Should torsemide and lisinopril be held in a patient with worsening renal function?

Management of Worsening Renal Function with Torsemide and Lisinopril

Do not hold either torsemide or lisinopril based solely on this creatinine rise from 1.72 to 2.05 mg/dL. This modest increase (approximately 19%) likely represents hemodynamic changes from effective decongestion or RAAS inhibition rather than true tubular injury, and continuing guideline-directed medical therapy (GDMT) is associated with better long-term outcomes in heart failure patients 1.

Understanding the Creatinine Rise

Distinguishing Hemodynamic from Structural Kidney Injury

• A creatinine rise of less than 30% above baseline within the first 2 months of ACE inhibitor therapy is expected and associated with long-term renoprotection, not harm 2. Your patient's rise of 19% falls well within this acceptable range.

• Worsening kidney function during decongestion does not reflect true tubular injury in most heart failure patients 1. In fact, successful decongestion with rising creatinine is associated with lower mortality and reduced hospitalization rates compared to failure to decongest with stable creatinine 1.

• The clinical context matters critically: Look for signs of true acute tubular necrosis such as sepsis, hypotension, or bleeding 1. If absent and the patient is euvolemic or improving clinically, this creatinine rise represents hemodynamic adjustment, not kidney damage.

When to Continue Both Medications

Lisinopril Should Be Continued If:

• The creatinine rise is less than 30% above baseline (yours is 19%) 2
• Potassium remains below 5.6 mEq/L 2
• The patient is clinically stable or improving with decreasing congestion 1
• No evidence of volume depletion, hypotension, or concurrent NSAID use 3, 2

The FDA label for lisinopril states to "consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function" 3—but a 19% rise without other concerning features does not meet this threshold.

Torsemide Should Be Continued If:

• The patient requires ongoing diuresis for volume management 1, 4
• Electrolytes are being monitored appropriately 4
• The patient is not showing signs of severe volume depletion 5

Critical Monitoring Requirements

Immediate Assessment Needed:

• Check volume status clinically: Is the patient euvolemic, hypervolemic, or hypovolemic? 1
• Measure potassium level: Hyperkalemia (K+ ≥5.6 mEq/L) would require intervention 2
• Review for precipitating factors: Recent NSAID use, dehydration, gastroenteritis, or excessive diuresis 2
• Assess BUN-to-creatinine ratio: A low BUN (16 mg/dL in the case example) with rising creatinine suggests RAAS inhibition rather than prerenal azotemia 1

Follow-Up Monitoring:

• Recheck renal function and electrolytes in 1-2 weeks after any medication adjustment 4
• Monitor for stabilization: Creatinine typically stabilizes after 4 weeks of ACE inhibitor therapy if salt and fluid intake are normal 2

When to Hold or Adjust Medications

Hold Lisinopril If:

• Creatinine rises more than 30% above baseline within the first 2 months 2
• Potassium exceeds 5.6 mEq/L despite management 2
• Signs of true acute kidney injury develop (oliguria, uremic symptoms, rapid creatinine doubling) 3
• Severe hypotension occurs (SBP <100 mmHg with symptoms) 3

Reduce or Hold Torsemide If:

• Clinical signs of volume depletion emerge (orthostatic hypotension, dizziness, prerenal azotemia) 5
• The patient becomes euvolemic or hypovolemic and no longer requires diuresis 1
• Severe electrolyte abnormalities develop despite supplementation 5

Common Pitfalls to Avoid

• Do not reflexively discontinue ACE inhibitors for modest creatinine rises: Patients with the most advanced renal insufficiency at baseline show the maximum benefit from ACE inhibitors, but they also experience the largest early creatinine rises 2. This is expected and beneficial.

• Avoid combining torsemide with NSAIDs: NSAIDs block diuretic effects and worsen renal function 4.

• Do not ignore volume status: A rising creatinine in an overloaded patient who needs more diuresis is fundamentally different from one in a depleted patient 1.

• Remember that diuretic-associated creatinine rises may reflect more advanced heart failure rather than direct nephrotoxicity 1. Higher diuretic doses are often a marker of disease severity.

Evidence-Based Rationale

The 2025 American Journal of Kidney Diseases guidelines emphasize that creatinine increases during decongestion or RAAS inhibitor initiation frequently occur without actual tubular damage 1. The landmark study by Ahmad et al. demonstrated that worsening renal function during aggressive diuresis is not associated with tubular injury markers 1.

For ACE inhibitors specifically, a comprehensive review of 12 randomized trials involving 1,102 patients showed that those with chronic renal insufficiency who experienced an early 25% creatinine rise had a 55-75% lower risk of long-term renal function deterioration compared to those without the rise 2. The key threshold is 30% above baseline—below this, continue therapy unless other contraindications emerge.