Nosocomial infections in renal transplant patients: risk factors and treatment implications associated with urinary tract and surgical site infections.

A prospective cohort study was conducted from January 2000 to December 2001 to determine the rate of bacterial nosocomial infections in renal transplant recipients. The patients were divided into two groups according to the origin of the allograft, namely deceased or living related donors. One hundred and sixty-three renal transplant recipients were reviewed during hospitalization; 110 (67.5%) kidneys were from deceased donors and 53 (32.5%) kidneys were from living related donors. The median length of hospitalization was 12 days for transplants from living related donors and 26 days for transplants from deceased donors (P<0.0001). Twenty-one (39.6%) recipients of kidneys from living related donors and 68 (61.8%) recipients of kidneys from deceased donors had bacterial nosocomial infectious episodes (P=0.019). The post-transplant nosocomial infections diagnosed during hospitalization included urinary tract infections (UTIs) (44.8%), surgical site infections (SSIs) (11%), pneumonia (6.1%), catheter-related bloodstream infections (4.2%) and others (1.8%). Risk factors for UTI included: recipient of kidney from a deceased donor, substitution of the initial immunosuppressive regimen, duration of urinary bladder catheterization, and length of hospitalization before the infection. Six Enterobacter cloacae strains with multiple resistances to antibiotics were identified in UTIs, and hospital dissemination was documented using molecular typing. UTI was the single most important hospital infection and was significantly higher in recipients of kidneys from deceased donors (P=0.001).

Cardiovascular response to the injection of acetylcholine into the anterior cingulate region of the medial prefrontal cortex of unanesthetized rats.

Injection of acetylcholine (ACh) (2.5-60 nmol) into the anterior cingulate cortex caused dose-dependent hypotensive responses (Emax = -25.3 mmHg) and no change in the heart rate. The hypotensive response to 30 nmol of ACh was blocked by local pretreatment with atropine (3 nmol) or 4-DAMP (6.7 nmol), a non-tropine muscarinic antagonist. When the same dose of atropine was injected i.v., no changes were observed in the hypotensive response to intracortical ACh. This observation rules out the possible leakage of ACh into the peripheral circulation and favors the idea of a cortical site of action. The injection of the same dose of ACh into the corpus callosum or the occipital cortex did not cause changes in the cardiovascular system. The present results confirm earlier evidence that the cingulate cortex is involved in the control of the autonomic system and indicate that cholinergic muscarinic receptors in the cingulate cortex mediate a hypotensive response without a change in heart rate.