During the first decade of this century, Veit and later Weichart suggested that toxemia of pregnancy may be an immunologically conditioned process. No proof was submitted and the idea remained dormant. Later investigations on the etiologic mechanisms of eclampsia centered about the accompanying hypertension and renal changes; a strong case was being built around the nephropathy-hypertension-toxemia axis.
In recent years, when electron microscopic investigations have disclosed the immunologic aspects in experimentally produced glomerulonephritis, the attention of some scientists turned to a similar possibility in toxemia.
Boss,1 in 1965, demonstrated that microsomal fractions of human placenta are capable of elaborating antigens and that fluorescent antibodies to antiwhole human kidney and to placenta localize exclusively in the basement membranes of the kidney. In 1967, Robertson, Brosens, and Dixon2 pointed to a significant similarity between the arteriolar changes of the placental bed in patients with toxemia of pregnancy and arteriolar changes