Predicting Contrast-induced Renal Complications.

Chronic kidney disease is an independent risk factor for the development of coronary artery disease and overlaps with other risk factors such as hypertension and diabetes. Percutaneous coronary intervention is a cornerstone of therapy for coronary artery disease and requires contrast media, which can lead to renal injury. Identifying patients at risk for contrast-associated acute kidney injury (CA-AKI) is critical for preventing kidney damage, which is associated with both short- and long-term mortality. Determination of the potential risk for CA-AKI and a new need for dialysis using validated risk prediction tools identifies patients at high risk for this complication. Identification of patients at risk for renal injury after contrast exposure is the first critical step in prevention. Contrast media volume, age and sex of the patient, a history of chronic kidney disease and/or diabetes, clinical presentation, and hemodynamic and volume status are factors known to predict incident contrast-induced nephropathy. Recognition of at-risk patient subpopulations allows for targeted, efficient, and cost-effective strategies to reduce the risk of renal complications resulting from contrast media exposure.

Bruchpiloting synaptic connections: Egfr in autophagy-mediated neuronal circuit development.

Macroautophagy/autophagy is involved in many aspects of human development including the formation of neuronal circuits. A recent study from Dutta et al. found that the recruitment of Egfr (Epidermal growth factor receptor) to synapses suppresses autophagic degradation of presynaptic proteins, a requirement for proper neuronal circuit development. The findings suggest that Egfr inactivation during a distinct critical interval in late development results in increased levels of autophagy in the brain and decreased neuronal circuit development. Furthermore, the presence of brp (bruchpilot) in the synapse is critical for proper neuronal functioning over this same period. Dutta and colleagues found that increased autophagy due to Egfr inactivation results in decreased brp levels and, therefore, reduced neuronal connectivity. Through live cell imaging, it was determined that only the synaptic branches that accumulate both Egfr and brp are stabilized, allowing for the persistence of active zones, further supporting the importance of both Egfr and brp in the brain. While Dutta and colleagues collected these data based on studies conducted on Drosophila brains, the findings provide great insight as to how these different proteins may be implicated in human neurology.