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TRADITIONALLY, the term "prerenal failure" was used to describe a clinical situation in which the structurally intact kidney fails as a result of an impairment in glomerular perfusion. The decreased delivery of blood to the glomerulus was thought to precipitate a fall in the glomerular filtration rate, with subsequent development of azotemia. Our current understanding of this syndrome, however, is much more complicated than this earlier, simplistic formulation, in which renal function was viewed as being generally subservient to alterations in the systemic circulatory status, particularly cardiac output. In addition to the retention of salt and water, induced by adaptations . . .
Epstein et al. (Thu,) studied this question.