Diabetic nephropathy (DN) is the leading cause of end-stage renal failure worldwide. Besides, diabetic nephropathy is associated with cardiovascular disease, and increases mortality of diabetic patients. Several factors are involved in the pathophysiology of DN, including metabolic and hemodynamic alterations, oxidative stress, and activation of the renin-angiotensin system. In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in the pathogenesis of diabetic nephropathy. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. In this paper we review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines, and take part in other mediators of inflammation, as adhesion molecules.
Our results showed a significant association between hyperuricemia and metabolic syndrome in low-income young adults in Mexico. DR is associated with estimated risk of CVD in type 2 diabetic patients.
BackgroundBiopterins have a crucial role in the function of nitric oxide synthase, uncoupling of the enzyme leads to endothelial dysfunction and vascular damage, The aim of this study was to evaluate the relationship between the levels of biopterins with carotid intima-media thickness (CIMT) in hypertensive type-2 diabetic patients.MethodsWe studied 30 hypertensive type-2 diabetic patients and 30 normotensive non-diabetic age-matched subjects, in whom biopterins levels were measured by reverse phase high performance liquid chromatography with fluorescence detection. Additionally, the CIMT of both the common and internal carotid arteries was measured. The levels of biopterins and CIMT were correlated using the Pearson correlation coefficient test.ResultsWe did not find a significantly correlation between biopterins levels and CIMT. However, we found a significantly inverse correlation between the BH4/BH2 ratio and the CIMT in patients (r = -0.54, p < 0.01). A multiple regression analysis revealed that the CIMT correlated significantly and independently with the BH4/BH2 ratio.ConclusionOur results suggest that the BH4/BH2 ratio seems to be a better marker of vascular disease than biopterin levels.
Hyperuricemia leads to endothelial dysfunction and insulin resistance, and has been associated with diseases such as hypertension. Antihypertensive drugs modify serum uric acid levels, however, few data are available about their combinations on uricemia. In this study we evaluate the effect of two combinations of losartan, with amlodipine or with hydrochlorothiazide, on serum uric acid levels in hypertensive patients. Methods: A total of 60 hypertensive patients were randomized in two groups; group LA received losartan/amlodipine (100/5 mg) once a day, whereas LH group received losartan hydrochlorothiazide (100/12.5 mg) once a day for 3 months. In both groups serum uric acid levels were measured at the beginning and end of the study. Patients were evaluated monthly for blood pressure (BP) and adverse events. Statistical analysis was performed with a two-way analysis of variance (ANOVA) for repeated measures. Results: All patients experienced a significant reduction of BP to the same extent (LA 155/94 to 123/79, LH 157/92 to 124/78 mmHg, p > 0.05). In the LA group, serum uric acid decreased from 6.5 ± 1.6 to 4.6 ± 1.3 mg/ml (p = 0.0001), whereas in the LH group there was a nonsignificant increase from 5.82 ± 1.4 to 5.85 ± 1.5 mg/ml, (p = 0.936). When both groups were compared, we found a significant reduction (p < 0.00013) on serum uric acid levels in the LA group. Conclusions: Both combinations decrease BP values to the same extent, however, LA combination showed a reduction on serum uric acid levels, which may contribute to a reduction in the metabolic risk in hypertensive patients.
Prehypertensive patients had lower ABI and higher prevalence of peripheral artery disease when compared with normotensive subjects; this fact increases their cardiovascular risk. ABI must be included in global evaluation of prehypertensive subjects.
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