Article Text

  1. E. P. Cohen,
  2. H. Kobori,
  3. J. E. Moulder,
  4. B. L. Fish,
  5. L. G. Navar
  1. Medical College of Wisconsin and Hypertension and Renal Center of Excellence, Tulane University


Radiation nephropathy leads to renal failure, but that evolution may be interrupted by antagonists of the renin-angiotensin system (RAS). Furthermore, angiotensin II (AII) infusion worsens experimental radiation nephropathy. Assays for renin and AII, systemic and intrarenal, have not shown activation of the RAS in radiation nephropathy. Intrarenal angiotensinogen (AGT) may provide additional insight to the status of the RAS in kidney diseases. We therefore tested intrarenal AGT in this model. 24 barrier-maintained WAG/Rij/MCW rats underwent 17 Gy total body irradiation then syngeneic marrow transplant. 24 control rats were un-irradiated. Intrarenal cortical AGT was measured by Western blot analysis and normalized to b-actin. The ratio of irradiated-to-control AGT to β-actin optical density increased with time after irradiation, being 1.0 ± 0.3 at day one, 1.3 ± 0.5 at day 22, 1.3 ± 1.4 at day 41, and 1.6 ± 0.4 at day 63 (data as means, 95% CI). The individual irradiated to control values were not statistically different for days 1, 22, and 41, but did achieve significance at day 63 (p = .04 for trend). The interval of week 3 to week 10 after irradiation is the time when proteinuria, azotemia, and hypertension develop in this model. The trend toward an early increase in tissue AGT suggests that radiation may stimulate intrarenal AGT production and may play an initiating role in radiation nephropathy. The significant trend with time supports a sustaining role for the intrarenal RAS-mediated injury in radiation nephropathy.

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