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István Wittmann, Péter Degrell, Gergő A. Molnár, Mónika Tamaskó, Károly Kalmár Nagy, Erzsébet Schmidt, Eszter Fehér, László Kalabay, Boglárka Laczy, László Wagner, Zoltán Wagner, Judit Nagy, Diagnosis and successful management of calciphylaxis in a pancreas–kidney transplant patient, Nephrology Dialysis Transplantation, Volume 20, Issue 7, July 2005, Pages 1520–1521, https://doi.org/10.1093/ndt/gfh896
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1Second Department of Medicine and Nephrological Center2 Surgical Department3 Department of Nuclear Medicine University of Pécs Hungary4 Third Department of Medicine Semmelweis University Budapest Hungary Email: [email protected]
Sir,
We would like to refer to a case of fatal calciphylaxis developed 2 years after kidney transplantation published in the December 2004 issue of Nephrology Dialysis Transplantation [1].
We report a case of a 49-year-old woman who suffered from type 1 diabetes mellitus for 40 years. She became uraemic and underwent haemodialysis for 2 years, and finally received a pancreas–kidney transplant. Three months after transplantation, painful dry gangrene developed on her upper extremities and legs.
Two years after transplantation she was admitted with acral gangrene and osteomyelitis of the left hallux. Peripheral pulses were palpable, suggesting non-atherosclerotic lesions. The left hallux was amputated and histological examination showed all criteria of calciphylaxis. On admission, the patient had normal kidney and endocrine pancreas function (haemoglobin A1c, 4.9%; fructosamine, 222 µmol/l; BUN, 4.9 mmol/l; serum creatinine, 63 µmol/l). Oral glucose tolerance test and calculated insulin sensitivity indices [2] (ISIStumvoll = 0.14; HOMAIR = 2.26) showed increased insulin sensitivity. Extraosseal calcium-deposition in the connective tissues is characteristic for calciphylaxis [3]; however, in our case, bone scintigraphy and X-ray examinations were negative. Secondary hyperparathyroidism, a common cause of calciphylaxis was excluded (serum calcium, 1.99 mmol/l; phosphorous, 1.15 mmol/l; parathyroid hormone, 2.4 pmol/l). As hypofetuinaemia also predisposes to calciphylaxis [4], we measured serum fetuin level, which proved to be subnormal (408 µg/ml) [5]. Signs of autonomic neuropathy and day-time hypotension indicated sympathetic hypoactivity. The dose of methylprednisolone was increased to 24 mg/day [3]. The patient also received pentoxifylline, pentosan polysulfate and thioctic acid infusions on 5 consecutive days, which were repeated seven times in 2 years.
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