Meyrier A, Becquemont L, Simon P, Laaban J P
Service de Néphrologie, Hôpital Avicenne, Bobigny, France.
Nephrol Dial Transplant. 1990;5(3):174-8. doi: 10.1093/ndt/5.3.174.
Anuria complicated the malignant phase of hypertension in twelve patients (ten males and two females). Five were black; five had primary hypertension; one had HBs virus angiitis; the six remaining cases suffered from previously documented renal disease, including two with Berger's disease. Renal angiography showed interruption of renal blood flow as far as the main branches of the renal artery and/or a false impression of 'cortical necrosis' and of 'renal infarcts'. In contrast, renal biopsy did not show irreversible vascular damage. Thus, anuria was mainly functional and due to active renal vasoconstriction. This was confirmed by the subsequent course; diuresis resumed after 1 week to 24 months of dialysis. Repeat angiography in six cases showed recovery of renal circulation and disappearance of 'cortical infarcts', even when plasma renin activity remained elevated and hypertension was not controlled. In one case captopril induced a new reversible episode of anuria. These observations suggest that active vasoconstriction with prolonged anuria might be due to some vasoconstrictive substance other than angiotensin II.
12例患者（10例男性，2例女性）在高血压恶性阶段出现无尿。5例为黑人；5例患有原发性高血压；1例患有乙肝病毒血管炎；其余6例患有先前记录的肾脏疾病，其中2例患有伯杰氏病。肾血管造影显示肾血流中断至肾动脉主要分支处，和/或出现“皮质坏死”和“肾梗死”的假象。相比之下，肾活检未显示不可逆的血管损伤。因此，无尿主要是功能性的，是由活跃的肾血管收缩引起的。这一点在随后的病程中得到了证实；在透析1周 至24个月后，尿量恢复。6例患者再次进行血管造影显示肾循环恢复，“皮质梗死”消失，即使血浆肾素活性仍然升高且高血压未得到控制。在1例患者中，卡托普利诱发了新的可逆性无尿发作。这些观察结果表明，伴有长时间无尿的活跃血管收缩可能是由血管紧张素II以外的某种血管收缩物质引起的。
