The Glomerulus in Acute Renal Failure

Abstract

During the past 10–12 years, investigators in medical renal physiology have altered their focus from the examination of normal regulatory mechanisms to focus in part upon a variety of pathophysiologic models of altered renal function. One of the most active and initial arenas of pathophysiologic evaluation has been examination of the mechanism of acute renal failure (ARF). Several of the initial studies, derived from both this country and Europe, provided an initial unitary hypothesis which postulated a pivotal role for renal vasoconstriction in the pathogenesis of acute renal failure (Ayer et al., 1971; Oken et al., 1966; Henry et al., 1968; Thiel et al., 1967). Studies supported the concept that major reductions in renal blood flow (RBF) and renal plasma flow (RPF) occurred early in the initiating phase of acute renal failure (Ayer et al., 1971; Chedru et al., 1972; Hsu et al., 1977; Flamenbaum et al., 1972b; Munck, 1958; Hollenberg et al., 1968). These findings led to the view commonly and logically held at that time that acute renal failure was a “vasomotor nephropathy.”