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Potassium Channel Syndrome Caused by Nicorandil in Chronic Kidney Disease: A Case Report and Literature Review.
Electrolyte Blood Press
June 2022
Division of Nephrology and Hypertension, Department of Internal Medicine, Inha University College of Medicine, Incheon, Republic of Korea.
Nicorandil is an anti-anginal drug that is commonly used in the treatment of ischemic heart disease. Nicorandil acts as a nitrate donor and ATP-sensitive potassium channel agonist, inducing coronary artery vasodilation. Potassium efflux through ATP-sensitive potassium channels activated by nicorandil can cause refractory hyperkalemia, particularly in patients with chronic kidney disease (CKD).
View Article and Find Full Text PDFNicorandil-Induced Hyperkalemia in a Hemodialysis Patient.
Am J Med Sci
April 2017
Division of Nephrology, Department of Medicine, Taipei Veteran General Hospital, Taipei, Taiwan; School of Medicine, National Yang Ming University, Taipei, Taiwan. Electronic address:
Intractable hyperkalemia due to nicorandil induced potassium channel syndrome.
Ann Card Anaesth
September 2015
Department of Cardiac Anaesthesiology, Care Hospital, Bhubaneswar, Odisha, India.
Nicorandil is a commonly used antianginal agent, which has both nitrate-like and ATP-sensitive potassium (K ATP ) channel activator properties. Activation of potassium channels by nicorandil causes expulsion of potassium ions into the extracellular space leading to membrane hyperpolarization, closure of voltage-gated calcium channels and finally vasodilatation. However, on the other hand, being an activator of K ATP channel, it can expel K + ions out of the cells and can cause hyperkalemia.
View Article and Find Full Text PDFNicorandil-induced hyperkalemia in a uremic patient.
Case Rep Med
November 2012
Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, No. 100, Tzyou 1st Road, Kaohsiung 80756, Taiwan.
Nicorandil is an antianginal agent with nitrate-like and ATP-sensitive potassium channel activator properties. After activation of potassium channels, potassium ions are expelled out of the cells, which lead to membrane hyperpolarization, closure of voltage-gated calcium channels, and finally vasodilation. We present a uremic case suffering from repeated junctional bradycardia, especially before hemodialysis.
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