A case of chronic renal failure followed by cold agglutinin due to Mycoplasma pneumoniae infection.
A case of chronic renal failure followed by cold agglutinin due to Mycoplasma pneumoniae infection.
复制标题
肺炎支原体感染导致慢性肾功能衰竭并发冷凝集素一例。
作者：
T. Shibasaki;H. Gomi;I. Ohno;F. Ishimoto;O. Sakai
Toshiaki Shibasaki，MD，The Jikei University School of Medicine，3-25-8 NishiShinbashi，Minato-ku，Tokyo 105（Japan）尊敬的先生，众所周知，冷凝集素可能由自身免疫机制的作用诱导[1，2]，然后是血红蛋白尿和皮肤疼痛，由外周毛细血管疾病引起，但经常观察到溶血性贫血与寒冷有关致敏[3]。红细胞表面存在三种抗凝集素的抗原，如I、i和Pr [4，5]，通过激活与补体的结合诱导溶血。冷凝集素可在各种疾病[6，7]中形成，如特发性、恶性淋巴瘤、肿瘤和感染[8，9]，主要如肺炎支原体、巨细胞病毒和EB病毒。温凝集素抗体在慢性肾功能衰竭（CRF）患者中的存在早有报道。然而，这是第一例冷凝集素与M。1例膜增生性肾小球肾炎（MPGN）所致CRF患者出现肺炎链球菌感染。一名31岁的男性自1979年6月以来一直在另一家医院接受MPGN治疗。1987年7月来我科时，他只有CRF，数据如下：每日尿蛋白排泄量为7-10 g，血清肌酐为4.8 mg/dl。1988年1月，他诉称喉咙痛、全身不适、咳嗽、发烧（37-38 ℃）和氮质血症加重，因此入院接受进一步检查。入院时，他的体温为37.1 ℃，血压为164/90 mm Hg，并观察到心脏杂音和胸部湿罗音。实验室检查示红细胞140 × 105 mm ~ 3，血红蛋白5.5 g/dl，红细胞压积15.3%，但结合珠蛋白112 mg/dl，血清铁80 μg/dl，糖水和火腿试验均在正常范围内。每日尿蛋白排泄量为15.8 g，血清总蛋白降至5.6 g/dl。观察到明显的代谢性酸中毒，包括pH 7.30和HCOi 14.3 mmol/l，以及明显的肾功能不全，显示为血尿素氮78 mg/dl和血清肌酐12.3 mg/dl。对于血清学和免疫学数据，冷凝集素的滴度在15 °C的体外温度下显示为2，048 ×，Coombs试验为阳性。抗各种感染的血清滴度仅为
Toshiaki Shibasaki, MD, Second Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 NishiShinbashi, Minato-ku, Tokyo 105 (Japan) Dear Sir, It is well known that cold agglutinin may be induced by the effect of autoimmune mechanisms [1, 2], and then hemoglobinuria and skin pain caused by disorders of the peripheral capillaries but in frequently hemolytic anemia are observed associated with cold sensitization [3]. There are three kinds of antigens against agglutinin such as I, i and Pr located on the surface of erythrocytes [4, 5], and hemolysis is induced by the activation of binding to the complement. Cold agglutinin might be formed in various diseases [6, 7] such as idiopathic, malignant lymphoma, neoplasms, and infections [8, 9] mainly such as Mycoplasma pneumoniae, cytomegalovirus and Epstein-Barr virus. The presence of warm agglutinin antibody in the patient with chronic renal failure (CRF) has been reported earlier. However, this is the first case of the cold agglutinin associated with M. pneumoniae infection appearing in a patient with CRF derived from membranoprolifera-tive glomerulonephritis (MPGN). A 31-year-old male had been treated for MPGN at another hospital since June 1979. When he came to our department in July 1987, he only had CRF with the following data: daily urinary excretion of protein was 7–10 g and the serum creatinine was 4.8 mg/dl. In January 1988, he complained of a sore throat, general malaise, cough, fever (37–38 °C) and the exacerbation of azotemia, and so he was admitted for further examinations. On admission, he had a body temperature of 37.1 °C, blood pressure of 164/90 mm Hg, and the presence of a heart murmur and moist rales in his chest were observed. Regarding, laboratory data, there existed marked anemia such as RBC 140 × lOVmm3, hemoglobin 5.5 g/dl and hematocrit 15.3%, but haptoglobin 112 mg/dl, serum Fe 80 μg/dl, and sugar water and Ham tests were within normal limits. Daily excretion of proteinuria was 15.8 g and serum total protein was decreased to 5.6 g/dl. Marked metabolic acidosis was observed including pH 7.30 and HCOi 14.3 mmol/l, and marked renal dysfunction shown as blood urea nitrogen 78 mg/dl and serum creatinine 12.3 mg/dl. For serological and immunological data, the titer of cold agglutinin showed 2,048 × at a temperature of 15 °C in vitro and Coombs tests were positive. The serum titer against various infections was only