Correlated Morphologic and Functional Studies of Acute Renal Failure in the Rat

摘要

The recent work concerning the pathophysiology of Acute Renal Failure (ARF) has clarified several important points. We have shown a clear dissociation of tubular necrosis and the initiation of ARF in this model. This finding minimizes the importance of both tubular obstruction and backleak, in the initiation of HgCl2-induced ARF. Instead, the importance of the sublethal changes described in the P1 and P2 segments is emphasized. We suggest that these changes may result in impaired electrolyte reabsorption which may act as an initiating mechanism via tubuloglomerular feedback. Evidence indicating the involvement of the renin-angiotensin system in such a feedback mechanism has been obtained in the study of Sato et al., and the chronic salt loading experiments of Barnes et al. It should be pointed out, however, that the evidence at this point is circumstantial. Additional work is needed to more clearly evaluate the role of this and/or other vasoconstrictor stimuli.