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Kidney Week

Abstract: PO1131

When Sipping K Is Not OK

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Rajasekaran, Arun, The University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Hasnie, Ammar, The University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Tolwani, Ashita J., The University of Alabama at Birmingham, Birmingham, Alabama, United States
Introduction

Hyperkalemia is one of the most common and potentially lethal electrolyte abnormalities that occurs in approximately 1% to 10% of hospitalized patients. It is associated with an increased risk of arrhythmias, poor cardiovascular outcomes, and increased morbidity and mortality. We highlight an unusual etiology of severe hyperkalemia in a patient with underlying CKD.

Case Description

A 74-year-old Black male with known arterial hypertension, coronary artery disease, CKD 3 [baseline serum creatinine (Cr) 1.7 mg/dl] presented with syncope secondary to severe bradycardia (heart rate 30/min) consequent to severe hyperkalemia, which necessitated a pacemaker placement, and non-oliguric AKI on CKD. Pertinent serum labs on presentation include Cr 2.8 mg/dl, potassium (K) 7.6 mmol/L, and bicarbonate 19 mmol/L. Serum osmolarity, glucose, and creatinine kinase levels were within normal limits. Urine pH was 5. Renal imaging was unremarkable. He was not on any medication(s) commonly attributed with a propensity to elevate serum K, including renin angiotensin inhibitors, non-selective β blockers, or non-steroidal anti-inflammatory agents. Given that the hyperkalemia was out of proportion to his kidney injury, upon further questioning he attributed consuming a diet rich in K along with drinking multiple cups of Essiac tea daily for the last 2 months. Hyperkalemia was managed medically, including initial temporizing measures, bicarbonate supplementation, K binders, and intravenous crystalloids to enhance distal nephron K excretion. Emphasis was placed on consuming a K restricted diet along with discontinuing Essiac tea use. Serum K normalized in 3 days; however Cr was 3 mg/dl on discharge.

Discussion

Essiac tea contains red clover, sheep sorrel, burdock root, and rhubarb which has extremely high potassium content. It is hepatotoxic and nephrotoxic when consumed in large amounts. We highlight the importance of obtaining a thorough dietary history, especially when the degree of hyperkalemia cannot be solely attributed to the extent of kidney injury. Dietary counselling is paramount in such cases.