A 24-year-old man presented to the interventional department for left upper-limb swelling for 2 months. He denied abdominal pain, nausea, vomiting, chest pain, or dyspnea. On admission his temperature was 36.6°C, blood pressure 93/75 mmHg, heart rate 95 bpm, respiratory rate 20 breaths/min. Physical examination was unremarkable apart from findings related to the dialysis access and cardiac assessment.

The patient had a solitary kidney, persistent urinary incontinence, and congenital genital hypoplasia. He underwent right nephrectomy at age 3 months, enterostomy at age 8 months, and intestinal surgery with stoma at age 1 year. He began maintenance hemodialysis in 2017 (three times a week) and had a functioning left forearm arteriovenous fistula reconstructed in March 2020.

Electrocardiogram (ECG) showed complete left bundle branch block (cLBBB) with pathological Q waves in leads I, aVL, V5 and V6, without clear ST-T elevation (Figure 1A). Prior ECGs (Figure 1B) confirmed chronic cLBBB with an rS pattern in V5 and an Rs pattern in V6.

Transthoracic echocardiography (TTE) demonstrated global cardiac enlargement, markedly reduced left ventricular systolic and diastolic function (LVEF ≈ 22%; LVEDD ≈ 80 mm). A linear hyperechoic band was seen in the high lateral wall, and an irregular hyperechoic mass at the apex measuring approximately 3.0 × 4.0 cm with posterior acoustic shadowing suggested myocardial calcification (Figure 2, red arrows).

Chest contrast CT showed a markedly enlarged, globular heart (Figure 3A), linear calcification in the high lateral wall (Figure 3B, red arrow), and a hemispherical calcified lesion at the apex measuring about 3.0 × 4.0 cm (Figure 3C, red arrow).

Laboratory tests: serum creatinine 827 µmol/L (reference 57–97 µmol/L), urea 19.58 mmol/L (3.1–8.0 mmol/L). Cardiac biomarkers: troponin I 0.216 ng/ml (0–0.045 ng/ml), myoglobin >1,000 ng/ml (0–110 ng/ml), CK-MB 2.35 ng/ml (0–5.0 ng/ml), NT-proBNP 32,961 pg/ml (0–125 pg/ml). Infection markers: WBC 7.30 × 10⁹ /L (3.5–9.5 × 10⁹ /L), neutrophils 71.8% (40%–75%), lymphocytes 13.5% (20%–50%), monocytes 11.3% (3%–10%), CRP 16.51 mg/L; blood cultures negative. Historical data showed prolonged mineral metabolism disturbance: serum calcium 1.88 mmol/L (ref 2.11–2.52), serum phosphorus 3.27 mmol/L (ref 0.85–1.15), 25-OH vitamin D 13.05 ng/ml (ref >30), and iPTH ≈ 2,000 pg/ml (ref 18.5–88.0).

Pathological Q waves conventionally indicate transmural myocardial necrosis. We hypothesize that severe focal calcification may produce “pseudo-Q waves” by (1) mechanical compression, fibrosis and cell necrosis creating electrically silent zones, and (2) microvascular/ischaemic microenvironment changes and structural remodeling that reduce depolarization contribution from the affected region, producing prominent Q waves in corresponding leads. Direct histopathological confirmation is lacking, so this mechanism remains speculative.

Troponins and CK-MB can be elevated in CKD patients in the absence of acute ischemia, partly due to chronic myocardial injury or systemic inflammation, and their elevation correlates with worse prognosis. In this case the biomarker pattern (mild troponin elevation, marked myoglobin rise, non-concordant CK-MB) is more compatible with chronic/metabolic myocardial injury or stress rather than acute extensive myocardial necrosis (4).

Early recognition and aggressive control of CKD-MBD (phosphate binders, vitamin D analogues, phosphate-lowering strategies, and consideration of parathyroidectomy when indicated) are essential to reduce soft tissue and myocardial calcification risk. Imaging (cardiac CT and echocardiography) is valuable to define extent and morphology of calcification. Patients with severe myocardial calcification or related cardiac dysfunction require multidisciplinary evaluation (cardiology, cardiac surgery, nephrology, endocrinology) to individualize management.

This report lacks myocardial histopathology (no myocardial biopsy) to directly characterize the calcified tissue and cell changes. Systematic long-term imaging follow-up and invasive coronary evaluation were not performed to fully exclude chronic coronary artery disease. Future reports should, when feasible, include tissue diagnosis or more detailed serial imaging to corroborate pathogenesis.