Landerer C, Dambacher M A, Staub J J, Truniger B
Schweiz Med Wochenschr. 1983 Feb 5;113(5):162-70.
The syndrome of uremic arteriopathy with ischemic skin manifestations--livedo reticularis, skin infarction and ulcerative necrosis--is described in a series of 6 patients. In all patients (3 female and 3 male, age 53-73 years) the syndrome occurred after slowly progressive renal failure and in 5 cases during temporary exacerbation of chronic renal failure and after alkalinizing treatment for marked metabolic acidosis. All patients had evidence of secondary hyperparathyroidism. In 4 the Ca X P product was in excess of 4.90, but only once above the critical product of 5.60 (greater than 70 when conventional units are used). Diagnosis was based on the clinical appearance of the skin involvement and the finding of vascular calcifications (x-ray and skin biopsy). The secondary hyperparathyroidism appears to play an important role in the pathogenesis of the syndrome. An increase in plasma phosphate or Ca X P product, calciphylaxis and/or alkalinizing therapy may release the precipitation of calcium salts in the interstitium or in the vessel walls. Therapy is confined to decreasing plasma phosphate and therewith the Ca X P product by means of phosphate binders or a diet low in phosphate. The unpredictable, often rapid success of parathyroidectomy awaits further clarification.
本文描述了6例伴有缺血性皮肤表现（网状青斑、皮肤梗死及溃疡性坏死）的尿毒症性动脉病综合征。所有患者（3例女性，3例男性，年龄53 - 73岁）均在缓慢进展的肾衰竭后出现该综合征，5例发生于慢性肾衰竭暂时加重期以及针对明显代谢性酸中毒进行碱化治疗后。所有患者均有继发性甲状旁腺功能亢进的证据。4例患者的钙磷乘积超过4.90，但仅1次超过临界值5.60（使用传统单位时大于70）。诊断基于皮肤受累的临床表现以及血管钙化的发现（X线及皮肤活检）。继发性甲状旁腺功能亢进似乎在该综合征的发病机制中起重要作用。血浆磷酸盐或钙磷乘积增加、钙化防御及/或碱化治疗可能促使钙盐在间质或血管壁中沉淀。治疗仅限于通过使用磷结合剂或低磷饮食降低血浆磷酸盐及钙磷乘积。甲状旁腺切除术不可预测且往往迅速起效，有待进一步阐明。
