Abstract
CHASIS, Goldring, and Baldwin in 1949 reported on the favorable use of methyl-bis (β-chloroethyl) amine hydrochloride (nitrogen mustard) in glomerulonephritis.1 Their rationale for using this drug was based on "the assumption that human glomerulonephritis is the result of tissue alterations in the kidneys induced by an antigen-antibody complex."2 Nitrogen mustard is known to inhibit antibody production. Several confirmatory reports of the use of the agent in the nephrotic syndrome have appeared in the literature.* In a recent paper Baldwin, McLean, Chasis, and Goldring stated that the evidence favoring the use of nitrogen mustard in human glomerulonephritis is equivocal.2 Dustan, Corcoran, and Haserick first used this drug in systemic lupus erythematosus with renal involvement.5 Rohn and Bond administered nitrogen mustard to five patients who had systemic lupus erythematosus without renal damage. Three cases were benefited.6 Since Duston's preliminary report, in 1951, we have treated 20 patients with active acute and subacute