ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO1477

Pseudohypophosphatemia Caused by Severe Leukocytosis in a Patient with Chronic Lymphocytic Leukemia (CLL) and Tumor Lysis Syndrome (TLS)

Session Information

Category: Trainee Case Report

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

Authors

  • Jafarizade, Mehrian, Lehigh Valley Health Network, Allentown, Pennsylvania, United States
  • Chong, Grace Yun, Lehigh Valley Health Network, Allentown, Pennsylvania, United States
  • Guzzo, Joseph C., Lehigh Valley Health Network, Allentown, Pennsylvania, United States
  • Kopyt, Nelson P., Lehigh Valley Health Network, Allentown, Pennsylvania, United States
  • Duffy, Margaret, Lehigh Valley Health Network, Allentown, Pennsylvania, United States
Introduction

TLS is an oncologic emergency, which can cause life-threatening electrolyte derangements. Classic laboratory abnormalities in TLS include hyperphosphatemia, hyperkalemia, hypocalcemia, and hyperuricemia. In cases of severe hyperleukocytosis, false laboratory abnormalities can occur, and can lead to apply inaccurate, potentially harmful treatments.

Case Description

A 71-year-old man with a history of CLL was admitted for dyspnea and volume overload. He had recently started venetoclax one week prior to presentation. Labs revealed a WBC of 79,300/cm2 (33% blasts), creatinine 1.49 mg/dL (baseline 0.80 mg/dL), serum potassium 7.2 mmol/L, CO2 8 mmol/L, calcium <5.0 mg/dL, phosphorus 0.5 mg/dL, and uric acid 8.9 mg/dL. He was diagnosed with TLS and treated with rasburicase. Despite aggressive phosphorus repletion, the patient remained severely hypophosphatemic, though he was never symptomatic. Given the incongruence between lab values and clinical status, we suspected a lab error. We ordered STAT labs, sent on ice, which revealed normal serum phosphorus (4.5 mg/dL) on the same day that labs processed by standard protocol revealed a low level (0.9 mg/dL). Other discordant results noted were hyperkalemia (>9.5 mmol/L but 3.7 on a point-of-care arterial blood sample), hypoxemia (pO2 <48 mmHg on ABG but 98% on pulse oximetry room air), and hypoglycemia (serum blood glucose 9 mg/dL but 86 on point-of-care finger testing).

Discussion

This abstract reports the first case of reported pseudohypophosphatemia in a patient with CLL. The pathophysiology of pseudohypophosphatemia is thought to involve a sodium-phosphate co-transporter, though the exact underlying pathophysiology is unknown. Pseudohypoxemia and pseudohypoglycemia, also described in hematologic disorders, are thought to be due to increased metabolic demands by blasts, which decrease oxygen tension and glucose levels in vitro. Increased leukocyte fragility in CLL patients can lead to pseudohyperkalemia.
In conclusion, it is crucial to verify lab abnormalities in patients with hyperleukocytosis with point-of-care or deliberate (i.e. arterial blood sample on ice or STAT) sample collection. Failure to recognize psuedohypophosphatemia may result in unnecessary phosphorus repletion, leading to potential harm for the patient.