Abstract

Reconsideration of the initial descriptions of “lower nephron nephrosis” coupled with an examination of laboratory models leads to a reintroduction of tubular obstruction by casts and cell debris as a likely definitive etiologic mechanism. The use of experimental models confirms that the clinical course and pathologic anatomy may be recreated with laboratory situations in which various proteins are precipitated in the renal tubule. Whether induced by water-loading or by solute diuresis, urine production prevents or ameliorates the renal lesion, presumably by the creation of more rapid tubular flow and more dilute tubular urine. The properties of mannitol, the most simple, reliable, and effective compound to produce osmotic diuresis, are described. In light of the foregoing information it seems reasonable to expect that the kidney which is making urine in adequate quantities may well be protected against the “acute tubular necrosis” type of insult. A plan is hereby presented for the administration of mannitol in both emergency and elective situations with a view toward the elimination of this unfortunate renal complication.

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