report the incidence of AKI in a distinct geographic population base, in patients with stroke. Baseline renal function emerged as both a significant independent marker for short-term survival after an acute stroke (even after adjustment for baseline comorbidities) and as a risk factor for subsequent AKI.

Rosiglitazone demonstrated its nephro- and neuroprotective effects in normoalbuminuric patients with type 2 diabetes mellitus by the end of the follow-up period and these effects were beyond glycemic control. Urinary beta2- and a1-microglobulin are significant biomarkers for incipient diabetic nephropathy and diabetic cerebral microangiopathy. These biomarkers showed that proximal tubule dysfunction may develop before the stage of microalbuminuria.

CVR is impaired in normotensive NIDDM patients. These cerebral hemodynamic changes correlate significantly with the duration of DM, parameters of inflammation, proteinuria and serum creatinine.

Introduction: The aim of our study was to clarify the hypothesis that proximal tubule (PT) dysfunction may be responsible for early diabetic nephropathy (DN), independently of preceding glomerular endothelial dysfunction. The pattern of endothelial dysfunction and its potential variability was evaluated in two vascular beds, the kidney and the brain. Methods: A total of 68 normoalbuminuric type 2 diabetes mellitus (DM) patients were enrolled in a cross-sectional study and the following parameters were assessed: urinary albumin:creatinine ratio (UACR), urinary α₁-microglobulin, urinary β₂-microglobulin, plasma asymmetric dimethyl-arginine (ADMA), serum creatinine, glomerular filtration rate (GFR), C-reactive protein (CRP), fibrinogen, HbA_1c; pulsatility and resistance indices in the internal carotid artery and middle cerebral artery and intima-media thickness (IMT) in the common carotid artery; cerebrovascular reactivity was evaluated through the breath-holding test. Results: Plasma ADMA was increased in 12 patients (17.5%), urinary α₁-microglobulin in 19 patients (27.9%) and urinary β₂-microglobulin in 16 patients (23.5%). Cerebral hemodynamic indices correlated with plasma ADMA, CRP, fibrinogen, duration of DM, HbA_1c and GFR. ADMA correlated with fibrinogen, CRP, HbA_1c, duration of DM and GFR. There were no correlations between ADMA and UACR, and urinary α₁-/β₂-microglobulin. Also, no correlations were found between urinary α₁-/β₂-microglobulin and UACR, HbA_1c, duration of DM and GFR. Conclusion: The increase in urinary α₁-/β₂-microglobulin precedes the stage of albuminuria. It may be assumed that early DN is related to PT dysfunction. Endothelial dysfunction plays a pivotal role in the brain vasculature, while its involvement in the development of early DN is not conditional on the occurrence of albuminuria.

No abstract