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Objective: The study was to evaluate neurotoxicity caused by antibiotics in dialysis patients, including incidence, clinical features, treatments and prognosis. Methods: In this retrospective study, we reviewed the medical records of 1066 dialysis patients (254 peritoneal dialysis [PD] cases and 812 hemodialysis [HD] cases) who also received intravenous antibiotics in our hospital during July 2006 - April 2012. Naranjo scale was used for estimating the probability of an adverse drug reaction. Results: The incidence of antibiotic-induced neurotoxicity was 5.66% in patients receiving HD, and 7.87% in patients receiving PD. There was no significant difference between the two dialysis modalities about the incidence of antibiotic-induced neurotoxicity ( p > 0.05). The risk factors included extremely old age, history of central nervous system disorder, low residual renal function, hypoalbuminemia, and the use of multiple antibiotics that share one mechanism. The neurotoxic antibiotics included cephalosporins, penicillins, carbapenems and quinolones in our study. Most patients could be properly diagnosed early according to their medical history, symptoms, signs, electroencephalography (EEG), other related auxiliary examination, and with the help of experienced neurologists. Most neurotoxic patients showed clinical improvement after the discontinuation of antibiotics and active treatment. Conclusions: The adverse neurotoxic effects of antibiotics were common in dialysis patients due to wide and incorrect usage. Neurotoxicity could be prevented in high-risk cases with dosage adjustments. Better prognosis can be achieved with early and proper diagnosis, decisive withdrawal, and aggressive treatment including enhanced HD. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) remains the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Although traditional risk factors, such as diabetes mellitus, hypertension, dyslipidemia and advanced age, are prevalent in ESRD patients they may not be sufficient by themselves to account for the high prevalence of CVD in patients with this condition. Thus, the search for other, non-traditional, risk factors that may be involved in the pathogenesis of uremic CVD has been an area of intense study. Data suggest that the accelerated atherosclerotic process of ESRD may involve several interrelated processes, such as oxidative stress, endothelial dysfunction and vascular calcification, in a milieu of constant low-grade inflammation. The cause(s) of inflammation in ESRD are multifactorial and, while it may reflect underlying CVD, an acute-phase reaction may also be a direct cause of vascular injury via several pathogenetic mechanisms. Available data suggest that pro-inflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation and atherosclerosis (MIA syndrome) would improve survival in dialysis patients. Recent evidence has demonstrated strong associations between inflammation and both increased oxidative stress and endothelial dysfunction in ESRD patients. As there is not yet any recognized, or even proposed, treatment for ESRD patients with chronic inflammation it would be of obvious interest to study the long-term effect of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as outcome of these patients. [ABSTRACT FROM AUTHOR]