Issue 3, 2011 May 2011 Welcome to the 3rd issue of Kidney and Blood Pressure Research Digest (KBPR Digest) in 2011. We would like to draw your attention to articles of outstanding importance in the field of nephrology and hypertension, presenting short summaries of these articles to the scientific community in the form of KBPR Digest. KBPR Digest provides readers from all over the world with a free and concise overview on interesting topics which are part of the current issue of Kidney and Blood Pressure Research. We hope that you will be inspired to get to know more about the articles which are presented below. Professor Thomas Quaschning, MD, PHD On behalf of the Editorial Board of Kidney and Blood Pressure Research mail@thomas-quaschning.de  Digest of issue 3/2011 Issue 3/2011 of Kidney and Blood Pressure Research covers a wide spectrum of clinical and preclinical topics. It contains a study which investigates the effects of blockade of the renin-angiotensin system on cardiovascular status in hypertensive patients with renal failure as well as an evaluation of the association of coronary artery calcification with arterial stiffness in hemodialysis patients. Furthermore, the issue contains a study which explores the impact of candesartan on genomic damage in lymphocytes of hemodialysis patients. Hypertension is commonly associated with conditions such as diabetes mellitus and chronic kidney disease (CKD). In the pathophysiological background of these diseases, the increased renin-angiotensin system (RAS) activity plays a major role. The treatment of these high-risk patients is complex, but the main goal is to reduce the grade of albuminuria and other clinical and subclinical organ damage. Dual RAS blockade has no more efficiency to decrease cardiovascular mortality than mono-blockade. Nagy and coworkers (Kidney Blood Press Res 2011;34:150-157) aimed to explore differences between other cardiovascular markers in patients with RAS blockade. They therefore analyzed two groups of patients treated with a long-term ACE inhibitor (MONO-group, n = 20) and an ACE inhibitor and angiotensin II receptor blocker (DUAL-group, n = 15). Ambulatory blood pressure monitoring, echocardiography, arterial stiffness and levels of catecholamine, endogenous ouabain (EO), pro-brain natriuretic peptide and more types of urinary albumin measurements were performed. In the DUAL-group, the authors found significantly better cardiac parameters, but the levels of EO and urinary albumins were similar in both groups. The level of EO correlated with nighttime mean arterial blood pressure and arterial stiffness. Urinary immuno-unreactive albumin showed a relationship with diastolic dysfunction of the heart. In summary, cardiac parameters were more prosperous in the DUAL-group, but the levels of EO did not differ between the groups. Since urinary immuno-unreactive albumin was correlated with diastolic dysfunction, this parameter may advance to become be new marker of cardio-vascular conditions. Despite the fact that traditional cardiovascular risk factors are significantly over-represented in patients with chronic kidney disease (CKD) on maintenance dialysis (CKD-5), they do not seem to fully explain the incidence of cardiovascular diseases (CVD) observed in CKD-5. It is well recognized that vascular calcification (VC) represents a frequent finding in patients undergoing CKD-5. Evidence suggests that vascular calcification portends poor cardiovascular prognosis in patients undergoing maintenance dialysis. Nonetheless, how VC might predispose to cardiovascular mortality still remains to be clarified. Herein, an Italian group of scientists (Kidney Blood Press Res 2011;34:180-187) reported on the association between coronary artery calcification (CAC) progression and changes in cardiac repolarization as well as arterial stiffness. The authors included 132 patients new to dialysis. Demographic and clinical characteristics were collected at study entry and during the 12-month follow-up. CAC, 12-lead ECG and pulse wave velocity (PWV) were assessed at baseline and study completion. Uni- and multivariable analyses were applied to detected factors associated with worsening of cardiac repolarization (QTd) and arterial stiffness (PWV). In the present study, uni- and multivariable analyses revealed that CAC progression was associated with a significant increase in both QTd and PWV. Every 20-unit increase in the CAC score corresponded to a significant 23 percent and 32 percent increase in the risk of experiencing a 1-m/s increase in PWV and 1 ms in QTd, respectively. The most notable finding of these results is that CAC progression is associated with a progressive deterioration of parameters of arterial stiffness and cardiac repolarization. These results indicate that CAC could represent a step in the continuum of events responsible for the cardiovascular mortality in CKD-5. Nonetheless, future studies should confirm that preventing or attenuating CAC progression results in a better prognosis among patients receiving hemodialysis. In end-stage renal disease (ESRD), genomic damage is enhanced, as shown in peripheral blood lymphocytes by the micronucleus frequency test and the single cell gel electrophoresis-comet assay. Unrepaired or improperly repaired DNA lesions may have serious consequences, such as premature ageing, atherosclerosis and cancer predisposition. Angiotensin II (ANG II) and advanced glycation end products (AGEs) exert genotoxic effects in vitro which were prevented by the AT1 receptor blocker, candesartan. A stimulation of the renin-angiotensin system and accumulation of AGEs could be involved in enhanced genomic damage in ESRD. Therefore, Schupp et al. (Kidney Blood Press Res 2011;34:167-172) investigated whether oral co-administration of candesartan modulates enhanced DNA damage in ESRD patients. Fifteen maintenance hemodialysis (MHD) patients with mild hypertension were treated with candesartan for 4.5 months. Fourteen MHD patients served as conventionally treated uremic controls. DNA damage was measured as micronucleus frequency (MNF) in peripheral blood lymphocytes and was evaluated three times before candesartan therapy and afterwards every 6 weeks. Compared to 14 healthy controls, MNF at baseline was significantly elevated in MHD patients. While in the conventionally treated MHD patients the enhanced DNA damage persisted, the co-administration of candesartan ameliorated the genomic damage significantly and independently of blood pressure changes. The authors conclude that blockade of AT1 receptors with candesartan is able to reduce DNA damage in MHD patients. Nevertheless, long-term studies in larger patient groups are needed to investigate whether reduced genomic damage consecutively lowers atherosclerotic complications and development of cancer. For submission of articles or sign-ups to ToC Alerts, please go to the journal's homepage © S. Karger AG - Medical and Scientific Publishers Allschwilerstrasse 10, P.O. Box, CH-4009 Basel (Switzerland) Tel. +41 61 306 11 11, Fax +41 61 306 12 34, publications@karger.com. Please read the Karger Privacy Policy. If you have received this email by mistake, click here and we will take you off this mailing list.