Articles: cations.
-
Cerebral arteriovenous malformations (AVMs) are dynamic neurovascular disorders that occur mainly in young adults, presenting an annual risk of rupture of 2% - 4% per year.1 They can be asymptomatic, representing an incidental radiologic finding, or present with neurologic deficits according to their brain location, size, and presence or absence of bleeding.2,3 AVMs located in eloquent areas4 represent a great challenge for neurosurgeons, sometimes directed to alternatives therapies (e.g., embolization, radiotherapy) due to the difficulty in planning and surgical technique. Despite the complexity, we consider that there is benefit to removing these lesions; this can be done safely, as with the adequate microsurgical strategy and neuroanatomic knowledge. ⋯ He presented with intermittent left-hand paresthesia followed by an episode of involuntary movements in the left arm without loss of consciousness and with spontaneous resolution. Angiography showed an AVM feed by branches of the middle cerebral artery and multiple venous drainage for the Trolard complex and superficial middle cerebral vein, with a 4-cm nidus, making it grade III in the Spetzler-Martin classification.4 The patient underwent surgery with total resection of the lesion without any complication or new neurologic deficits.
-
Sepsis-associated acute kidney injury (SA-AKI) is a frequent complication of sepsis, yet the pathophysiologic mechanisms of SA-AKI are incompletely understood. PERSEVERE is a clinically validated serum biomarker panel with high sensitivity in predicting mortality from sepsis, and recent evidence suggests it can also predict severe, persistent SA-AKI at day 3 of hospitalization among septic children. We developed a murine model of PERSEVERE (mPERSEVERE) to further interrogate the sepsis-related biological underpinnings of SA-AKI using candidate biomarkers within mPERSEVERE. ⋯ The combination of plasma CCL3+KC can predict SA-AKI development in mice at 24-hours following CLP Of these two biomarkers, only renal expression of KC is increased in mice with SA-AKI. Further studies are required to determine if KC directly contributes to the underlying pathobiology of SA-AKI.