Bronchial aspirates glucose level as indicator for methicillin-resistant staphylococcus aureus [MRSA] in intubated mechanically ventilated patients

This study evaluated if the level of glucose in bronchial aspirate serves as indicator for the risk of MRSA infection in intubated mechanically ventilated ICU patients.A total of 50 critically ill patients was enrolled and were under tight glycemic control to abolish the effect of hyperglycemia on bronchial secretion, if they were expected to require mechanical ventilation for more than 48 hours. Bronchial aspirates were detected for glucose and sent twice weekly for microbiological analysis and whenever an MRSA was expected.The results showed that all the patients had glucose tested in bronchial aspirates. Glucose was detected in bronchial aspirates of 28 of the 50 patients. Glucose in bronchial aspirates in these patients ranged between [2.9-5.lmmol/1]. MRSA was detected in 22 patients where 28 were MRSA free of the MRSA patients 19 had positive glucose where glucose was positive in 28 patients of them 19 [86.4%]where MRSA positive to 9 with no MRSA [32.1%].The risk of having MRSA present markedly increased significantly in the presence of glucose: [p value .001]

Heat preconditioning reduces subsequent ischemia reperfusion injury in rat kidney: a possible role for HSP-72

Improving the ability of the kidney to tolerate ischemic injury has important implication in renal transplantation. On the other hand, thermo tolerance describes the process in which hyperthermia induces a transient resistance of the stressed cells to subsequent episodes of oxidative stress. The current study was performed to evaluate the beneficial effect of heat preconditioning induced HSP-72 formation on renal ischemia reperfusion [I/R] induced damage. Four groups of rats [n=20/group] were included: Control sham-operated group [group I], heat-preconditioned sham-operated group [group II], I/R injury group [group III] and heat pre-conditioned I/R injury group [group IV]. Heat-preconditioning was induced 24h prior to sham operation and or I/R injury by increasing the core body temperature to [41 +/- 0.5°C] for 20min. The rat kidneys were subjected to ischemia by 20min of bilateral renal artery occlusion followed by reperfusion for 24 and 48h. After 24 and 48h of reperfusion, serum urea, creatinine, 24h urine out put and albumin content as well as the renal HSP-72 gene expression and MDA level were measured. Also light microscopic examination of renal tissue specimens was performed. It was found that group IV had a significant increase in renal HSP-72 gene expression compared to group III [898.36 +/- 107.82 versus 572.88 +/- 47.08 micro g/g tissue], associated with a significant improvement of its renal functions including serum urea, creatinine and 24h urine volume out put. Also there was a reduction in renal tissue injury detected by a significant decrease in urine albumin content, a significant decrease in renal MDA level and improvement in specimen microscopic picture compared to group III. The increase in HSP-72 expression and its renoprotective effect were significantly greater 24h after I/R than after 48h. Thus it can be concluded that upregulation of HSP-72 after heat preconditioning has a renal beneficial effect and can be a target for protection of renal functions during I/R injury

Gene expression of vasopressin receptor type 2 and aquaporin 2 in acute renal failure versus chronic renal failure in rats

Urinary concentration decreases in response to a reduction of functioning renal mass. Although a variety of factors have been implicated, the pathogenesis of impaired urinary concentration ability in acute renal failure [ARF] and in chronic renal failure [CRF] especially the cellular and molecular defects, were poorly understood. Our study therefore aimed to present a possible explanation for the pathogenesis of impaired urinary concentration and the molecular defect in kidney tissue of experimental ARF and CRF rat models and aimed to find and compare any molecular defect difference between ARF and CRF. Thirty albino adult male rats were used in our study and the animals were divided into three groups. Group I: Sham-operated controls [n=10]. Group II: Renal ischemia-reperfusion injury group [n=10] in which the renal artery and vein were bilaterally exposed and occluded for 30min with vascular clamps to produce renal ischemia-induced acute renal failure [ARF], the clamps were removed to allow kidney reperfusion then the animal sacrified after 24H. Group III: Chronic renal failure group [n=10], this group of animals underwent right total nephrectomy and removal of 2/3 of the left kidney and the experimental protocol lasted about one month then the animals were sacrified. Blood, urine and kidney tissue samples were collected from the three groups to measure serum urea and creatinine and 24 hour-urinary albumin for evaluation of kidney function and to measure aquaporin 2 water channel and vasopressin-receptor type 2 [V[2]] gene expressions in kidney tissue. Kidney function tests as regards serum urea, serum creatinine and 24 hour-urinary albumin in group II and group III showed a significant [p<0.05] increase in comparison to control group [group I]. Ischemic-reperfusion rats [group II] showed the highest of these parameters indicating that, they had the worst kidney function. A significant [p<0.05] decrease in vasopressin-receptor type 2 [V[2]] mRNA expression in kidney tissue was shown in group II [ARF] and group III in comparison to the control rats [group I] with the highest reduction in group II. A similar result was found as regards Aquaporin 2 water channel mRNA expression with a significant [p<0.05] reduction in group II and group III in comparison to group I, and the highest reduction was seen in group II among the three studied groups. In both ischemia-reperfusion rats and CRF rats, the ischemic and nephrectomy insults were associated with decreased mRNA expression of the aquaporin 2 and vasopressin-receptors type 2 [V[2]] in the kidney tissue, coinciding with the impairment of kidney function. This may contribute to the impairment in urinary concentration in the post-ischemic period and the urinary concentration defect associated with CRF