Efficacy and safety of nicotinamide in haemodialysis patients: the NICOREN study.

Background: Nicotinamide (NAM) has been proposed as an alternative treatment to phosphate binders for hyperphosphataemia in chronic kidney disease.

Methods: The NICOREN multicentre, open-label and randomized study was designed to examine non-inferiority and safety of NAM when compared with sevelamer (SEV) in chronic haemodialysis patients. One hundred patients were randomized to either NAM or SEV treatment for 24 weeks.

The Association between 25-Hydroxyvitamin D and Hemoglobin A1c Levels in Patients with Type 2 Diabetes and Stage 1-5 Chronic Kidney Disease.

Aim. To examine the relationship between plasma 25-hydroxyvitamin D (25(OH)D) levels and blood hemoglobin A1c (HbA1c) levels in diabetic patients at various stages of chronic kidney disease (CKD). Methods.

Use of nicotinamide to treat hyperphosphatemia in dialysis patients.

Hyperphosphatemia in chronic kidney disease (CKD) has been associated with elevated cardiovascular morbidity and mortality. Serum phosphate control remains a cornerstone of the clinical management of patients with CKD, in order to both attenuate the progression of secondary hyperparathyroidism or bone disease and (possibly) reduce the risk of vascular calcification. Despite technical improvements in dialysis and the use of dietary restrictions, drug therapy is often required to control phosphate levels in patients with end-stage renal disease (ESRD).

Serious spontaneous epistaxis and hypertension in hospitalized patients.

The aim of the study was to evaluate the role of hypertension in patients hospitalized for serious spontaneous epistaxis. This 6-year retrospective study was based on 219 patients hospitalized in a University Hospital ENT and Head and Neck surgery department for serious spontaneous epistaxis. The following parameters were recorded: length of hospital stay, history of hypertension, blood pressure (BP) recordings (on admission, during hospitalization and on discharge), epistaxis severity criteria, including medical and/or surgical management of epistaxis (blood transfusion depending on blood count, embolization, surgery), medications affecting clotting.

Prevention of dementia by antihypertensive drugs: how AT1-receptor-blockers and dihydropyridines better prevent dementia in hypertensive patients than thiazides and ACE-inhibitors.

Our review of cohort studies and clinical trials evaluating antihypertensive drugs in the prevention of cognition decline and all dementia in patients with hypertension indicates that two antihypertensive drug classes have greater protective effects, independent of blood pressure decrease: dihydropyridine calcium-channel blockers as shown in the Syst-Eur trial and angiotensin-AT1 receptor blockers as found in the MOSES and ONTARGET trials. By contrast, diuretics and angiotensin-converting enzyme-inhibitors (ACEIs) prevent dementia only in patients with a stroke history, provided they are combined, and prevent stroke recurrence. A Japanese cohort study and a small trial in patients already suffering from Alzheimer's disease (AD) suggest, however, that the BBB-penetrating ACEI may slow down cognitive decline.

Angiotensin AT1-receptor blockers and cerebrovascular protection: do they actually have a cutting edge over angiotensin-converting enzyme inhibitors?

First, an update of the vascular systemic and tissue renin-angiotensin-aldosterone system is provided to explain how it is regulated at the systemic and tissue levels, and how many angiotensin peptides and receptors can be modulated by the various antihypertensive drugs. Second, experimental data is presented to support the hypothesis that antihypertensive drugs that increase angiotensin II formation, such as diuretics, AT1-receptor blockers and dihydropyridines, may have greater brain anti-ischemic effects than antihypertensive drugs that decrease angiotensin II formation, such as beta-blockers and angiotensin-converting enzyme inhibitors, because they increase activation of angiotensin AT2 and AT4 receptors. Indeed, these trigger brain anti-ischemic mechanisms by favouring cerebral blood flow (angiogenesis and recruitment of pre-existing collateral circulation, specifically in the ischemic brain where AT2 receptors are overexpressed) or by directly increasing neuronal resistance to anoxia.

Vitamin D affects survival independently of vascular calcification in chronic kidney disease.

Background And Objectives: Cardiovascular disease is the main cause of mortality in chronic kidney disease (CKD) patients. Vitamin D might have beneficial effects on vascular health. The aim of this study was to determine the prevalence of vitamin D deficiency (25-hydroxyvitamin D [25D] View Article and Find Full Text PDF

Protective effect of candesartan in experimental ischemic stroke in the rat mediated by AT2 and AT4 receptors.

Objectives: The contribution of the AT2 and AT4 angiotensin receptors to the protective role of the AT1 receptor blocker candesartan in acute ischemic stroke was investigated.

Methods: Embolic stroke was induced by injection of calibrated microspheres (50 microm) in the right internal carotid in Sprague-Dawley rats.

Results: Inhibition of production of endogenous angiotensins by pretreatment for 24 h with lisinopril significantly increased mortality and infarct volume, whereas candesartan for 24 h reduced blood pressure to the same extent but had no deleterious effect.

Antihypertensive treatment and stroke prevention in patients with and without chronic kidney disease: a review of controlled trials.

Background: Stroke is the leading cause of serious long-term disability and the third leading cause of death in the Western world. In patients with chronic kidney disease (CKD), stroke and vascular dementia are significantly more prevalent than in the general population. However, the optimal stroke prevention strategy in these patients is unclear, because controlled studies are scarce.

[Diuretic-based therapy].

Diuretics are pharmacological agents that increase natriuresis through inhibition of tubular re-absorption of sodium. The mechanisms and site of this inhibition differ with each drug class, accounting for their additive effects on natriuresis increase and their hydroelectrolytic side effects. The response to a given diuretic dose depends on the diuretic concentration on the urine at its action site.

Does a change in angiotensin II formation caused by antihypertensive drugs affect the risk of stroke? A meta-analysis of trials according to treatment with potentially different effects on angiotensin II.

Background: Stroke prevention by antihypertensive therapy is believed to be related to the fall in blood pressure (BP). Experimental data have documented that activation of non-AT1 receptors of angiotensin II may exert anti-ischaemic mechanisms in the brain. The present meta-analysis of various randomized clinical trials attempts to relate stroke risk to angiotensin II formation during antihypertensive therapy.

[Which optimal antihypertensive bitherapy for kidney patients?].

In this editorial review on the optimal antihypertensive treatment for chronic kidney disease (CKD) patients, we start with the controversy triggered by Casas et al., for proposing a bitherapy optimal not only for nephroprotection, but also for global cardiovascular protection. The incidence of cardiovascular complications are indeed much greater than the occurrence of end stage renal disease (ESRD) in these patients, so that their prevention has at least the same priority.

Insulin maintains plasma antioxidant capacity at an early phase of kidney transplantation.

Background: Ischaemia-reperfusion and hyperglycaemia are two main sources of oxidative stress that plays an important role in the pathophysiology of tissue injury in transplant recipients. We hypothesized that controlling hyperglycaemia with insulin during the first hours following kidney transplantation could improve antioxidant defences and therefore decrease ischaemia-reperfusion-induced injury.

Method: We performed a prospective randomized study in non-diabetic dialysed patients receiving a first cadaveric renal allograft, and assigned them to receive either 200 g/day of glucose infusion (control group, n=23) or the same glucose infusion and intravenous insulin to maintain blood glucose<10 mmol/l (insulin group, n=20).