Giacobetti R, Feldman S A, Ivanovich P, Huang C M, Levin M L
Nephron. 1977;19(5):295-300. doi: 10.1159/000180903.
A 42-year-old male was hemodialyzed for 2 years with excellent control of calcium-phosphate metabolism. He received a cadaveric renal transplant but experienced a prolonged episode of acute tubular necrosis during which he could not tolerate phosphate-binding antacids. His calcium X phosphate product became markedly elevated for 20 days. Following a brief period of function, the homograft was removed on the 45th post-transplant day after severe rejection and subsequent infection. Chest X-ray was normal. Six days after graft nephrectomy, he became acutely dyspneic and markedly hypoxemic. Diffuse, flocculent pulmonary infiltrates appeared on the chest film. The patient expired 1 day later. At postmortem examination, there was severe, diffuse pulmonary alveolar calcification demonstrated by chemical and histologic examination. Although unlikely, the prolonged post-transplant period characterized by elevated calcium X phosphate product may have played a pathogenetic role. Calciphylaxis may have occurred, with hyperparathyroidism as the sensitizing agent and any of several drugs acting as challenger.
一名42岁男性接受血液透析2年，钙磷代谢控制良好。他接受了尸体肾移植，但在急性肾小管坏死的一段较长时间内，无法耐受磷结合抗酸剂。他的钙磷乘积在20天内显著升高。在短暂的功能期后，移植肾在移植后第45天因严重排斥反应及随后的感染而被切除。胸部X线检查正常。移植肾切除术后6天，他突然出现呼吸困难和明显低氧血症。胸部X线片上出现弥漫性、絮状肺部浸润影。患者1天后死亡。尸检时，化学和组织学检查显示有严重的弥漫性肺泡钙化。尽管可能性不大，但移植后钙磷乘积升高的这段较长时间可能起到了致病作用。可能发生了钙化防御，甲状旁腺功能亢进作为致敏剂，几种药物中的任何一种作为激发因素。
