Management of Hypertensive Patient with AKI
In hypertensive patients with AKI, immediately discontinue ACE inhibitors, ARBs, NSAIDs, and diuretics, initiate volume resuscitation with isotonic crystalloids, and target a blood pressure of <130/80 mmHg once volume status is optimized, using non-RAAS blocking agents initially. 1, 2, 3
Immediate Medication Review and Discontinuation
The first critical step is stopping medications that worsen AKI:
- Immediately discontinue ACE inhibitors and ARBs, as these can cause AKI and hyperkalemia, particularly in volume-depleted states 1, 2, 4, 3
- Stop all NSAIDs immediately, as they increase AKI risk more than twofold in volume-depleted patients 2, 4, 3
- Withdraw all diuretics to prevent exacerbation of prerenal AKI 2, 4, 3
- Hold aminoglycosides and other nephrotoxic medications to prevent further kidney damage 2, 3
This represents a departure from chronic management, where ACE inhibitors/ARBs are cornerstone therapy for hypertensive CKD patients. However, the ACC/AHA guidelines explicitly state that these agents can cause AKI and require careful monitoring 1.
Volume Resuscitation Strategy
Use isotonic crystalloids (normal saline or Ringer's lactate) as first-line therapy for volume expansion 2, 4, 3:
- Avoid starch-containing colloid solutions, which are associated with harm in AKI 2, 4, 3
- Monitor closely for pulmonary edema during fluid administration 2
- In select cases with concurrent cirrhosis or severe sepsis, consider albumin 1 g/kg on day 1 followed by 20-40 g daily 1, 3
Blood Pressure Targets During AKI
The target blood pressure depends on baseline hypertension status and volume optimization:
For Patients WITHOUT Pre-existing Hypertension:
- Target MAP 65-73 mmHg and DBP 50-60 mmHg once volume resuscitated 5
For Patients WITH Pre-existing Hypertension:
- Target MAP 70-80 mmHg and DBP 54-62 mmHg once volume resuscitated 5
- Long-term goal remains <130/80 mmHg after AKI resolution 1
The 2017 ACC/AHA guidelines recommend <130/80 mmHg for all CKD patients, but this target should be approached cautiously during acute AKI 1. Research demonstrates that hypertensive AKI patients require higher perfusion pressures than normotensive patients to maintain renal perfusion 5.
Antihypertensive Medication Selection During AKI
Once volume status is optimized and blood pressure remains elevated:
First-line agents (avoiding RAAS blockade initially):
- Dihydropyridine calcium channel blockers (amlodipine, nifedipine) 1
- Thiazide-like diuretics (chlorthalidone, indapamide) ONLY after volume repletion is complete 1
- Beta-blockers if concurrent coronary disease or heart failure 1
Avoid initially:
- ACE inhibitors and ARBs until kidney function stabilizes 1, 2
- Combination ACE inhibitor + ARB therapy is contraindicated 1
- Mineralocorticoid receptor antagonists carry hyperkalemia risk 1
Monitoring Parameters
Daily monitoring requirements 2, 4, 3:
- Serum creatinine daily to assess AKI trajectory
- Electrolytes (particularly potassium and bicarbonate)
- Urine output with goal >0.5 mL/kg/hour
- Blood pressure measurements
Within 2-4 weeks of any medication change, check basic metabolic panel to monitor for electrolyte abnormalities and changes in kidney function 1.
Common Pitfall: Intensive BP Lowering in Severe Hypertension
Caution with severe presentation hypertension (SBP ≥220 mmHg): Patients presenting with SBP ≥220 mmHg who undergo intensive BP lowering to <140 mmHg have significantly higher rates of AKI (odds ratio 2.6) compared to those with lower presentation BP 6. This suggests more gradual BP reduction may be safer in extreme hypertension with concurrent AKI.
Renal Replacement Therapy Indications
Initiate RRT when conservative management fails and any of the following develop 2, 4, 3:
- Severe oliguria/anuria persisting >48 hours despite optimal fluid resuscitation
- Refractory hyperkalemia
- Severe metabolic acidosis
- Volume overload with pulmonary edema
- Uremic complications
- Stage 3 AKI (creatinine >3× baseline) failing to improve
Prefer continuous RRT over intermittent hemodialysis in hemodynamically unstable patients, as it causes lower fluid shifts and reduced hemodynamic instability 4, 3.
Reintroduction of RAAS Blockade
Once AKI resolves and kidney function stabilizes:
Resume ACE inhibitor or ARB therapy for long-term management if 1:
- Albuminuria ≥300 mg/day or ≥300 mg/g creatinine ratio present
- CKD stage 3 or higher
- Diabetes with any degree of albuminuria
The 2019 KDOQI commentary emphasizes that continuation of ACE inhibitors/ARBs as kidney function declines to eGFR <30 mL/min/1.73 m² may provide cardiovascular benefit without significantly increasing risk of end-stage kidney disease 1.
Long-Term Follow-Up Strategy
Monitor serum creatinine every 2-4 weeks for 6 months after discharge to detect recurrent AKI 2, 4, 3. Evaluate kidney function at 3 months post-AKI to assess for resolution, new-onset CKD, or worsening of pre-existing CKD 4, 3.
Target intensive follow-up to high-risk populations: those with Stage 3 AKI, incomplete recovery at discharge, or baseline CKD 2, 4.