Why was Spironolactone (an aldosterone antagonist) discontinued in a patient with cirrhosis and ascites?

Why Spironolactone Was Likely Discontinued

The provider most likely discontinued spironolactone due to hyperkalemia (potassium >5.5 mEq/L), worsening renal function (creatinine >2.5 mg/dL), or severe hyponatremia (sodium <120-125 mmol/L), as these are the primary indications for stopping aldosterone antagonists in cirrhotic patients with ascites. 1, 2, 3

Primary Reasons for Discontinuation

Hyperkalemia

• Hyperkalemia is the most common reason to stop spironolactone, particularly when potassium exceeds 5.5 mEq/L 2
• The long half-life of spironolactone (with metabolites lasting 13.8-16.5 hours) increases the risk of potassium accumulation, which is why it's no longer recommended as monotherapy except in minimal fluid overload 1, 4
• Risk factors that make hyperkalemia more likely include: baseline creatinine >1.6 mg/dL, baseline potassium >5.0 mEq/L, concomitant ACE inhibitors or NSAIDs, diabetes, elderly age, and dehydration 2
• Patients with underlying parenchymal renal disease (diabetic nephropathy, IgA nephropathy) tolerate less spironolactone due to hyperkalemia 1

Worsening Renal Function

• Spironolactone must be stopped immediately if creatinine rises to >3.5 mg/dL (310 μmol/L) 2
• If creatinine reaches 2.5 mg/dL (220 μmol/L), the spironolactone dose should be halved 2
• Spironolactone is substantially excreted by the kidney, and the risk of adverse reactions is greater in patients with impaired renal function 4
• The drug is contraindicated when creatinine clearance falls below 30 mL/min 2

Severe Hyponatremia

• Diuretics should be reduced or stopped when serum sodium drops below 120-125 mmol/L 1, 2
• Spironolactone can cause sudden alterations in fluid and electrolyte balance that may precipitate hepatic encephalopathy and coma in cirrhotic patients 4
• Although cirrhotic patients typically don't develop symptoms from hyponatremia until sodium is below 110 mmol/L (unless the decline is rapid), severe hyponatremia warrants fluid restriction and diuretic adjustment 1

Secondary Considerations

Hepatic Encephalopathy

• Diuretics should be reduced or stopped if hepatic encephalopathy develops, as spironolactone can precipitate impaired neurological function and worsening encephalopathy in patients with cirrhosis and ascites 3, 4

Drug Interactions

• NSAIDs or COX-2 inhibitors are absolute contraindications to aldosterone antagonist use 2
• Concomitant lithium use requires discontinuation of spironolactone due to reduced renal clearance of lithium and high risk of toxicity 4
• Aspirin (600 mg dose) can inhibit the natriuretic effect of spironolactone by blocking tubular secretion of its active metabolite canrenone 4

Transition to Alternative Management

• If ascites persists despite maximum doses (spironolactone 400 mg + furosemide 160 mg), the patient has refractory ascites and should transition to large-volume paracentesis with albumin replacement (8g per liter removed) 2
• In diuretic-resistant patients with tense ascites, serial paracentesis becomes more appropriate than continuing ineffective diuretic therapy 1

Clinical Context

The decision to discontinue spironolactone reflects careful monitoring of the three critical parameters: potassium levels (checked at 3 days, 1 week, then monthly for 3 months), creatinine, and sodium 2. Given that spironolactone is the cornerstone of therapy in cirrhotic ascites due to hyperaldosteronism 2, discontinuation is never taken lightly and indicates a significant complication has developed that outweighs the drug's benefits for managing ascites.