Hideto Yano

Acute renal failure due to cholesterol crystal embolism treated with LDL apheresis followed by corticosteroid and candesartan

Cholesterol crystal embolism (CCE) is caused by the shedding of cholesterol crystals into the bloodstream, and it has been recently recognized as a serious complication after vascular procedures. Our case of CCE, which was diagnosed by skin and renal biopsies, occurred in a patient with hypertension and diabetes mellitus, 3 months after coronary angiography, with the development of renal failure and blue toes. After low-density lipoprotein apheresis (LDL-A), the skin lesions, including livedo reticularis and pain from the acrocyanotic toes, dramatically improved, with partial recovery of renal function. Following the administration of low-dose corticosteroid and candesartan – an angiotensin II type 1 receptor antagonist (ARB) – the eosinophilia disappeared and renal function improved gradually with a decrease in urinary protein excretion. Therefore, a combination therapy of LDL-A, low-dose corticosteroid, and an ARB is a possible treatment for CCE, although the possibility of spontaneous recovery of renal function cannot be eliminated for this patient.

Long-Term Survivor With Pulmonary Veno-Occlusive Disease

A 51-year-old woman was admitted to our hospital because of shortness of breath. Her mean pulmonary artery pressure was 52 mm Hg, and idiopathic pulmonary artery hypertension was diagnosed. She received beraprost sodium, imidapril, warfarin, and home-based oxygen therapy. At 67 years of age, dyspnea on effort worsened to New York Heart Association functional class III. The plasma level of brain natriuretic peptide was 57 pg/mL. Transthoracic echocardiography showed an enlarged right ventricle, severe tricuspid regurgitation, and a large pericardial effusion. At 68 years of age, she was urgently admitted to our hospital because of severe dyspnea at rest. A chest x-ray showed bilateral pulmonary artery enlargement (Figure 1). Computed tomography of the chest revealed that both main bronchi were compressed by the pulmonary artery aneurysms, with no mural thrombus in the pulmonary arteries (Figure 2). The diameters of the right and left main pulmonary arteries were 69.8 and 55.5 mm, respectively. Bronchoscopy during mechanical ventilation confirmed nearly complete extrinsic compression of the left and right main stem bronchi without positive airway pressure (Figure 3 …