Abstract
In Reply. —We welcome the opportunity to respond to the letter by Rossi et al. Basically we have no argument regarding the role of angiotensin II in maintaining filtration pressure and thus preserving renal function in the presence of renal artery stenosis. Studies in animals 1,2 and human beings 3,4 have reported this important function of angiotensin II in preserving renal autoregulation. Although this mechanism could have played an important role in the development of azotemia in our patients, other factors however, should be considered. Two of our patients had generalized skin rash with fever, eosinophilia, and eosinophiluria compatible with interstitial nephritis, and two patients (Nos. 2 and 3) had evidence of hypotension and volume contraction, respectively. Volume contraction has been a factor for serum urea nitrogen elevation in the range of 52 mg/dL, in three patients in a blind study comparing captopril with enalapril maleate (MK-421). Rehydration of these patients
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