Rockville, Md. —There has been extensive research of ischemic acute kidney injury focused on the belief that prolonged low oxygen levels (hypoxia) cause injury to the kidney’s tubular tissue lining, resulting in continued kidney risk. Ischemic acute kidney injury happens when kidney cells have impaired oxygen and nutrient delivery or waste removal due to a sudden drop in blood flow.
David Pollock, PhD, FAPS, a professor at the University of Alabama at Birmingham, recently embarked to determine if all scientists are truly open to new ideas and novel mechanisms that contribute to the onset of kidney disease. To help explain, he reviewed the work of colleagues in a recent article in Function that explores why the complexities of acute kidney injury are not fully understood. Pollock’s review also detailed the many changing names for ischemic acute kidney injury over the years.
Pollock’s findings’ which he spelled out in his own Function article, included:
- The source of a large amount of injury to the outer medulla of the kidney following ischemia is related to the toxic effects of red cells contents and are identified within the damaged renal tubular lining.
- Well-established findings demonstrating the presence of hemoglobin within renal tubules following ischemia appear to be largely forgotten in much of the recent research of ischemic acute kidney injury.
“… it may be worth resurrecting the name ‘hemoglobinuric nephrosis,’ at least in concept, to explain the pathogenesis of outer-medullary tubular injury in ischemic [acute kidney injury],” Pollock wrote.
Read the full article, “Rethinking ischemic acute kidney injury as nephrotoxicity,” published ahead of print in the journal Function. Contact APS Media Relations or call 301.634.7314 to schedule an interview with a member of the research team.
