Role of angiotensin converting enzyme inhibitors and angiotensin receptor blockers in hypertension of chronic kidney disease and renoprotection. Study results.

Chronic kidney disease (CKD) is a global health problem associated with considerable morbidity and mortality and despite advances in the treatment of end stage renal disease (ESRD) mechanisms to prevent and delay its progression are still being sought. The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in many of the pathophysiologic changes that lead to progression of renal disease. Traditionally RAAS was considered as an endocrine system and its principal role was to maintain blood pressure (BP). In recent years local RAAS has been described to operate independently from systemic and local angiotensin II (AngII) in the kidney to contribute in hypertension and kidney damage. The benefits of strict BP control in slowing kidney disease progression have been demonstrated in several clinical trials and the question whether specific agents like angiotensin converting enzyme antagonists (ACEIs) and angiotensin receptor blockers (ARBs) provide renoprotective benefits beyond BP lowering is to be answered. Several studies support these agents reduce proteinuria and protect renal function, whereas the opposite is stated by others. According to guidelines, their use is recommended as first line agents in diabetic renal disease and non diabetic renal disease with albuminuria, whereas there is no data to support the same in non diabetic nonalbuminuric renal disease. Dual blockage of RAAS with the combination of ACEIs and ARBs could offer an alternative in strict RAAS blockade, but studies up to now can not prove its safety and the combination is not recommended until ongoing trials will provide new and unarguable results.

[Biological factors associated with depression in patients with type ΙΙ diabetes mellitus].

This study was undertaken in order to identify the prevalence and factors associated with depression in a group of patients with type II diabetes mellitus. 200 patients (127 women/73 men) with type II diabetes mellitus, from Diabetic Clinic of 1st Propedeutic Medical Department of Aristotle's University of Thessaloniki, AHEPA Hospital, were enrolled in our study. Patients, sex, age, duration of diabetes, antidiabetic treatment, diabetic complications, body mass index (BMI), waist circumference, blood pressure, smoking, physical exercise and alcohol intake were assessed. BDI-II(Beck Depression Inventory-II) scale was used to measure the presence of depression. Prevalence of depression was high in the total of our patients (31.5%) and also in men (26%) and women (34.6%) separately. Depression appeared not to be related to patients' age, duration of diabetes, smokingand physical exercise, in the total of them (p>0.05). Patients, who were prescribed insulin, seemed to be more often depressed compared to those undertaking oral antidiabetic medication. The presence of depression was statistically significant increased in patients with diabetic complicationsin the total (p=0.013) and in men (p=0.001), while it was almost significantly increased in patients with diabetic nephropathy (p=0.052) and stroke (p=0.097). Depression was statistically significant related to obese patients compared to normal weight patients, in the total (p=0.003), and in menseparately (p=0.013), and also statistically significant was the relationship of depression with central obesity in the total (p=0.011) and in men (p=0.014). Statistically important was the relationship of arterial hypertension with depression in diabetic men (p=0.030), while in the limits of statistical importance was the relationship between depression and modest to heavy alcohol consumption in women (p=0.063). In a clinical aspect, depression seems to influence the development of type II diabetes mellitus, as it is shown by the significant association of diabetic complications anddepressive symptoms. The development of depression has often been considered a secondary response to the onset of complications, but depression might also play a primary role in the development or exacerbation of diabetic complications. It would be reasonable to speculate that obesity and arterial hypertension are biological variables that may interact with depression to produce diabetic complications. Further studies are needed to identify the pathways that mediate this association. These observations demonstrate that depression has a significant role in the development of type II diabetes mellitus, implying the necessity of its diagnosis and treatment, for the most optimal confrontation of the diabetic patient.

Stroke and conditions that mimic it: a protocol secures a safe early recognition.

OBJECTIVE: Certain disorders may be falsely diagnosed as stroke. We examined the efficacy of the diagnostic protocol that is followed in our stroke unit and was designed in order to early differentiate more efficiently between stroke and conditions that mimic it. METHODS-PATIENTS: Three hundred sixty-two elderly patients (196 male, 166 female with average age 74.56 years), who were hospitalized at our stroke center between January of 2005 and June of 2007 and diagnosed at admission as stroke patients, were retrospectively studied in order to investigate if the final diagnosis agreed with the initial diagnosis of stroke on admission.Our diagnostic protocol included medical history of the patient, assessment of state of consciousness, blood pressure, electrocardiogram, complete blood cell count (hematocrit/hemoglobin, leukocytes, platelets), clotting mechanism (prothrombin time, activated partial thromboplastin time), glucose, electrolytes (Na, K, Ca), renal (blood urea nitrogen, creatinine) and liver function (SGOT, SGPT), as well as imaging methods like chest X-Ray and brain CT scan. RESULTS: In 95% of patients, the final diagnosis agreed with the initial diagnosis of stroke at admission. According to final diagnosis, 344 (95%) of them had stroke -either hemorrhagic or ischemic-, while from the rest 18 (5%), 12 (66.7%) were found to have metastatic neoplasm of brain, 3 (18.7%) had primal tumour of brain, whereas 3 (18.7%) suffered from other diseases (respiratory infection, meningoencephalitis, thyrotoxicosis). The principal symptoms of the conditions that mimicked a stroke were: aphasic disturbances (27.3%), dizziness/fainting (27.3%), headache/diplopia (11.1%), dysarthria (11.1%), hiccup and/or swallow disturbances (5.6%). CONCLUSION: Our diagnostic protocol seems to ensure a high degree of differential diagnosis between stroke and conditions that mimic it.

Neuropeptide Y and alpha-melanocyte-stimulating hormone: interaction in obesity and possible role in the development of hypertension.

AIM: Obesity and hypertension frequently coexist and both represent important risk factors for cardiovascular disease. The mechanisms implicated in the regulation of food intake have not been completely elucidated. Recent data suggests that peripheral and central neuropeptides play an important role in the maintenance of energy balance. More specifically, leptin, neuropeptide Y (NPY) and alpha-melanocyte-stimulating hormone (a-MSH) appear to be implicated in the pathogenesis of obesity and also contribute to the development of hypertension in obesity. METHODS: Analysis of the pertinent bibliography published in PubMed database. RESULTS: Leptin is produced in the adipose tissue directly correlated with fat tissue mass. Leptin acts on two distinct neural populations in the hypothalamus: the first expresses the orexigenic peptides NPY and agouti-related protein (AgRP), the second pro-opiomelanocortin (POMC). The activation of POMC neurons increases the production of the anorexigenic hormone a-MSH and inhibits the release of NPY and AgRP. In addition, the hypothalamus integrates the neuroendocrine systems with the autonomic nervous system and controls the activity of the latter. Stimulation of hypothalamic nuclei elicits sympathetic responses including blood pressure elevation. Both NPY and a-MSH appears to be implicated in the hypothalamic regulation of sympathetic nervous system (SNS) activity. CONCLUSION: Alterations in leptin, NPY and a-MSH are frequently observed in obesity and might stimulate SNS activity, contributing to the development of hypertension in obese patients. These neuropeptides might provide a pathophysiologic link between excess weight and hypertension. However, more research is needed before the pharmacologic manipulation of these complex neuroendocrine systems can be applied in the treatment of obesity and hypertension.