In normal subjects, the rate of aldosterone secretion fluctuates widely according to the state of salt and water balance, but the pathways mediating this relationship are still to be identified. Hypersecretion of aldosterone occurs in malignant nephrosclerosis (2). Angiotensin, the pressor peptide released from plasma by renin, increases both the adrenal secretion (3) and the urinary excretion (4) of aldosterone in man. These observations support the suggestion (5) that a renaladrenal interaction might be involved in the normal regulation of sodium and potassium balance. By this mechanism, the kidney, perhaps sensitive to diminished arterial filling or ischemia, secretes renin, generating angiotensin, which then stimulates aldosterone secretion. Aldosterone, in turn, restores renal perfusion by promoting sodium and water retention.In malignant hypertension this mechanism may become deranged, leading to the coexistence of increased amounts of both angiotensin and aldosterone in the blood, a possibility that derives additional support from the earlier report (6) of increased blood angiotensin in these patients. On the other hand, since neither renin nor angiotensin has been conclusively demonstrated in normal human plasma, elaboration of these substances in malignant hypertension might be simply a consequence of severe renal damage.Our more recent work has investigated the possibility that this renal-adrenal interaction participates in normal homeostasis, as well as in the *This report was presented in part at the 54th an-
In 17 out of 29 hospitalized patients (58.6%) with internal arteriovenous fistula (AVF) thrombosis a systemic streptokinase infusion was used as an alternative to urgent surgical declotting. In the remaining 12 patients (41.4%) fibrinolytic treatment was contraindicated due to the necessity for immediate dialysis, uncontrolled hypertension, active peptic ulcer, known multilevel stenoses of the fistula, or operation 8 days prior to the thrombosis. The systemic streptokinase therapy alone was successful in 9 of 17 patients treated (52.9%), 5 of 17 patients (29.4%) needed the combined therapy (streptokinase plus surgery) and in 3 of 17 patients (17.6%) the fibrinolytic therapy was unsuccessful. No serious complications attributable to the streptokinase infusion were observed. Systemic streptokinase treatment for acute AVF declotting followed by the radiological evaluation of the vessels can be a reasonable alternative to ‘blind’ surgical emergency reconstruction. The method makes it possible to identify those underlying anatomic abnormalities of the draining vein which may be localized at some distance from the anastomosis and so overlooked during surgery.
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