A woman in her 70s, with a medical history of hypertension, diabetes, and dyslipidemia, died at home 35 days after undergoing coronary stenting via the femoral approach. Despite an uneventful postoperative course and improved cardiac function parameters, she became bedridden following discharge. Initially, this was presumed to be due to senility post-hospitalization, but a forensic autopsy was conducted to evaluate the potential involvement of the cardiovascular procedure.

The deceased was 141 cm tall, weighed 29.1 kg, and exhibited disuse atrophy of the extremities. The left toes showed blue discoloration with a well-defined border (Fig. 1a, b). The heart weighed 324 g, with no evidence of restenosis at the coronary stent graft. The aorta, with marked atherosclerosis, displayed multiple sac-like aneurysmal structures (Fig. 2a). The aortic intima was friable with a shaggy appearance, and multiple atheromatous ulcerated plaques were either thrombus-covered or exposed to the necrotic core of a sac-like structure (Fig. 2b, c). The kidneys exhibited slight atrophy, particularly cortical atrophy, and fine granular changes. The left and right kidneys weighed 65 g and 54 g, respectively (Fig. 2d).

(a) Gross appearance of the sole. (b) Blue left hallux. Area of resection with spindle-shaped biopsy from the border of the blue toe (enclosed by a dashed line)

(a) Gross surface of the abdominal aorta; multiple aneurysmal sac-like structures. (b) Severely friable aortic intima; atherosclerotic ulcers are covered by a mature thrombus (white arrow). The necrotic core of the sac is exposed (yellow arrow). (c) Cross-section of the aneurysmal sac. (d) Cut surface of the kidney

An excision biopsy of the left hallux, taken from the border of the blue discoloration (Fig. 1b), revealed CCE in the subcutaneous artery (Fig. 3a, b). The sac-like structure of the aortic intima contained cholesterol crystals, necrotic cell fragments, and lipids encased by a fibrous capsule (Fig. 2c). CCs were also lodged in the interlobular and central arteries (Fig. 3d, e). Segmental fibrinoid necrosis was observed in the upper cortex of the glomeruli, accompanied by mild interstitial fibrosis. Some afferent arteries showed hyaline degeneration, though there was no evidence of significant inflammatory infiltration, glomerular hypercellularity, crescents, nodular mesangial expansion, glomerular basement membrane thickening, or Kimmelstiel–Wilson nodules.

Microscopic findings. (a) CCE in subcutaneous tissue (yellow arrow). (b) Subcutaneous artery filled with CCs. (c) Core of the sac containing CCs covered by a fibrous capsule. (d) Interlobular artery. (e) Central artery. (a–e) Hematoxylin and eosin staining

The serum urea nitrogen level was elevated at 35.4 mg/dL (normal range: 8–22 mg/dL) and serum creatinine levels of 2.52 mg/dL (normal range: 0.47–0.79 mg/dL).

The cause of death was determined to be CCE, primarily due to latent and progressive RF complicated by cardiac catheterization against a background of severe aortic sclerosis and mild hypertensive nephrosclerosis.

A woman in her 80s, with a medical history of hypertension, chronic RF, and a stent graft treatment for an aortic aneurysm five years prior, died in a nursing home. Although initially diagnosed as senility, a forensic autopsy was requested by the bereaved family.

The deceased was 151 cm tall, weighed 47.3 kg, and exhibited no signs of trauma. The right second toe had been amputated (Fig. 4a, b), and the tip of the right third toe displayed a spot with reddish-purple discoloration (Fig. 4b). A stent graft was found in the thoracic aorta (Fig. 5a). The kidneys had coarsely granular surfaces, and the cut surface revealed an irregularly narrowed cortex, with the left and right kidneys weighing 80 g and 79 g, respectively (Fig. 5b).

(a) Gross appearance of the right sole. (b) The second toe was amputated (black arrow); spotty reddish-purple discoloration of the third toe (area of excisional biopsy enclosed by a dashed line)

(a) Gross surface of the thoracoabdominal aorta; stent graft in the thoracic aorta. Ostium of the renal arteries (white arrow). (b) Cut surface of the kidney

An excision biopsy of the right third toe, taken from the discolored skin spot (Fig. 4b), revealed CCEs with significant thrombofibrotic changes in the subcutaneous arteries (Fig. 6a–c). The interlobular arteries contained fresh, nonfibrotic CCs (Fig. 6d), and the arterial walls showed myointimal thickening. The glomeruli exhibited global sclerosis, while the interstitium displayed patchy fibrosis with mild lymphocyte infiltration. There was no evidence of glomerulonephritis or diabetic nephropathy. The central artery demonstrated marked intimal thickening (Fig. 6e).

Microscopic findings. (a) CCE in subcutaneous tissue (yellow arrow). (b, c) CCE with highly thrombo-fibrotic changes. (d) Interlobular artery. (e) Central artery. Hematoxylin and eosin (a, b, d, e) and Elastica van Gieson (c) staining

The serum urea nitrogen level was elevated at 49.6 mg/dL, and serum creatinine levels of 3.65 mg/dL.

A review of the patient’s medical history indicated the involvement of BTS in toe amputation and the subsequent chronic RF. Numbness in the right second toe was reported 95 days after aortic repair, followed by necrosis and amputation 97 days later; both attributed to BTS. While severe hypertensive nephrosclerosis was identified as the primary cause of chronic RF, the presence of fresh CCE in the kidney (Fig. 6d) suggested that BTS played a persistent role in the progression of renal failure.