SummaryAn anticoagulant occurring in 4 of 6 patients with SLE has been demonstrated by a sensitive assay utilizing an ammonium sulfate fraction of serum. The anticoagulant functions as an inhibitor of the activation of prothrombin. No species specificity was demonstrable. The inhibitor behaves clinically and chromatographically as an immunoglobulin, although an attempt to demonstrate directly the antibody nature of the inhibitor was not successful.A severe, apparently independent, decrease in the level of prothrombin was observed in the patient with hemorrhagic symptoms. In contrast to the anticoagulant activity, the low prothrombin has persisted during treatment.
A single injection of any one of several long-acting adrenal corticosteroids at birth induces progressive cystic changes in nephrons which develop in the subcapsular zone of the rabbit kidney until 10 days after birth. These cystic lesions enlarge progressively and become visible within a few days after birth. When the animal is 2 weeks old, renal size has become three times as large as that of uninjected littermates. Adrenal corticosteroids prolong the duration of nephrogenic activity in the renal cortex. The cysts are blind and represent dilatation of the developing end of the collecting ducts. When the steroid-induced hypokalemia is prevented with repeated potassium chloride injections, renal cystic disease is almost completely prevented. Certain long-acting steroids induce cystic renal changes without systemic signs of toxicity.
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