Can Vidaza (Azacitidine) cause hyperkalemia?

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Last updated: March 12, 2025View editorial policy

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From the Guidelines

Vidaza (azacitidine) can cause hyperkalemia, which is an elevated level of potassium in the blood, as a potential side effect, particularly during the first 1-2 treatment cycles. This medication, commonly used to treat myelodysplastic syndromes and certain leukemias, has been associated with electrolyte abnormalities including hyperkalemia. Hyperkalemia typically develops as part of tumor lysis syndrome, where rapid destruction of cancer cells releases intracellular contents including potassium into the bloodstream. Additionally, Vidaza can cause kidney dysfunction in some patients, which may impair potassium excretion 1. Patients receiving Vidaza should have their electrolyte levels, including potassium, monitored regularly throughout treatment, especially during the initial cycles. Signs of hyperkalemia to watch for include muscle weakness, fatigue, numbness, tingling, irregular heartbeat, or palpitations. If hyperkalemia develops, dose adjustment, temporary discontinuation of Vidaza, or specific treatments to lower potassium levels may be necessary depending on the severity. According to recent guidelines, therapies aimed at lowering K+ levels and enabling patients to continue RAASi therapy should be considered, and the use of K+ binders such as patiromer sorbitex calcium (PSC) or sodium zirconium cyclosilicate (SZC) may be beneficial in managing hyperkalemia 1. It is essential to evaluate the patient's diet, use of supplements, and concomitant medications that may contribute to hyperkalemia, and to closely monitor K+ levels to protect against development of hypokalaemia. In general, RAASi therapy should be started at a low dosage and titrated to the maximum tolerated evidence-based doses shown to reduce the risk of cardiovascular and renal events in clinical trials 1.

Some key points to consider:

  • Hyperkalemia can be life-threatening and requires immediate treatment
  • Vidaza can cause kidney dysfunction, which may impair potassium excretion
  • Patients receiving Vidaza should have their electrolyte levels monitored regularly
  • K+ binders such as PSC or SZC may be beneficial in managing hyperkalemia
  • Close monitoring of K+ levels is essential to protect against development of hypokalaemia. In patients with K+ levels >5 on maximum tolerated, guideline-recommended dose of RAASi therapy, treatment with a K+ lowering agent may be initiated as soon as K+ levels >5 mEq/L, and K+ level should be monitored according to the clinical status and K+ lowering treatment should be maintained unless another aetiology for hyperkalaemia is identified 1.

From the Research

Hyperkalemia and Vidaza (Azacitidine)

  • There is no direct evidence in the provided studies that Vidaza (Azacitidine) can cause hyperkalemia 2, 3, 4, 5.
  • The studies primarily focus on the treatment and management of hyperkalemia in patients with kidney disease, heart failure, and those taking certain medications 2, 3, 4, 5.
  • Azacitidine (Vidaza) is mentioned in one study as a treatment for higher-risk myelodysplastic syndromes/acute myeloid leukaemia, with its tolerability profile and adverse events discussed, but hyperkalemia is not mentioned as a potential side effect 6.
  • Hyperkalemia is associated with life-threatening cardiac arrhythmias and increased mortality, and is often observed in patients with chronic kidney disease and/or those taking certain medications 2, 3, 4, 5.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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