The Degree of Leukocytosis and Urine GATA-3 mRNA Levels Are Risk Factors for Severe Acute Kidney Injury in Puumala Virus Nephropathia Epidemica

Peer reviewe

Can Calcium And Sodium Channel Blockers Attenuate Hemodynamic Responses To Endotracheal Intubation?

Aim: Direct laryngoscopy and endotracheal intubation following induction of anesthesia almost always triggers powerful cardiovascular responses. The purpose of this study was to investigate the efficacy of diltiazem (calcium channel blocker), lidocaine (sodium channel blocker) and a combination of these two drugs in the attenuation of circular responses to endotracheal intubation in normotensive patients. Methods: 120 Patients were randomly assigned to one of the following four groups. Group I received a single 0.2 mg/kg IV bolus of diltiazem 1 minute prior to laryngoscopy and intubation (n=30), Group II received a single 1.5 mg/kg IV bolus of lidocaine (n=30) 3 minutes prior and Group III received combination of these two drugs 1 minute prior to laryngoscopy and intubation (n=30). Group IV served as the control and received a single 5 mL IV bolus of normal saline. Changes in heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were measured and then compared within and between groups. Rate pressure product (RPP) was calculated and evaluated as well. Results: Either diltiazem or lidocaine alone blunts unwanted hemodynamic responses to intubation. However, significantly less circulatory responses were experienced by patients receiving both than those receiving either lidocaine or diltiazem alone. Conclusion: Given the difference in the pharmacological mechanisms of these two drugs, the prophylactic therapy with combination of diltiazem+lidocaine is significantly more effective than any one alone for attenuating hemodynamic changes to laryngoscopy and tracheal intubation, without producing increased risk of hypertension

Urinary sediment GATA-3 mRNA levels are elevated and T-bet mRNA levels are decreased during acute illness in PUUV-induced severe AKI.

<p>Severe AKI is >3-fold rise in serum Cr during acute illness compared to a 6 month baseline. Illness day 1 is the first calendar day of reported fever. a) Urinary sediment CD3ε mRNA relative expression compared to 2 week baseline value b) Urinary sediment GATA-3 mRNA relative expression compared to 2 week baseline value c) Urinary sediment T-bet mRNA relative expression compared to 2 week baseline value. Symbols and error bars are mean±S.E.</p

Maximum urine IL-6, plasma IL-6, and urine IL-8 concentrations are positively correlated with the degree of PUUV-induced AKI.

<p>a) maximum urine IL-6 levels b) maximum plasma IL-6 levels c) maximum urine IL-8 levels d) maximum plasma IL-8 levels.</p

Characteristics of study subjects with PUUV nephropathia epidemica.

a<p>AKI = acute kidney injury; severe AKI = >3-fold rise in serum creatinine during acute illness compared to a 6 month baseline value.</p>b<p>Values are median (95% confidence interval of median).</p

Clinical laboratory indicators in study subjects with PUUV nephropathia epidemica.

a<p>AKI = acute kidney injury; severe AKI = >3-fold rise in serum creatinine during acute illness compared to a 6 month baseline value.</p>b<p>Values are median (95% confidence interval of median).</p

Multivariate statistical models for acute kidney injury in study subjects with PUUV nephropathia epidemica.

a<p>Odds ratio (OR) for developing severe PUUV-induced acute kidney injury (AKI) compared to non-severe AKI. Severe AKI = >3-fold rise in serum creatinine during acute illness compared to a 6 month baseline value.</p>b<p>95% confidence interval (CI) for the Odds Ratio.</p>c<p>log₁₀ transformed variable.</p>d<p>White blood cell (WBC).</p>e<p>Linear regression of log₁₀ transformed peak creatinine ratio vs. log₁₀ transformed variables.</p>f<p>95% confidence interval (CI) for the linear regression coefficient.</p