TUBULOINTERSTITIAL INJURY AND IMPAIRED RENAL-FUNCTION AFTER RECOVERY FROM ACUTE PUROMYCIN NEPHROSIS

Renal function was assessed at 2 and 8 wk after infusion of puromycin into the left renal artery of Munich Wistar rats. At 2 wk, albumin exc retion averaged 90 +/- 12 mu g/min in the left kidney and 4 +/- 1 mu g /min in the right kidney. Unilateral nephrosis was accompanied by redu ction in the glomerular filtration rate (GFR) (left, 0.71 +/- 0.04; ri ght, 1.31 +/- 0.02 ml/min) and by impaired excretion of sodium (FE(Na) ; left, 0.025 +/- 0.004; right, 0.064 +/- 0.006%). Reductions in GFR a nd FE(Na) in the nephrotic kidney were not reversed by acute angiotens in II receptor blockade with losartan. At 8 wk, albumin excretion aver aged 6 +/- 1 in the left kidney and 8 +/- 1 mu g/min in the right kidn ey. Recovery from nephrosis was accompanied by persistent reduction in GFR (left, 1.05 +/- 0.05 right, 1.41 +/- 0.05 ml/min) and impairment of sodium excretion in the previously nephrotic left kidney (left, 0.0 31 +/- 0.004; right, 0.051 +/- 0.004%). Losartan again did not return GFR and FEN, toward normal. The reductions in GFR and FEN, in the prev iously nephrotic left kidney were associated with structural changes, including intratubular casts, an increased fractional volume of the in terstitium (left, 25 +/- 1; right, 15 +/- 1%), decreased fractional vo lume of tubules (left, 66 +/- 2; right, 77 +/- 1%), and glomerular col lapse (left, 15 +/- 2; right, 1 +/- 1%). These findings suggest that t ubulointerstitial. injury can cause persistent reduction in GFR and im pairment of sodium excretion after recovery from acute nephrosis.