Should a patient with Acute Kidney Injury (AKI) discontinue Furosemide, Empagliflozin (Empagliflozin), or Gabapentin?

Management of Furosemide, Empagliflozin, and Gabapentin in Acute Kidney Injury

In a patient with AKI, you should immediately discontinue gabapentin and empagliflozin, while furosemide should be continued or initiated if volume overload is present but discontinued if the patient is volume depleted or has progressive oliguria despite treatment.

Gabapentin: Discontinue Immediately

• Gabapentin must be discontinued immediately in AKI because it is entirely renally excreted and accumulates rapidly, causing severe neurotoxicity including altered mental status and coma 1
• The drug requires dose adjustment even in mild renal impairment, and continued use during AKI episodes represents a significant iatrogenic overdose risk 1
• All potentially nephrotoxic or renally-cleared medications should be discontinued immediately, as drugs account for 20% of community-acquired AKI episodes requiring hospitalization 2

Empagliflozin: Discontinue Immediately

• Empagliflozin should be discontinued immediately in AKI because SGLT2 inhibitors cause osmotic diuresis leading to volume depletion, worsen acute hemodynamic renal changes, and can rarely cause acute interstitial nephritis 3, 4
• The FDA label explicitly warns that empagliflozin causes intravascular volume contraction and increases serum creatinine with decreases in eGFR, particularly in patients with moderate renal impairment 3
• Biopsy-proven AIN secondary to empagliflozin has been documented, requiring discontinuation and corticosteroid treatment for recovery 4
• The acute impairment in renal function from empagliflozin reverses after treatment discontinuation, confirming that acute hemodynamic changes play a central role 3

Furosemide: Context-Dependent Decision

Continue or Initiate Furosemide If:

• The patient has volume overload or acute lung injury requiring fluid removal 5, 6
• The patient has AKI with preserved urine output (>500 mL/12h) and creatinine clearance >20 mL/min 7
• The patient has AKI stage 2-3 by urine output criteria, where furosemide is associated with improved survival and renal recovery 5

Discontinue Furosemide If:

• The FDA label mandates discontinuation if "increasing azotemia and oliguria occur during treatment of severe progressive renal disease" 8
• The patient is volume depleted or has prerenal AKI, as diuretics worsen hemodynamic compromise 2
• The patient has AKI stage 2-3 by serum creatinine criteria or acute-on-chronic kidney disease, where furosemide shows no mortality benefit 5

Furosemide Administration Protocol in AKI:

• Use continuous infusion rather than bolus dosing for superior diuretic response at the same total dose 7
• For septic shock patients on continuous renal replacement therapy, maximum diuretic response occurs at 20 mg/hour continuous infusion, achieving safe plasma levels <20 mg/L 7
• The FDA warns against rapid injection in severe renal impairment due to ototoxicity risk; controlled IV infusion not exceeding 4 mg/minute is recommended 8

Critical Monitoring Requirements

• Perform immediate comprehensive medication reconciliation and adjust all drug doses based on current GFR 2
• Monitor daily serum creatinine, eGFR, and electrolytes (especially potassium) during the acute phase 2
• Assess volume status immediately and correct volume depletion or overload before making diuretic decisions 2
• The decision framework should consider: renal versus non-renal excretion, potential for nephrotoxicity, strength of indication for the drug, and availability of suitable alternatives 9

Key Pitfalls to Avoid

• Never continue gabapentin without dose adjustment in any degree of renal impairment, as off-label use during acute illness should be discouraged 1
• Never combine multiple nephrotoxins, as each additional nephrotoxin presents 53% greater odds of developing AKI 2
• Never use furosemide to "reverse" established AKI in oliguric patients, as this leads to inappropriate fluid overload without benefit 9
• Recognize that AKI impairs hepatic cytochrome P450 activity, affecting drug metabolism even for medications primarily cleared by the liver 2