Unilateral hematuria is a vaso-occlusive complication of the sickle syndromes, especially the sickle cell trait. Treatment is usually ineffective, and the duration is variable, often prolonged and subject to recurrences. In sickle cell trait hematuria is usually the only consequence of sickling, possibly because the unique renal countercurrent mechanism may result in a milieu more prone to sickling in the medullary circulation than in the vasculature of other organs. Urea in vitro inhibits gelation of deoxygenated sickle hemoglobin. In 2 previously reported cases of sickle cell trait hematuria ceased within 3 days with oral urea therapy. We describe another such patient in whom hematuria also ceased by day 3 with oral urea. Although clinical trails with intravenous urea were ineffective in shortening the course of sickle crisis, urea may have an enhanced effectiveness in the renal medulla where the propensity for sickling may be much greater than in other organs. If these observations are confirmed in a controlled study, oral urea therapy would emerge as an effective, relatively innocuous and inexpensive treatment for this frustrating condition.

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In speculating upon the probable role of desoxyribonuclease (DNase) in the depolymerization of desoxyribonucleic acid (DNA), which characterizes (1) the "lupus erythematosus (L.E.) cell" (2), we have suggested (3), as have Klemperer and his associates (4), that an increased serum enzyme activity, potentiation of an intracellular DNase, or destruction of an intracellular inhibitor of DNase by a serum factor, might be responsible. In a previous communication (5) we reported evidence which excludes the serum DNase from responsibility for the phenomenon. Studies on the interaction of leucocytes and serum, in an approach to the alternative possibilities, disclosed the presence of a specific intracellular inhibitor of human serum DNase and an inhibitor of the "L.E.cell" phenomenon (6, 7). In the present paper, we shall report upon some of the characteristics of these factors.