Glomerular injury after trauma, burn, and sepsis

Acute kidney injury development after trauma, burn, or sepsis occurs frequently but remains a scientific and clinical challenge. Whereas the pathophysiological focus has mainly been on hemodynamics and the downstream renal tubular system, little is known about alterations upstream within the glomerulus post trauma or during sepsis. Particularly for the glomerular endothelial cells, mesangial cells, basal membrane, and podocytes, all of which form the glomerular filter, there are numerous in vitro studies on the molecular and functional consequences upon exposure of single cell types to specific damage- or microbial-associated molecular patterns. By contrast, a lack of knowledge exists in the real world regarding the orchestrated inflammatory response of the glomerulus post trauma or burn or during sepsis. Therefore, we aim to provide an overview on the glomerulus as an immune target but also as a perpetrator of the danger response to traumatic and septic conditions, and present major players involved in the context of critical illness. Finally, we highlight research gaps of this rather neglected but worthwhile area to define future molecular targets and therapeutic strategies to prevent or improve the course of AKI after trauma, burn, or sepsis. [GRAPHICS]

Automated summary

Acute kidney injury is a common occurrence after trauma, burn, or sepsis and remains a challenging issue in the scientific and clinical field. While much is known about the effects on the renal tubular system, little is understood about the changes that occur within the glomerulus. This article aims to provide an overview of the immune response and inflammatory processes within the glomerulus during these critical illnesses, and identify potential targets for future research and treatment strategies.