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  • Title: [Renal thrombotic microangiopathy with benign hypertension and uremia secondary to oral contraceptives (author's transl)].
    Author: Brass H, Lapp H.
    Journal: Med Klin; 1976 Sep 24; 71(39):1617-22. PubMed ID: 979870.
    Abstract:
    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. The case of a 34-year-old woman who developed uremia secondary to renal thrombotic microangiopathy after taking oral contraceptives for 3 years is reported. The case is unusual in that the clinical manifestations of nephropathy and terminal kidney failure were preceded by an almost 1-year development with benign hypertension. During the final stage (3-4 weeks prior to complete development of uremia), hemolysis was observed only once and malignant hypertension not at all. The question, if and when reversible hypertension due to oral contraceptives becomes persistent renal hypertension, can be answered only after long-term observations with careful documentation (renal biopsy and nephrologic functional diagnosis). This case suggests that benign hypertension does not cause renovascular damage and renal failure. Plasma renin activity was found to be basically elevated and, furthermore, stimulated by e.g., dialysis. However, this single case does not permit any conclusions about a pathogenetic role of renin in creating hypertension by e.g., renal vasoconstriction or despite hypertension - collapse of the capillary network.
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