Clinical scenarios where ACE inhibitors and ARBS are likely to cause AKI

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What are the clinical scenarios where ACE inhibitors and ARBS are likely to cause AKI?

Any clinical circumstance where perfusion to the kidney is impaired will cause a decline in glomerular filtration rate (GFR) and AKI by inducing efferent arteriolar vasodilatation through blockade of angiotensin II production or receptor binding. Clinical scenarios include:

  • • Disease states associated with hypotension
  • • Decreased blood volume (i.e., diuretics, diarrhea, vomiting, etc.)
  • • Decreased effective circulating blood volume (i.e., CHF, cirrhosis, nephrotic syndrome, etc.)
  • • Critical renal artery stenosis
  • • Treatment with medications such as NSAIDs, calcineurin inhibitors (CNIs), and vasoconstrictors

The typical scenario is that the GFR continues to decline with ACE inhibitor/ARB therapy and does not stabilize until drug withdrawal or correction of the underlying disease process.

Stabilization of kidney function, without hyperkalemia or hypotension, with continued ACEi/ARB therapy is likely associated with beneficial effects on both the heart and the kidneys.

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