Vancomycin-induced renal toxicity was reported in 10-20 % and 30-40 % of patients following conventional and high doses of vancomycin therapy, respectively .The most probable mechanism for its nephrotoxicity can be at least partially attributable to an increased production of reactive oxygen species and oxidative stress. There are a number of different risk factors which could accelerate or potentiate the occurrence of vancomycin-induced nephrotoxicity, with the most documented risk factors being high trough vancomycin level (especially >20 mg/L) or doses (>4 g/day), concomitant treatment with nephrotoxic agents, prolonged therapy (even more than 7 days), and admittance to an intensive care unit (especially prolonged stay). It is necessary to carry out more studies, especially those focused on the association between nephrotoxicity and high trough levels of vancomycin.
Medication errors occur frequently in medical wards. Clinical pharmacists' interventions can effectively prevent these errors. The types of errors indicate the need for continuous education and implementation of clinical pharmacist's interventions.
PurposeHealthcare workers have a main role in detection, assessment and spontaneous reporting of adverse drug reactions (ADRs), and improvement of their related knowledge, attitude and perception is essential. The goal of this study was evaluation of clinical pharmacists' interventions in improvement of knowledge, attitude and perception of healthcare workers about ADRs in a teaching referral hospital, Tehran, Iran.MethodChanges in knowledge, attitude and perception of healthcare workers of Imam teaching hospital about ADRs were evaluated before and after clinical pharmacists' interventions including workshops, meetings and presentations.ResultsFrom the 100 participated subjects, 82 of them completed the study. 51% of the health workers have been aware of the Iranian Pharmacovigilance Center at the ministry of health before intervention and after that all the participants knew this centre. About awareness and detection of ADRs in patients, 69 (84.1%) healthcare workers recognised at least one, and following interventions, it was improved to 73 (89%). Only seven (8.5%) subjects have reported ADRs in before intervention phase that were increased significantly to 18 (22%) after intervention.ConclusionClinical pharmacists' interventions were successful in improvement of healthcare workers' knowledge, attitude and perception about ADRs and spontaneous reporting in our hospital.
Depression is a common psychiatric disorder in patients with advanced chronic kidney diseases (CKDs). Strong correlation has been reported between depression and patients' morbidity and mortality among dialysis patients. On the contrary, chronic inflammation may be a major contributor to morbidity and mortality in these patients. Elevated plasma levels of proinflammatory cytokines, especially C-reactive protein and interleukin (IL)-6, have been correlated with cardiovascular events, hospitalization, and all-cause and cardiovascular-associated mortality in dialysis patients. Studies suggested that inflammation-mediated atherosclerotic cardiovascular diseases are the possible reasons for depression-induced mortality among patients without renal diseases. Several studies found significant elevations in circulating levels of proinflammatory cytokines, particularly IL-6 and tumor necrosis factor-α, in patients with major depression. Furthermore, depressive mood and behaviors, including sadness and suicidal ideation, were observed in patients who received repeated injections of recombinant cytokines. A thorough literature review indicates that while depressive symptoms and elevated inflammatory cytokine levels coexist in CKD and dialysis patients, their association is uncertain. Depression seems to be more associated with elevated serum levels of IL-6 than other cytokines in these patients. Further studies are needed to clarify the possibility of a causal relationship between inflammation and depressive symptoms in CKD and dialysis patients.
Several predisposing factors including elevated baseline SCr, concomitant nephrotoxic medications, low body weight, advanced age, tenofovir disoproxil fumarate (TDF) dose and duration of treatment and lower CD4 cell count were identified as risk factors for development of TDF-induced nephrotoxicity. Cellular accumulation through increased entry from the human organic anion transporters and decreased efflux into tubular lumen is main mechanism of nucleotide analogue antiviral induced nephrotoxicity. Renal function assessment and monitoring at baseline and during TDF treatment are the main approach of prevention of TDF-induced nephrotoxicity. Rosiglitazone may be helpful in patients presenting with TDF-induced nephrotoxicity. Pretreatment with melatonin prevented all known histological changes in proximal tubular mitochondira induced by TDF. Use of antioxidants with mitochondria-targeted properties such as MitoQ or Mito-CP may prevent proximal tubular mitochondrial against TDF damage. Vitamin E, ebselen, lipoic acid, plastoquinone, nitroxides, SOD enzyme mimetics, Szeto-Schiller (SS) peptides, and quercetin are other potential agents for prevention of TDF-induced nephrotoxicity. However, data regarding effectiveness of nephroprotective agents against TDF-induced nephrotoxicity are not conclusive. Before extrapolation of the preclinical evidence to clinical practice, these evidence should be confirmed in future human studies.
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