Brass H, Lapp H
Med Klin. 1976 Sep 24;71(39):1617-22.
A 34-year-old woman developed uremia secondary to severe renal thrombotic microangiopathy after 3 years intake of oral contraceptives. In this particular case manifestation of end stage renal failure was preceded by an unusually long lasting period of nine months with benign hypertension. Even during the final stage (3-4 weeks) prior to complete development of uremia only once hemolysis but no malignant hypertension was observed. Only close long term follow up including renal biopsy and subtile functional tests may provide information whether and/or when hypertension due to oral contraceptives turns to become--at least in part--renal hypertension and also becomes persistent. This observation does not give evidence that benign hypertension causes renovascular damage and thus renal failure. Plasma renin activity was found to be basically elevated and furthermore stimulated e.g. by dialyses. However, this single observation does not permit any conclusion about a pathogenetic role of renin in creating hypertension by e.g. renal vasoconstriction or--despite hypertension--collapse of the capillary network.
一名34岁女性在服用口服避孕药3年后,继发严重肾血栓性微血管病,发展为尿毒症。在这个特殊病例中,终末期肾衰竭出现之前,有长达9个月的良性高血压期。即使在尿毒症完全发展前的最后阶段(3 - 4周),仅观察到一次溶血,但未出现恶性高血压。只有通过包括肾活检和精细功能测试在内的密切长期随访,才能提供信息,了解口服避孕药所致高血压是否以及何时(至少部分地)转变为肾性高血压并持续存在。该观察结果并未证明良性高血压会导致肾血管损伤进而引起肾衰竭。发现血浆肾素活性基本升高,并且例如通过透析会进一步受到刺激。然而,这一单一观察结果无法就肾素通过例如肾血管收缩或(尽管存在高血压)毛细血管网络塌陷在引发高血压过程中的致病作用得出任何结论。