In a patient who develops acute kidney injury while on torsemide, should the medication be stopped or the dose reduced?

Management of Torsemide in Acute Kidney Injury

In a patient who develops AKI while on torsemide, the decision to stop or reduce the medication depends on whether the patient has volume overload: discontinue torsemide immediately if the patient is euvolemic or hypovolemic, but continue (potentially at reduced dose) if documented volume overload persists in a hemodynamically stable patient. 1, 2

Clinical Decision Algorithm

Step 1: Assess Volume Status and Hemodynamic Stability

• Stop torsemide immediately if any of the following are present: 1, 2

  • Patient is euvolemic or hypovolemic
  • Hemodynamic instability (hypotension, requiring vasopressors)
  • Oliguria with serum creatinine >3 mg/dL
  • Within 12 hours of last fluid bolus or vasopressor administration

• Consider continuing torsemide only if: 2

  • Patient is hemodynamically stable (MAP ≥60 mmHg, off vasopressors ≥12 hours)
  • Documented volume overload is present (pulmonary edema, peripheral edema, elevated CVP)
  • Patient is producing adequate urine output (>0.5 mL/kg/h)

Step 2: Evaluate Torsemide as Potential AKI Cause

Discontinue torsemide if: 1

• A causal relationship exists between torsemide and the AKI (temporal association, no other clear etiology)
• The drug is deemed non-essential after reassessment
• A less nephrotoxic alternative is available for the underlying indication

The ADQI consensus guidelines explicitly state that nephrotoxins should be discontinued when they are the potential cause of AKI or when they are non-essential. 1

Step 3: Assess for Polypharmacy Nephrotoxicity

• Immediately stop torsemide if the patient is receiving multiple nephrotoxic agents concurrently (NSAIDs, aminoglycosides, ACE inhibitors, contrast media), as each additional nephrotoxin increases AKI risk by 53%. 1, 2

• Loop diuretics combined with other nephrotoxins substantially amplify kidney injury risk. 2

When Torsemide May Be Continued Despite AKI

Torsemide can be maintained at reduced doses if: 2, 3

• Volume overload is life-threatening (severe pulmonary edema, anasarca)
• The patient's AKI trajectory is stable or improving
• No suitable alternative exists for managing fluid overload
• Hemodynamic parameters remain stable

Torsemide has pharmacokinetic advantages over furosemide in AKI: 3, 4, 5

• Higher bioavailability (90% vs 50-60% for furosemide)
• Primarily hepatic elimination, making it effective even with reduced GFR
• Longer duration of action (12-16 hours vs 6-8 hours for furosemide)
• Does not accumulate in renal failure

Monitoring Requirements if Torsemide Is Continued

Implement intensive monitoring: 1, 2

• Measure serum creatinine and eGFR at minimum every 48 hours during acute phase
• Monitor hourly urine output during IV diuretic therapy
• Check electrolytes every 12-24 hours (risk of hypokalemia, hyponatremia)
• Reassess volume status after each dose administration

Dose Adjustment Strategy

If continuing torsemide for persistent volume overload: 4, 5

• Reduce to the minimum effective dose that maintains adequate diuresis (target 0.8-1.5 mL/kg/h urine output)
• In one study of AKI patients recovering from continuous renal replacement therapy, torsemide doses were successfully titrated from median 29 mg every 6 hours with dose-dependent diuretic effect
• High-dose torsemide (100-200 mg daily) remains effective even in advanced renal failure, with a potency ratio of 1:2.5 compared to furosemide orally

Critical Pitfalls to Avoid

Never use torsemide to "reverse" or "treat" AKI itself—diuretics do not prevent AKI and may increase mortality. 1, 2 The KDIGO guidelines provide a Level 1B recommendation against using loop diuretics to prevent AKI, based on evidence that furosemide does not prevent AKI and may worsen outcomes. 1, 2

Do not attempt to convert oliguric to non-oliguric AKI with diuretics—this practice lacks evidence of benefit and causes harm. 2

Avoid extrapolating chronic kidney disease dosing guidelines to AKI patients, as hepatic blood flow, protein binding, and cytochrome P450 activity differ markedly in the acute setting. 1

Recognize that oliguria has multiple etiologies beyond volume overload: 2

• Acute compensated hypovolemia may require volume replacement, not diuresis
• Early biomarker-positive AKI does not automatically indicate volume overload requiring treatment

Special Populations

In cirrhotic patients with AKI: 2

• Withdraw all diuretics immediately as first-line management for AKI stage 1
• Discontinue if severe hyponatremia, worsening hepatic encephalopathy, or incapacitating muscle cramps develop

In elderly patients (≥75 years): 2

• Exercise particular caution, as loop diuretics are potentially inappropriate medications in this age group for certain indications

In patients with hypoproteinemia (nephrotic syndrome): 2

• Torsemide's effect may be weakened and ototoxicity potentiated
• Requires careful dose titration and monitoring

Evidence Quality and Nuances

The guideline evidence strongly supports a conservative approach to diuretics in AKI, with the ADQI 16 Workgroup consensus (2017) providing the most comprehensive framework for nephrotoxin management. 1 While torsemide has favorable pharmacokinetic properties compared to furosemide 3, 4, 6, 5, no loop diuretic should be used to treat AKI itself—only to manage volume overload in stable patients. 1, 2

Research evidence from cardiac surgery patients recovering from AKI after continuous renal replacement therapy suggests torsemide may have a better dose-dependent diuretic effect than furosemide, with less pronounced increases in serum creatinine and blood urea nitrogen. 4 However, this does not justify continuing torsemide in euvolemic or unstable AKI patients.