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.