2. Both Evans and Wistar rats usually recovered quickly from the acute injury, and between the 2nd and 5th months after injection they excreted normal or only slightly abnormal urines. During this period of absence of clinical signs of disease, histopathological examination of their kidneys revealed only minor scarring in the glomerular tufts.

3. Most of these apparently recovered rats subsequently developed a slowly progressing chronic glomerulonephritis irrespective of whether they were fed a basal or high protein diet.

4. Histopathologically similar renal lesions were present in all three strains of rats with active chronic nephritis regardless of whether the chronic disease followed immediately the acute nephrotoxic injury or was separated from it by an interval of months. These lesions were somewhat more severe, however, in Whelan rats.

5. Some intraglomerular scarring was present in the kidneys of all rats which survived acute nephrotoxic nephritis. It was especially prominent in those animals that remained clinically cured for as long as a year.

6. The permanent clinical recovery of certain animals, which were found to have moderate glomerular fibrosis on postmortem examination, suggests that factors other than this residual scarring contributed to the development of the recurrent nephritis observed in most of the Evans and Wistar rats. These unknown factors may produce varying degrees of renal functional trauma affecting both glomeruli and tubules.