About this Research Topic
Acute kidney injury (AKI) is a syndrome characterized by the rapid loss of the kidney's excretory function and is typically diagnosed by the accumulation of end products of nitrogen metabolism (urea and creatinine) or decreased urine output, or both. AKI is often secondary to extrarenal events, such as sepsis, major cardiac surgery, renal ischemia, the use of contrast media, and nephrotoxic drugs, among others. However, the mechanisms by which these events cause acute kidney injury remain controversial. No specific therapies have emerged that can attenuate acute kidney injury or expedite recovery, thus, treatment is supportive. New diagnostic techniques (eg. novel blood or urine biomarkers) might help with early diagnosis.
In this Research Topic, we aim to explore innovative mechanisms of AKI occurrence, investigate the effects of immune inflammation, hemodynamic abnormalities, and nephrotoxic substances on renal parenchymal cells, vascular endothelial cells, immune cells, etc., and delve into the subcellular mechanisms and signaling pathways involved. This research is intended to provide new targets for the early intervention and treatment of AKI. Encouraging the discovery and validation of new injury markers will promote early diagnosis of AKI and reduce the progression of AKI to Acute Kidney Disease (AKD)/Chronic Kidney Disease (CKD), thereby improving patient renal prognosis.
We welcome submissions on the following topics, but not limited to:
• Investigating the mechanisms of AKI occurrence, especially subcellular injury mechanisms, such as the role and mechanisms of organelle stress and dysfunction in AKI, including mitochondria, endoplasmic reticulum, ribosomes, etc.
• Discussing the molecular biology mechanisms underlying the transition of AKI to AKD/CKD.
• Exploring new injury markers that facilitate early diagnosis of AKI or the transition of AKI to AKD/CKD.
Manuscript Types: Original Articles (with a preference for basic research), Reviews, and Case Reports.
In this Research Topic, we aim to explore innovative mechanisms of AKI occurrence, investigate the effects of immune inflammation, hemodynamic abnormalities, and nephrotoxic substances on renal parenchymal cells, vascular endothelial cells, immune cells, etc., and delve into the subcellular mechanisms and signaling pathways involved. This research is intended to provide new targets for the early intervention and treatment of AKI. Encouraging the discovery and validation of new injury markers will promote early diagnosis of AKI and reduce the progression of AKI to Acute Kidney Disease (AKD)/Chronic Kidney Disease (CKD), thereby improving patient renal prognosis.
We welcome submissions on the following topics, but not limited to:
• Investigating the mechanisms of AKI occurrence, especially subcellular injury mechanisms, such as the role and mechanisms of organelle stress and dysfunction in AKI, including mitochondria, endoplasmic reticulum, ribosomes, etc.
• Discussing the molecular biology mechanisms underlying the transition of AKI to AKD/CKD.
• Exploring new injury markers that facilitate early diagnosis of AKI or the transition of AKI to AKD/CKD.
Manuscript Types: Original Articles (with a preference for basic research), Reviews, and Case Reports.
Keywords: acute kidney injury, subcellular mechanisms, blood or urine biomarkers, early diagnosis, transition of AKI to AKD/CKD
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
