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Kidney Week

Abstract: TH-PO0852

Ethacrynic Acid-Induced Severe Thrombocytopenia in Advanced CKD

Session Information

Category: Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)

  • 1900 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)

Authors

  • Salih, Noman, TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Ullah, Izhar, TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Khan, Asmad, TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Shah, Neal B., TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Arif, Ali, TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Hanif, Muhammad Owais, TidalHealth Peninsula Regional, Salisbury, Maryland, United States
  • Khan, Kazi S., TidalHealth Peninsula Regional, Salisbury, Maryland, United States
Introduction

Drug-induced immune thrombocytopenia (DITP) is an uncommon but important cause of abrupt, severe thrombocytopenia and is often misdiagnosed as immune thrombocytopenia (ITP). Loop diuretics are rarely implicated. We present a case of ethacrynic acid–associated DITP highlighting a classic but underrecognized diagnostic pattern.

Case Description

A 74-year-old woman with stage V CKD recently initiated on hemodialysis was started on ethacrynic acid for lower extremity edema during rehabilitation. Within days, her platelet count declined precipitously from ~150,000/µL to 13,000/µL, accompanied by lower-extremity purpura. Extensive evaluation did not identify alternative etiologies. Heparin-induced thrombocytopenia was unlikely (negative immunoassay; indeterminate serotonin release assay without clinical correlation). Thrombotic microangiopathy was excluded by a normal smear without schistocytes and normal LDH and haptoglobin. Normal fibrinogen with mild isolated D-dimer elevation argued against disseminated intravascular coagulation. Autoimmune and infectious workup was unrevealing, and there was no evidence of marrow suppression or vasculitis. Following discontinuation of ethacrynic acid, platelet recovery began within 48–72 hours and reached ~119,000/µL by day 5–6, despite only brief empiric dexamethasone.

Discussion

The temporal pattern of abrupt onset after exposure, profound nadir, and rapid recovery following withdrawal is highly characteristic of DITP. This trajectory contrasts with ITP, which typically demonstrates a slower response. The absence of laboratory or clinical evidence for TMA, DIC, infection, or autoimmune disease further supports a drug-mediated mechanism.

Ethacrynic acid can rarely cause severe DITP characterized by rapid platelet decline and brisk recovery after cessation. Recognition of the characteristic rapid decline-and-recovery pattern is critical to avoid misdiagnosis and unnecessary immunosuppression. Careful medication review remains essential in evaluating acute severe thrombocytopenia.