Methods: Septic patient with hyperlactatemia and metabolic acidosis were randomized to receive either high SID fl uid or Hartmann's solution during initial fl uid resuscitation. The primary outcome measures the pH and bicarbonate levels difference pre- and post- resuscitation.
Results: One hundred and sixty-two patients underwent randomization, 81 were assigned each to receive high SID fluid or Hartmann's solution. Both groups had similar baseline characteristics. High SID group received 23.5 mL/kg and the Hartmann's group received 22.7 mL/kg (p = 0.360). High SID fluid increased the mean (± SD) pH by 0.107 (± 0.09) vs. Hartmann's solution by 0.014 (± 0.12), p ≤ 0.001. Mean bicarbonate level increased signifi cantly in high SID group compared to Hartmann's (4.30 ± 3.76 vs. 1.25 ± 3.33, p ≤ 0.001). High SID group had higher post resuscitation lactate clearance than Hartmann's group (25.4 ± 28.3% vs. 12.0 ± 34.1%, p = 0.009). Shorter hospital stay was observed in highSID group 8.04 ± 5.96 days vs. Hartmann's group 12.18 ± 12.41 days (p = 0.048). Both groups showed no difference in incidence of pulmonary oedema, acute kidney injury and mortality.
Conclusions: Initial resuscitation using high SID fluid in selected septic patient improves pH and bicarbonate levels. The high SID group had better post resuscitation lactate clearance and shorter hospital stay.
METHODS: Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.
RESULTS: Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.
CONCLUSION: RESULTS from this study suggest that mefenamic acid as with other NSAIDs capable of producing nephrotoxicity. Therefore, the study of the exact mechanism of mefenamic acid induced severe nephrotoxicity can be done in this animal model.
METHODS: A multicenter cross-sectional study was performed from June 2014 to January 2015 using the EuroQOL-5 Dimensions instrument (EQ-5D-5L) for the assessment of HRQOL. ESRD patients undergoing HD in all dialysis centres in the West Bank of Palestine were approached and recruited for this study. Multiple linear regression was carried out to identify factors that were significantly associated with HRQOL.
RESULTS: Two hundred and sixty-seven patients were participated in the current study giving response rate of 96 %. Overall, 139 (52.1 %) were male, and the mean ± standard deviation age was 53.3 ± 16.2 years. The reported HRQOL as measured by mean EQ-5D-5L index value and Euro QOL visual analogue scale (EQ-VAS) score was 0.37 ± 0.44 and 59.38 ± 45.39, respectively. There was a moderate positive correlation between the EQ-VAS and the EQ-5D-5L index value (r = 0.42, p