Kidney Week

Abstract: TH-PO371

Back to Basics: Multiple Episodes of Hyperkalemia Due to Different Etiologies All Explained by Basic Physiologic Principles

Session Information

• Sodium, Potassium, and Volume Disorders: Clinical
  October 24, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolytes, and Acid-Base Disorders

• 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Portela, Rafael, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Rafael Portela, MD

• Matarneh, Ahmad, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Ahmad Matarneh, MD

• Sardar, Sundus, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Sundus Sardar, MD

• Llorens, Aidaliz, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Aidaliz Llorens, MD

• Abdulbasit, Muhammad, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Muhammad Abdulbasit, MD

Introduction

Potassium handling by the nephron is an important concept taught in medical school but, an intricate understanding of these processes usually develops during nephrology fellowship. Potassium disturbances are greatly influenced by intake, excretion and cellular shifts. We present a case of multiple episodes of hyperkalemia due to different etiologies all explained by basic physiology of potassium handling.

Case Description

57 year old female with chronic kidney disease stage 3a, MEN 2a syndrome status post right adrenal resection and gastric outlet obstruction with gastrojejunal (GJ) tube who presented for GJ tube dysfunction and stage 1 acute kidney injury. After unclogging the GJ tube, Peptamen 1.0 tube feeds (TF) were started (6 cans per day). After 48 hours, she developed unexplained hypotension. CT Chest revealed partial loculated pleural effusion. Labs showed hyperkalemia of 7.1 meq/L. She was treated medically and nephrology was consulted. At this point, acute kidney injury had resolved, but non anion gap metabolic acidosis (NAGMA) persisted (bicarbonate 20meq/L). Up to this point, hyperkalemia etiology was thought to be multifactorial: excess intake of potassium by TF (11 meq per bottle of Peptamen 1.0), NAGMA and underlying untreated primary adrenal crisis. Morning cortisol was low at 9.9 mcg/dL, consistent with our suspicion of primary adrenal insufficiency. She was treated with IV steroids accordingly and TF potassium content decreased and potassium remained stable at 4-5 meq/L. After 48 hours, had another hyperkalemic episode of 7.7 meq/L with worsening hyperglycemia of 409 mg/dL. Nephrology was reengaged and treatment with insulin was recommended. At this time, the culprit for hyperkalemia was increased insulin resistance in the setting of high dose steroid use, so steroids were tapered. Identifying each etiology of hyperkalemia episode led to prompt management and resolution of severe hyperkalemia.

Discussion

Here we portray multiple etiologies of hyperkalemia that every nephrologist should be aware. Prompt recognition of reversible causes of hyperkalemia such as increased dietary potassium intake, metabolic acidosis, adrenal insufficiency and insulin resistance are life saving and cost effective when managing admitted patients, avoiding invasive procedures, such as hemodialysis.