What is the role of depressed renal blood flow in the pathophysiology of acute kidney injury (AKI)?

Updated: Dec 24, 2020
  • Author: Biruh T Workeneh, MD, PhD, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Answer

Depressed RBF eventually leads to ischemia and cell death. This may happen before frank systemic hypotension is present and is referred to as normotensive ischemic AKI. The initial ischemic insult triggers a cascade of events, including production of oxygen free radicals, cytokines and enzymes; endothelial activation and leukocyte adhesion; activation of coagulation; and initiation of apoptosis. These events continue to cause cell injury even after restoration of RBF.

Tubular cellular damage results in disruption of tight junctions between cells, allowing back leak of glomerular filtrate and further depressing effective GFR. In addition, dying cells slough off into the tubules, forming obstructing casts, which further decrease GFR and lead to oliguria.

During this period of depressed RBF, the kidneys are particularly vulnerable to further insults; this is when iatrogenic renal injury is most common. The following are common combinations:

  • Radiocontrast agents, aminoglycosides, or cardiovascular surgery with preexisting renal disease (eg, elderly, diabetic, jaundiced patients)

  • Angiotensin-converting enzyme (ACE) inhibitors with diuretics, small- or large-vessel renal arterial disease

  • NSAIDs with chronic heart failure, hypertension, or renal artery stenosis


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