Acute kidney injury related to antihypertensive therapy can be caused by which of the following drug classes?

Acute kidney injury related to antihypertensive therapy can be caused by which of the following drug classes?

• A. ACE inhibitors, ARBs, and diuretics
• B. NSAIDs and acetaminophen
• C. Beta blockers and calcium channel blockers
• D. Aminoglycosides and vancomycin

Answer: (A)

Acute kidney injury from antihypertensive therapy is usually a hemodynamic problem tied to how these drugs alter renal blood flow and filtration pressure. ACE inhibitors and ARBs reduce angiotensin II–mediated constriction of the efferent arteriole, which lowers intraglomerular pressure and can decrease GFR. This effect becomes significant when renal perfusion is already compromised, such as with bilateral renal artery stenosis, heart failure with reduced effective arterial volume, or dehydration. Diuretics contribute by lowering circulating blood volume and renal perfusion, which can provoke prerenal AKI; this risk rises when a diuretic is used together with an ACE inhibitor or ARB, further reducing renal perfusion. Together, these classes are the ones most commonly associated with AKI in the context of antihypertensive therapy. NSAIDs and acetaminophen can affect the kidney but aren’t antihypertensive agents, beta blockers and calcium channel blockers aren’t typically linked to AKI in the same direct, hemodynamic way, and nephrotoxic antibiotics cause AKI via toxicity rather than through blood pressure–modulating effects.

Acute kidney injury from antihypertensive therapy is usually a hemodynamic problem tied to how these drugs alter renal blood flow and filtration pressure. ACE inhibitors and ARBs reduce angiotensin II–mediated constriction of the efferent arteriole, which lowers intraglomerular pressure and can decrease GFR. This effect becomes significant when renal perfusion is already compromised, such as with bilateral renal artery stenosis, heart failure with reduced effective arterial volume, or dehydration. Diuretics contribute by lowering circulating blood volume and renal perfusion, which can provoke prerenal AKI; this risk rises when a diuretic is used together with an ACE inhibitor or ARB, further reducing renal perfusion. Together, these classes are the ones most commonly associated with AKI in the context of antihypertensive therapy. NSAIDs and acetaminophen can affect the kidney but aren’t antihypertensive agents, beta blockers and calcium channel blockers aren’t typically linked to AKI in the same direct, hemodynamic way, and nephrotoxic antibiotics cause AKI via toxicity rather than through blood pressure–modulating effects.