Meta-analysis of AKI to CKD transition in perioperative patients.

BACKGROUND: Recent research shows AKI increases the risk of incident CKD. We hypothesized that perioperative AKI may confer increased risk of subsequent CKD compared to nonperioperative AKI. METHODS: A MEDLINE search was performed for "AKI, CKD, chronic renal insufficiency, surgery, and perioperative" and related terms yielded 5209 articles. One thousand sixty-five relevant studies were reviewed. One thousand six were excluded because they were review, animal, or pediatric studies. Fifty-nine studies underwent full manuscript review by two independent evaluators. Seventeen met all inclusion criteria and underwent analysis. Two-by-two tables were constructed from AKI +/- and CKD +/- data. The R package metafor was employed to determine odds ratio (OR), and a random-effects model was used to calculate weighted ORs. Leave-1-out, funnel analysis, and structured analysis were used to estimate effects of study heterogeneity and bias. RESULTS: Nonperioperative studies included studies of oncology, percutaneous coronary intervention, and myocardial infarction patients. Perioperative studies comprised patients from cardiac surgery, vascular surgery, and burns. There was significant heterogeneity, but risk of bias was overall assessed as low. The OR for AKI versus non-AKI patients developing CKD in all studies was 4.31 (95% CI 3.01-6.17; p < 0.01). Nonperioperative subjects demonstrated OR 3.32 for developing CKD compared to non-AKI patients (95% CI 2.06-5.34; p < 0.01) while perioperative patients demonstrated OR 5.20 (95% CI 3.12-8.66; p < 0.01) for the same event. CONCLUSIONS: We conclude that studies conducted in perioperative and nonperioperative patient populations suggest similar risk of development of CKD after AKI.

Post-exercise syncope: Wingate syncope test and visual-cognitive function.

Adequate cerebral perfusion is necessary to maintain consciousness in upright humans. Following maximal anaerobic exercise, cerebral perfusion can become compromised and result in syncope. It is unknown whether post-exercise reductions in cerebral perfusion can lead to visual-cognitive deficits prior to the onset of syncope, which would be of concern for emergency workers and warfighters, where critical decision making and intense physical activity are combined. Therefore, the purpose of this experiment was to determine if reductions in cerebral blood velocity, induced by maximal anaerobic exercise and head-up tilt, result in visual-cognitive deficits prior to the onset of syncope. Nineteen sedentary to recreationally active volunteers completed a symptom-limited 60° head-up tilt for 16 min before and up to 16 min after a 60 sec Wingate test. Blood velocity of the middle cerebral artery was measured using transcranial Doppler ultrasound and a visual decision-reaction time test was assessed, with independent analysis of peripheral and central visual field responses. Cerebral blood velocity was 12.7 ± 4.0% lower (mean ± SE; P < 0.05) after exercise compared to pre-exercise. This was associated with a 63 ± 29% increase (P < 0.05) in error rate for responses to cues provided to the peripheral visual field, without affecting central visual field error rates (P = 0.46) or decision-reaction times for either visual field. These data suggest that the reduction in cerebral blood velocity following maximal anaerobic exercise contributes to visual-cognitive deficits in the peripheral visual field without an apparent affect to the central visual field.

Neurovascular control following small muscle-mass exercise in humans.

Sustained postexercise vasodilation, which may be mediated at both a neural and vascular level, is seen in previously active skeletal muscle vascular beds following both large and small muscle-mass exercise. Blunted sympathetic vascular transduction and a downward resetting of the arterial baroreflex contribute to this vasodilation after cycling (large muscle-mass exercise), but it is unknown if these responses also contribute to sustained vasodilation following small muscle-mass exercise. This study aimed to determine if baroreflex sensitivity is altered, the baroreflex is reset, or if sympathetic vascular transduction is blunted following small muscle-mass exercise. Eleven healthy, college-aged subjects (five males, six females) completed one-leg dynamic knee-extension exercise for 1 h at 60% of peak power output. While cardiovagal baroreflex sensitivity was increased ~23% postexercise relative to preexercise (P < 0.05), vascular and integrated baroreflex sensitivity were not altered following exercise (P = 0.31 and P = 0.48). The baroreflex did not exhibit resetting (P > 0.69), and there was no evidence of changes in vascular transduction following exercise (P = 0.73). In conclusion, and in contrast to large muscle-mass exercise, it appears that small muscle-mass exercise produces a sustained postexercise vasodilation that is largely independent of central changes in the baroreflex.