What antihypertensive (blood pressure lowering) medications are recommended for patients with Acute Kidney Injury (AKI)?

Antihypertensive Management in Acute Kidney Injury

In patients with acute kidney injury (AKI), ACE inhibitors and ARBs should be temporarily discontinued, and calcium channel blockers or loop diuretics should be used as first-line antihypertensive agents instead. 1, 2

Immediate Management: Discontinue RAAS Blockers

ACE inhibitors and ARBs must be stopped during the acute phase of AKI because they reduce glomerular filtration pressure by blocking compensatory renal hemodynamic mechanisms, potentially worsening kidney function and increasing the risk of progression to acute kidney disease. 1, 2

• The combination of ACE inhibitors/ARBs with diuretics carries particularly high risk during AKI and should be avoided. 1, 3
• These medications alter intrarenal hemodynamics by reducing renal blood flow and glomerular filtration, which is especially problematic when kidney function is already compromised. 1
• Critical caveat: Small creatinine elevations up to 30% from baseline with RAAS blockers in stable chronic kidney disease are acceptable and should not be confused with true AKI—but this tolerance does NOT apply during acute kidney injury episodes. 1

First-Line Antihypertensive Options During AKI

Calcium Channel Blockers (Preferred)

Calcium channel blockers, particularly dihydropyridines like amlodipine, are the safest first-line choice because they have minimal effects on renal hemodynamics and do not compromise glomerular filtration. 1, 2

• Amlodipine 2.5-10 mg daily is well-tolerated and effective for blood pressure control without nephrotoxic effects. 1
• Non-dihydropyridine CCBs (diltiazem, verapamil) can also be used but should be avoided in heart failure with reduced ejection fraction. 1

Loop Diuretics (For Volume Overload)

Loop diuretics (furosemide, torsemide, bumetanide) are preferred when AKI is accompanied by volume overload or oliguria, particularly in moderate-to-severe kidney dysfunction. 1, 2

• These agents are more effective than thiazides when eGFR <30 mL/min/1.73 m². 1
• Loop diuretics may convert oliguric to non-oliguric AKI, facilitating fluid management, though they do not improve survival or renal recovery. 4
• Close monitoring of potassium and volume status is essential. 1

Thiazide-Like Diuretics (Limited Role)

Thiazide-like diuretics (chlorthalidone) can be considered in mild AKI but have reduced efficacy in moderate-to-severe kidney dysfunction. 1, 2

• The combination of thiazide diuretics with aldosterone antagonists (spironolactone) carries approximately three times higher risk of AKI compared to loop diuretic combinations and should be avoided. 3

Additional Considerations

Beta-Blockers

Beta-blockers can be used if the patient has concomitant ischemic heart disease or heart failure, though they are less effective for primary blood pressure control than other agents. 1, 2

Vasopressor Support (Critical Illness)

In hypotensive patients with AKI and vasodilatory shock, norepinephrine should be used to restore mean arterial pressure within autoregulatory range (typically >65 mmHg), as this improves renal perfusion and outcomes. 4, 5

• Vasopressin may provide additional benefit in less severe septic shock. 4
• Dopamine at renal doses has no proven benefit and should not be used. 4, 5

When to Reintroduce RAAS Blockers

RAAS blockers should only be reintroduced after:

1. GFR has stabilized
2. Volume status is optimized
3. The acute illness has resolved
4. Renal function and potassium are monitored within 1 week of restarting 2

• Start with lower doses and titrate slowly while monitoring closely. 2
• KDOQI guidelines recommend temporarily suspending RAAS antagonists during high-risk periods including intercurrent illness, IV radiocontrast administration, bowel preparation, and major surgery. 2

Critical Pitfalls to Avoid

Do not continue ACE inhibitors/ARBs during active AKI even if the patient was previously stable on these medications for chronic kidney disease—the acute setting fundamentally changes the risk-benefit calculation. 1, 2

Avoid nephrotoxic combinations, particularly:

• ACE inhibitor + ARB (dual RAAS blockade increases AKI risk). 1
• Thiazide + aldosterone antagonist in AKI setting. 3
• NSAIDs with any antihypertensive regimen. 1, 6

Remove all potential precipitating factors including diuretics initially, then reintroduce cautiously only if needed for volume management. 1