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Background. Shiga toxin-producing, enteroaggregative Escherichia coli was responsible for the 2011 outbreak of haemolytic uraemic syndrome (HUS). The present single-centre, observational study describes the 1-year course of the disease with an emphasis on kidney function. Outcome data after 1 year are associated with treatment and patient characteristics at onset of HUS. Methods. Patients were treated according to a standardized approach of supportive care, including a limited number of plasmapheresis. On top of this treatment, patients with severe HUS (n = 35) received eculizumab, a humanized anti-C5 monoclonal antibody inhibiting terminal complement activation. The per-protocol decision--to start or omit an extended therapy with eculizumab accompanied by azithromycin--separated the patients into two groups and marked Day 0 of the prospective study. Standardized visits assessed the patients' well-being, kidney function, neurological symptoms, haematological changes and blood pressure. Results. Fifty-six patients were regularly seen during the followup. All patients had survived without end-stage renal disease. Young(er) age alleviated restoring kidney function after acute kidney injury even in severe HUS. After 1 year, kidney function was affected with proteinuria [26.7%; 95% confidence interval (CI) 13.8-39.6], increased serum creatinine (4.4%, CI 0.0-10.4), increased cystatin C (46.7%, CI 32.1-61.3) and reduced (<90 mL/ min) estimated glomerular filtration rate (46.7%, CI 32.1-61.3). Nine of the 36 patients without previous hypertension developed de novo hypertension (25%, CI 10.9-39.1). All these patients had severe HUS. Conclusions. Although shiga toxin-producing Escherichia coli (STEC)-HUS induced by O104:H4 was a life-threatening acute disease, follow-up showed a good recovery of organ function in all patients. Whereas kidney function recovered even after longer duration of dialysis, chronic hypertension developed after severe HUS with neurological symptoms and could not be prevented by the extended therapy. [ABSTRACT FROM AUTHOR]

ANG II interacts with the sympathetic nervous system at central nervous blood pressure-regulating structures, including the baroreflex. It is unknown whether prolonged BP elevation mediated by high ANG II plasma levels could induce a persistent shift of the central nervous baroreflex setpoint, lasting beyond the short ANG II plasmatic half time of a few seconds, thereby consolidating elevated BP and/or increased SNA in healthy humans. In a blinded crossover design, ANG II or placebo (saline) was infused for a 6-h period in 12 resting normotensive students (6 males, 6 females) raising BP to borderline hypertensive levels. Between 60 and 120 min after the infusion period, muscle sympathetic nerve activity (MSNA) was assessed microneurographically and correlated with oscillometric BP measurements and heart rate at supine rest (baseline) and during pharmacologic baroreceptor challenge. Infusion of ANG II increased BP to borderline-hypertensive levels, as intended, whereas heart rate remained unaltered. At baroreflex assessment (i.e., 60-120 min after end of infusion period), systolic BP was significantly higher compared with placebo (Δ8.4 ± 3.1 mmHg; P < 0.05), whereas diastolic values were nearly equal between conditions. Baseline MSNA was neither decreased nor increased, and baroreflex sensitivity to vasoactive drug challenge was not altered. Our results show that elevation of ANG II plasma levels over 6 h was able to increase systolic, but not diastolic, BP far beyond blood-mediated ANG II effects. MSNA or heart rate did not counter-regulate this BP elevation, indicating that ANG II had sustainably reset the central nervous BP threshold of sympathetic baroreflex function to accept elevated BP input signals without counter-regulatory response., (Copyright © 2015 the American Physiological Society.)

Background: Preparing high quality discharge summaries is difficult for first year residents. For 5 years we have been training fourth year students how to write discharge summaries. Our goal is to facilitate the students' start into clinical work. Moreover, we intend to provide the students with a scheme to better memorize patients' histories. Two years after the tutorial the graduates were asked to evaluate the tutorial and to comment on its learning effects., Methods: A total of 1228 fourth year students wrote a discharge summary on a patient in whose care the specific student was involved during his or her training in internal medicine. All summaries were read, commented on and graded by a consultant. Two years after the tutorial 310 graduates were invited to complete an online survey on this tutorial., Results: 106 (34%) of all invited graduates completed the survey. The opinions on the tutorial greatly differed. In principal the students agreed that the tutorial was an important part of medical training and helped to better structure patients' medical data. The majority of the surveyed graduates, however, were not convinced of its practical usefulness for daily work. The students with the poorer grading found their grade less appropriate than the students with the better grading., Conclusions: Though our main goal could not be achieved in the view of the graduates, the overall opinion was rather positive. Problems with this kind of tutorial lay in the enormous effort of correction and in the discouraging effect of grading on the students with difficulties in the task.

Objective: Low birth weight (LBW) is associated with obesity and a higher cardiovascular risk in adult life. Since autonomic dysfunction could be a pathophysiological factor for this association, we assessed the impact of LBW on cardiac autonomic activity and metabolic rate in young adulthood. We hypothesized that the autonomic tone could be coupled with the metabolic rate in subjects with LBW., Methods: Heart rate variability (HRV) from 24-hour Holter-electrocardiograms was measured in 15 healthy adults aged 20 to 30 years with LBW (<2500g at term) and 15 paired subjects with normal birth weight (NBW). The pairs were closely matched by gender, age, and body mass index. Resting energy expenditure was measured by indirect calorimetry and body composition by bioimpedance., Results: Global HRV parameters were significantly higher in the LBW group and a marked difference was observed in the long wave fluctuations of the frequency domain (very low frequency). These fluctuations were positively correlated with the resting energy expenditure per body weight in the LBW and negatively in the NBW group. Only in the LBW group HRV was closely related to body fat., Interpretation: This case-control study indicates that autonomous nervous function is not generally deteriorated in young adults with LBW and has a significant association with metabolic rate. Thus, it may be a determinant of the body weight regulation in this group. The higher cardiovascular risk in ageing individuals with LBW would therefore rather be a consequence of weight gain than of a primary autonomous nervous dysfunction.

Nocturnal blood pressure (BP) decline or "dipping" is an active, central, nervously governed process, which is important for BP regulation during daytime. It is, however, not known whether the sleep process itself or, more specifically, slow-wave sleep (SWS) is important for normal dipping. Therefore, in the present study, healthy subjects (6 females, 5 males) were selectively deprived of SWS by EEG-guided acoustic arousals. BP and heart rate (HR) were monitored during experimental nights and the following day. Additionally, nocturnal catecholamine excretion was determined, and morning baroreflex function was assessed by microneurographic measurements of muscle sympathetic nerve activity (MSNA) and heart rate variability (HRV). Data were compared with a crossover condition of undisturbed sleep. SWS was successfully deprived leading to significantly attenuated mean arterial BP dipping during the first half (P < 0.05), but not during the rapid-eye-movement-dominated second half of total sleep; however, dipping still evolved even in the absence of SWS. No differences were found for nighttime catecholamine excretion. Moreover, daytime resting and ambulatory BP and HR were not altered, and morning MSNA and HRV did not differ significantly, indicating that baroreflex-mediated sympathoneural BP regulation was not affected by the preceding SWS deprivation. We conclude that in healthy humans the magnitude of nocturnal BP dipping is significantly affected by sleep depth. Deprivation of SWS during one night does not modulate the morning threshold and sensitivity of the vascular and cardiac baroreflex and does not alter ambulatory BP during daytime.