Kidney Week

Abstract: SA-PO0348

Unusual Presentation of AKI Secondary to Influenza A-Induced Rhabdomyolysis

Session Information

• AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Comerford, Gavin, Tallaght University Hospital, Department of Nephrology, Dublin, Ireland

Gavin Comerford

• Ali, Haider, Tallaght University Hospital, Department of Nephrology, Dublin, Ireland

Haider Ali, MD

• Bany Issa, Nawras, Tallaght University Hospital, Department of Nephrology, Dublin, Ireland

Nawras Bany Issa, MD

• McAnallen, Susan Marie, Tallaght University Hospital, Department of Nephrology, Dublin, Ireland

Susan Marie McAnallen, MBChB

• McEvoy, Caitríona M., Tallaght University Hospital, Department of Nephrology, Dublin, Ireland

Caitríona M. McEvoy, MBChB, PhD

Introduction

Influenza A is a common respiratory tract infection which can have a wide range of extra-pulmonary manifestations including rhabdomyolysis. We present a case of Influenza A-induced severe symptomatic rhabdomyolysis with AKI and multiple significant sequelae in an individual later found to have genetic abnormalities predisposing to rhabdomyolysis.

Case Description

A 28-year-old, with no past medical history, attended the Emergency Department with a three-day history of leg weakness and dark-coloured urine. There was no history of trauma, excessive exertion or recreational drug use. Initial investigations demonstrated apparent hepatic injury (AST 3170 IU/L, ALT 340 IU/L), raised inflammatory markers (CRP 100 mg/L), rhabdomyolysis (Creatinine Kinase (CK) >22,000 IU/L), and normal renal function (Creatinine 0.76 mg/dL). Toxicology, myositis and glomerulonephritis screens were normal. Viral screen revealed Influenza A positivity.
CK peaked at 284,050 IU/L and despite initial management the patient developed an AKI over subsequent days. Creatinine plateaued at 7 mg/dL on day 9, at which point the patient developed a hypertensive emergency manifested by headaches, blurred vision, a generalized tonic-clonic seizure, and systolic blood pressure >180mmHg requiring ICU transfer. MRI brain revealed changes suggestive of Posterior Reversible Encephalopathy Syndrome. T wave inversions in leads III and aVF, with an associated troponin rise were consistent with a type 2 myocardial infarction due to a hypertensive emergency. On day 14, Cr started to fall and the patient was discharged home on day 22 with Cr 1.23 mg/dL.
Given the magnitude of CK rise, genetic studies were conducted and revealed two distinct mutations of the CPT2 gene resulting in carnitine palmitoyltransferase II deficiency, predisposing to rhabdomyolysis.

Discussion

This case illustrates a serious complication of influenza infection and highlights the importance of screening for influenza in the setting of non-traumatic rhabdomyolysis, in the absence of typical symptoms and outside of the usual flu season. It also highlights the expanding role of genetic testing in the assessment of non-traumatic rhabdomyolysis.