Abstract
Acute kidney injury (AKI) is independently associated with increased morbidity and mortality. Ischemia is the leading cause of AKI, and short of supportive measures, no currently available therapy can effectively treat or prevent ischemic AKI. This paper discusses recent developments in the understanding of ischemic AKI pathophysiology, the emerging relationship between ischemic AKI and development of progressive chronic kidney disease, and promising novel therapies currently under investigation. On the basis of recent breakthroughs in understanding the pathophysiology of ischemic AKI, therapies that can treat or even prevent ischemic AKI may become a reality in the near future.
Highlights
Acute kidney injury (AKI) is independently associated with increased morbidity and mortality
AKI has been associated with increased length of hospital stay and adjusted odds ratios of 4.1 for hospital mortality and 2.0 for discharge to short- and long-term care facilities [1]
Recent experimental research has helped elucidate the pathophysiologic basis behind ischemic AKI, and therapies that can treat or even prevent ischemic AKI may become a reality in the near future
Summary
Acute kidney injury (AKI) is independently associated with increased morbidity and mortality. Pathobiology of ischemia While the human adult kidneys account for 2% of total body weight, they receive approximately 25% of the cardiac output This facilitates the high rates of glomerular filtration required for the precise regulation of the body’s fluid and electrolyte balance. The source of medullary blood flow arises from the efferent arterioles of the juxtamedullary glomeruli giving rise to the vasa recta This serially organized renal microvasculature allows for the countercurrent mechanisms vital for sodium balance. If the blood supply becomes interrupted transiently, the oxygen balance is maintained by reducing GFR and solute transport to the TAL This protective mechanism is undermined by production of reactive oxygen species that further decrease medullary blood flow and increase TAL activity.
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