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Objective: Acute kidney injury (AKI) is an important clinical entity that is known to increase mortality in patients with sepsis. Erythrocyte maturation and proliferation are inhibited by pro-inflammatory cytokines; these cytokines exert effects on red cell distribution width (RDW) well. Based on this knowledge; our aim in this study was to evaluate the impact of RDW on acute kidney injury in patients with sepsis. Methods: 120 patients diagnosed with sepsis and admitted to intesive care unit (ICU) and treated between 2009-2013 were retrospectively evaluated. Patients were divided into two groups as follows: group 1 (RDW≥16.8) and group 2 (RDW<16.8). Multiple logistic regression analysis was used to determine the association between RDW and AKI and mortality. Results: There was a statistically significant relationship between AKI and RDW (p<0.001, OR=11.52) but there were no statistically significant relationship between AKI and sex, age, serum lactate levels as well as SOFA score. Also, there were statistically significant relationship between mortality and RDW (p=0.044, OR=5), serum lactate levels (p=0.030) and SOFA score (p<0.001). RDW was found associated with both AKI and mortality. Conclusions: Results suggest that RDW is an important parameter for predicting development of AKI and mortality in ICU patients with sepsis. [ABSTRACT FROM AUTHOR]

Objectives: The early diagnosis of volume overload in chronic kidney disease (CKD) is very important. N-terminal probrain natriuretic peptide (NT-proBNP) is a valuable biomarker for this purpose. Our study aimed to detect the relationship between NT-proBNP and left ventricular hypertrophy (LVH), hypertension (HT), GFR, and proteinuria among diabetic patients with stage 3-4 CKD. Methods: 160 diabetic patients with stage 3-4 CKD [80 patients in stage 3 CKD (group 1) and 80 patients in stage 4 CKD (group 2)] were enrolled. NT-proBNP levels were evaluated in serum, and proteinuria was determined from 24-hour collected urine. Left ventricular hypertrophy was evaluated by M-mode echocardiography. NT-proBNP levels were compared according to their left ventricular hypertrophy, hypertension, and proteinuria levels. Results: NT-proBNP levels was significantly higher, and GFR was lower in group 2 compared to group1 (p < 0.05). NTproBNP was higher in patients with LVH (+) HT (+) and proteinuria = 1gr/d than patients with LVH (-), HT (-), and proteinuria < 1g/d (p < 0.05). We found a significant correlation between NT-proBNP levels and left ventricular posterior wall thickness, diastole (LVPWTd), proteinuria, SBP, and DBP. Proteinuria was the major contributor to increased NTproBNP levels among the independent variables. Conclusion: We detected that NT-proBNP levels are increased during the progression of CKD, and proteinuria is the major cause of increased NT-proBNP levels among the independent variables. [ABSTRACT FROM AUTHOR]

Objectives: The early diagnosis of volume overload in chronic kidney disease (CKD) is very important. N-terminal probrain natriuretic peptide (NT-proBNP) is a valuable biomarker for this purpose. Our study aimed to detect the relationship between NT-proBNP and left ventricular hypertrophy (LVH), hypertension (HT), GFR, and proteinuria among diabetic patients with stage 3-4 CKD. Methods: 160 diabetic patients with stage 3-4 CKD [80 patients in stage 3 CKD (group 1) and 80 patients in stage 4 CKD (group 2)] were enrolled. NT-proBNP levels were evaluated in serum, and proteinuria was determined from 24-hour collected urine. Left ventricular hypertrophy was evaluated by M-mode echocardiography. NT-proBNP levels were compared according to their left ventricular hypertrophy, hypertension, and proteinuria levels. Results: NT-proBNP levels was significantly higher, and GFR was lower in group 2 compared to group1 (p < 0.05). NTproBNP was higher in patients with LVH (+) HT (+) and proteinuria = 1gr/d than patients with LVH (-), HT (-), and proteinuria < 1g/d (p < 0.05). We found a significant correlation between NT-proBNP levels and left ventricular posterior wall thickness, diastole (LVPWTd), proteinuria, SBP, and DBP. Proteinuria was the major contributor to increased NTproBNP levels among the independent variables. Conclusion: We detected that NT-proBNP levels are increased during the progression of CKD, and proteinuria is the major cause of increased NT-proBNP levels among the independent variables. [ABSTRACT FROM AUTHOR]

Objective: Organophosphates are commonly used in agriculture and mostly lead to intoxication. In this study, we examined the sociodemographic features, clinical findings, and the relationship between time to treatment with pralidoxime and mortality in patients with organophosphate poisoning treated in our clinic. Methods: We retrospectively examined hospital records of 179 patients who were managed for organophosphate poisoning in our clinic, between January 2001 and November 2009. Sociodemographic data, clinical findings, laboratory results, complications during follow-up, and outcomes were recorded. The patients were grouped as died and survived, and comparison of sociodemographic and clinical features, laboratory results, and treatment outcomes were performed. Results: Among 179 patients, 133 (74.3%) were female, 46 (25.6%) were male and mean age was 27.1+11.7 years. Fifteen (8.3%) patients died. Illiteracy rate among those who died was 66.6%, while it was 30.4% in those who survived. Among those who died, 13 (86.6%) had nicotinic and 14 (93.3%) had CNS signs. Assessment of cases by the time to PAM administration revealed mortality rates of 4.47% (n=6), 19.4 % (n=7), and 22.2% (n=2) for the first 3 hours (n= 134), 3-6 hours (n=36), and after 6 hours (n=9), respectively. Conclusion: A great majority of patients presenting with organophosphate poisoning were of low educational status, which was linked with mortality, indicates the importance of education. In addition, mortality rate was lower in patients who were administered PAM at an earlier period in the treatment process, suggesting the role of early PAM administration in reducing mortality. [ABSTRACT FROM AUTHOR]