How to manage Hypertension in a patient with Acute Kidney Injury?

Management of Hypertension in Patients with Acute Kidney Injury

In patients with acute kidney injury (AKI) and hypertension, ACE inhibitors or ARBs should be used as first-line agents, with careful monitoring of renal function and potassium levels. 1, 2

Pathophysiology and Considerations

• Hypertension is highly prevalent in AKI patients, with rates varying by AKI etiology: 85% in post-renal AKI, 75% in intrinsic renal AKI, and 30% in pre-renal AKI 3
• Uncontrolled hypertension, along with edema and pulmonary congestion, may necessitate dialysis initiation in AKI patients 3
• Patients with AKI are often volume depleted due to pressure natriuresis, which can lead to precipitous BP falls when antihypertensive therapy is initiated 1

Treatment Algorithm

Step 1: Assess Hemodynamic Status and AKI Severity

• For hemodynamically unstable patients (requiring vasopressors), continuous renal replacement therapy (CRRT) is more appropriate than antihypertensive medications 1
• For stable patients with AKI, target BP <130/80 mmHg 1
• Consider fluid status carefully before initiating antihypertensive therapy 1

Step 2: First-Line Pharmacologic Therapy

• ACE inhibitors or ARBs are recommended first-line agents for hypertension in AKI patients 1, 2
• Start with low doses to prevent sudden decreases in BP, especially in volume-depleted patients 1
• For patients with CKD stage 3 or higher with albuminuria, ACE inhibitors are reasonable to slow kidney disease progression 1
• If ACE inhibitors are not tolerated, ARBs may be used as an alternative 1

Step 3: Diuretic Management

• Avoid using diuretics to prevent AKI 1
• Use diuretics only for management of volume overload in AKI patients 1
• For patients with heart failure with preserved ejection fraction (HFpEF) and hypertension, diuretics should be prescribed to control volume overload 1
• Loop diuretics (furosemide) are most commonly used (67.1%) for AKI patients with volume overload 4
• Consider combination therapy with loop diuretics and thiazides for resistant cases, but monitor potassium levels closely 1

Step 4: Special Considerations

• In patients with malignant hypertension and AKI, reduce mean arterial pressure by 20-25% over several hours using labetalol, nitroprusside, nicardipine, or urapidil 1
• For patients with hypertensive encephalopathy and AKI, labetalol may be preferred as it leaves cerebral blood flow relatively intact 1
• In AKI patients with liver disease, intravenous albumin administration appears beneficial for prevention of renal failure 1
• Avoid combination therapy with ACE inhibitors and ARBs due to increased risks of hyperkalemia and worsening AKI 1

Medication Precautions in AKI

• When initiating ACE inhibitors like lisinopril in patients on diuretics, reduce the starting dose to minimize hypotensive effects 5
• Monitor serum potassium frequently when using potassium-sparing diuretics with ACE inhibitors or ARBs 5, 6
• Avoid NSAIDs in AKI patients on ACE inhibitors or ARBs as they may cause deterioration of renal function 5, 6
• The combination of thiazide diuretics and aldosterone antagonists carries a higher risk of AKI than other diuretic combinations 7
• Avoid dual blockade of the renin-angiotensin system (combining ACE inhibitors, ARBs, or aliskiren) due to increased risks of hypotension, hyperkalemia, and worsening renal function 5, 6

Long-Term Outcomes

• ACE inhibitor/ARB use in post-AKI patients with hypertension is associated with better survival outcomes compared to non-users 2
• ACE inhibitor/ARB users are marginally less likely to progress to end-stage renal disease (adjusted HR 0.95) and significantly less likely to suffer from all-cause mortality (adjusted HR 0.93) 2

Monitoring and Follow-Up

• Monitor serum creatinine, potassium levels, and urine output closely when initiating antihypertensive therapy in AKI patients 1
• Target a diuresis of ≥0.5-1.0 ml/kg/h when using diuretics for volume management 4
• Consider transitioning from CRRT to intermittent hemodialysis when vasopressor support has been discontinued, hemodynamic stability achieved, and fluid balance can be adequately controlled 1, 8