Acute and chronic kidney diseases have devastating consequences on human health. Renal vascular function, glomerular filtration, and epithelial transport are required for water and electrolyte homeostasis. Nephrotoxicity and diseases such as hypertension, diabetes and metabolic syndrome contribute significantly to acute and chronic kidney diseases. These disease pathological states impact on renal vascular and epithelial function and the ability for the kidney to maintain water and electrolyte homeostasis. Evidence over the past decade have provided evidence for a transition from acute to chronic kidney injury. Acute kidney injury in the clinical setting can cause sustained alterations in epithelial transport and renal hemodynamics that increase the risk for developing chronic kidney disease. The objective of this Research Topic is to highlight several renal vascular and epithelial mechanisms that contribute to acute and chronic kidney diseases.
This is a timely Research Topic because there are extremely limited options to treat acute and chronic kidney diseases. There have also been great advances our understanding of organismal, cellular and molecular mechanisms that contribute to acute and chronic kidney diseases. This is now a very fast-moving field as indicated by recent publications and the tremendous need for therapeutics to treat acute and chronic kidney diseases.
The Research Topic should have broad interest since it covers acute kidney injury, chronic kidney disease, diabetes, hypertension, metabolic syndrome, and renal physiology. Research publications will span cell signaling, animal studies, disease pathology studies, renal hemodynamics, glomerular filtration, and renal epithelial transport studies. The Research Topic will present novel developments on renal dysfunction that contributes to acute kidney injury and chronic kidney diseases.
Topic Editor John D Imig is a Co-founder of Diplos Therapeutics (Ann Arbor, MI) and Nephraegis (Milwaukee, WI). All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Acute and chronic kidney diseases have devastating consequences on human health. Renal vascular function, glomerular filtration, and epithelial transport are required for water and electrolyte homeostasis. Nephrotoxicity and diseases such as hypertension, diabetes and metabolic syndrome contribute significantly to acute and chronic kidney diseases. These disease pathological states impact on renal vascular and epithelial function and the ability for the kidney to maintain water and electrolyte homeostasis. Evidence over the past decade have provided evidence for a transition from acute to chronic kidney injury. Acute kidney injury in the clinical setting can cause sustained alterations in epithelial transport and renal hemodynamics that increase the risk for developing chronic kidney disease. The objective of this Research Topic is to highlight several renal vascular and epithelial mechanisms that contribute to acute and chronic kidney diseases.
This is a timely Research Topic because there are extremely limited options to treat acute and chronic kidney diseases. There have also been great advances our understanding of organismal, cellular and molecular mechanisms that contribute to acute and chronic kidney diseases. This is now a very fast-moving field as indicated by recent publications and the tremendous need for therapeutics to treat acute and chronic kidney diseases.
The Research Topic should have broad interest since it covers acute kidney injury, chronic kidney disease, diabetes, hypertension, metabolic syndrome, and renal physiology. Research publications will span cell signaling, animal studies, disease pathology studies, renal hemodynamics, glomerular filtration, and renal epithelial transport studies. The Research Topic will present novel developments on renal dysfunction that contributes to acute kidney injury and chronic kidney diseases.
Topic Editor John D Imig is a Co-founder of Diplos Therapeutics (Ann Arbor, MI) and Nephraegis (Milwaukee, WI). All other Topic Editors declare no competing interests with regards to the Research Topic subject.