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This conference opened with an elaboration of the concept of the protective action of the normal kidney (Dr. Braun-Menéndez). After initiation of unilateral renal ischemia, the elevated blood pressure is reduced as the intact normal kidney hypertrophies to take over the work of the ischemic kidney. Removal of this intact kidney causes hypertension because the ischemic kidney cannot increase in size or function. As the protective action of the kidney is also lacking following bilateral nephrectomy, renoprival hypertension develops, providing the animals are kept alive long enough. The cause of renoprival hypertension remains obscure. Gross changes in salt and water metabolism do not have to be present (Dr. Grollman). The normal kidney may produce some material which lowers the blood pressure, or it may destroy or excrete a pressor substance (Dr. Handler). Excretory removal is not so likely as a cause, since the production of simple excretory failure by diverting urine back into the blood stream does not result in hypertension (Dr. Grollman). According to some participants, renoprival and chronic renal hypertension are not identical: Removal of a unilateral ischemic kidney causes the blood pressure to return to normal. This does not fit with the renoprival hypertension theory and is evidence that a pressor agent must be involved (Dr. Goldblatt). A further difference is that whereas antirenin lowers the blood pressure in chronic renal hypertension, it will not lower the blood pressure in renoprival hypertension (Dr. Helmer). Dr. Kolff, however cites reports, such as that of the failure of bilateral nephrectomy to cure renal hypertension, which favor the view that the mechanism of production is the same in both forms of hypertension. Both groups finally agreed that some cases of renal and of renoprival hypertension could not be explained by assuming a single mechanism of action.

Conference on Mechanism of Protective Action of Kidney and Relation of Renoprival to Chronic Renal Hypertension