Blue Toe Syndrome and Acute Kidney Injury Following Transcatheter Aortic Valve Replacement: A Biopsy-Proven Case of Cholesterol Embolization Syndrome
- 1Department of Internal Medicine, University of Central Florida, Orlando, USA
- 2Department of Medicine, Division of Nephrology, Orlando VA (Veterans Affairs) Healthcare System, Orlando, USA
Abstract
Cholesterol embolization syndrome (CES) is an underrecognized complication of arterial instrumentation caused by embolization of atheromatous debris into small- and medium-sized arteries. Acute kidney injury (AKI) is well described after transcatheter aortic valve replacement (TAVR), but biopsy-proven CES after TAVR is rarely reported. Its delayed presentation may be mistaken for contrast-associated nephropathy, rapidly progressive glomerulonephritis, or systemic vasculitis. A 77-year-old man with chronic kidney disease, type 2 diabetes, hypertension, and peripheral artery disease underwent transfemoral TAVR for severe aortic stenosis. Preprocedural computed tomography angiography showed a "shaggy aorta." One month later, he developed intermittent, painless violaceous discoloration of the left first through third toes. Approximately 2.5 months after TAVR, serum creatinine had risen from a baseline of 1.2-1.5 mg/dL to 4.24 mg/dL, prompting admission. Microscopic hematuria, mild eosinophilia (0.64 ×10³/µL), elevated inflammatory markers, and dysmorphic erythrocytes raised concern for glomerulonephritis and vasculitis, and empiric intravenous methylprednisolone was given while diagnostic evaluation proceeded. Kidney biopsy demonstrated atheroembolic cholesterol clefts in intrarenal arteries with ischemic changes, without glomerulonephritis or immune complex deposition. Preserved pedal pulses with an ankle-brachial index of 1.21 and toe-brachial index of 0.98 supported distal microembolization rather than large-vessel occlusion. Corticosteroids were stopped, nephrotoxins withheld, aspirin resumed, and high-intensity statin therapy was initiated; creatinine improved to approximately 3.1 mg/dL by discharge. CES should remain in the differential for progressive AKI with blue toe syndrome after TAVR, even when presentation is delayed, and initial findings suggest immune-mediated disease.
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BibTeX
@article{mehta2026blue,
title = {{Blue Toe Syndrome and Acute Kidney Injury Following Transcatheter Aortic Valve Replacement: A Biopsy-Proven Case of Cholesterol Embolization Syndrome}},
author = {Varun Mehta and Nelson Reyes Perez and Eleana Estrella and Shivam Joshi},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.117137},
url = {https://europepmc.org/article/PMC/PMC13717815},
note = {CC BY},
}
RIS
TY - JOUR
TI - Blue Toe Syndrome and Acute Kidney Injury Following Transcatheter Aortic Valve Replacement: A Biopsy-Proven Case of Cholesterol Embolization Syndrome
AU - Varun Mehta
AU - Nelson Reyes Perez
AU - Eleana Estrella
AU - Shivam Joshi
PY - 2026
DA - 2026/09/29
JO - Cureus
DO - 10.7759/cureus.117137
UR - https://europepmc.org/article/PMC/PMC13717815
AB - Cholesterol embolization syndrome (CES) is an underrecognized complication of arterial instrumentation caused by embolization of atheromatous debris into small- and medium-sized arteries. Acute kidney injury (AKI) is well described after transcatheter aortic valve replacement (TAVR), but biopsy-proven CES after TAVR is rarely reported. Its delayed presentation may be mistaken for contrast-associated nephropathy, rapidly progressive glomerulonephritis, or systemic vasculitis. A 77-year-old man with chronic kidney disease, type 2 diabetes, hypertension, and peripheral artery disease underwent transfemoral TAVR for severe aortic stenosis. Preprocedural computed tomography angiography showed a "shaggy aorta." One month later, he developed intermittent, painless violaceous discoloration of the left first through third toes. Approximately 2.5 months after TAVR, serum creatinine had risen from a baseline of 1.2-1.5 mg/dL to 4.24 mg/dL, prompting admission. Microscopic hematuria, mild eosinophilia (0.64 ×10³/µL), elevated inflammatory markers, and dysmorphic erythrocytes raised concern for glomerulonephritis and vasculitis, and empiric intravenous methylprednisolone was given while diagnostic evaluation proceeded. Kidney biopsy demonstrated atheroembolic cholesterol clefts in intrarenal arteries with ischemic changes, without glomerulonephritis or immune complex deposition. Preserved pedal pulses with an ankle-brachial index of 1.21 and toe-brachial index of 0.98 supported distal microembolization rather than large-vessel occlusion. Corticosteroids were stopped, nephrotoxins withheld, aspirin resumed, and high-intensity statin therapy was initiated; creatinine improved to approximately 3.1 mg/dL by discharge. CES should remain in the differential for progressive AKI with blue toe syndrome after TAVR, even when presentation is delayed, and initial findings suggest immune-mediated disease.
SN - 2168-8184
ER -