Accelerated atherosclerosis in a patient with post-BMT nephropathy

Abstract

CorrespondenceAccelerated atherosclerosis in a patient with post-BMT nephropathy BMT has been associated with a 20% incidence of renal failure (BMT-nephropathy), with or without hypertension, the combination of which is associated with a high morbidity and mortality.1 Few studies discuss long-term survival with this syndrome.We recently evaluated a patient who had received an HLA-identical sibling T cell-depleted allogeneic BMT for CLL in 1987 following a preparative regimen of cytarabine, cyclophosphamide and whole-body radiation (1375 cGy; delivered in nine fractions over 3 days). He developed BMT-nephropathy 6 months post-transplant, and became hemodialysis-dependent in 1995. He also had a history of well-controlled hypertension for the last 5 years. Family history was negative for premature atherosclerosis or cardiovascular diseases. He smoked around five cigarettes a day for the last 15 years. He was hospitalized in midDecember 1997 for diarrhea and abdominal pain. His stool was positive for Clostridium difficile-toxin and he was treated with metronidazole. Sigmoidoscopy was performed due to worsening of his abdominal pain and fever, which revealed no evidence of pseudomembranes, but patchy necrotic areas and ischemic changes on biopsy. He underwent an exploratory laparotomy resulting in a right hemicolectomy and colostomy, for treatment of his hemorrhagic necrosis. A second exploratory laparotomy ending in a left hemicolectomy and ileostomy, was performed 1 week later because of extension of the hemorrhagic necrosis which was confirmed on post-operative colonoscopy. Colonic biopsies showed full thickness ischemic necrosis without pseudomembranes, with no vasculitis. Computed tomographic (CT) scans done pre-operatively demonstrated focal splenic infarction, extensive arterial atherosclerosis involving the renal, splenic, iliac arteries, vas deferens, and mitral annular calcifications. Studies to evaluate a hypercoagulable status were negative. An embolic source was ruled out by transesophageal echocardiogram. His blood glucose and plasma lipid profile were normal. Bone marrow showed panhypoplasia, with no evidence of lymphoid aggregates or tumor. His hospital course was further complicated by unstable angina, enterococcal septicemia, and progressive multi-organ failure. Six weeks after his admission, life-support measures were discontinued.Autopsy showed: lungs, bilateral organizing bronchopneumonia and CMV was isolated; heart, left ventricular myocardial infarction and biventricular hypertrophy; bowels, ischemic small intestine but no infarction; kidneys, end-