The management of edema in patients with chronic glomerulonephritis complicated by the syndrome of hypoproteinemia and massive proteinuria continues to be unsatisfactory. The immediate cause of the edema is the reduced osmotic pressure resulting from the hypoproteinemia. No clinical methods are available at present by which one can stop the proteinuria or stimulate production of plasma protein so that the plasma protein concentration will rise sufficiently to eliminate the edema.
Administration of acacia in the treatment of nephrotic edema was first reported by Hartmann in 1933.1 Since that time, many clinical reports have appeared, and much experimental work has been done on this subject. For the most part these reports have been unfavorable, with the result that acacia is not used extensively in the treatment of nephrotic edema. The opposition to the use of acacia is based on the following observations:
Cases have been reported in which there
JOHNSON JB, NEWMAN LH. INTRAVENOUS INJECTION OF ACACIA: CLINICAL AND PHYSIOLOGIC EFFECTS ON PATIENTS WITH NEPHROTIC EDEMA. Arch Intern Med (Chic). 1945;76(3):167–173. doi:10.1001/archinte.1945.00210330038008
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