Reduced aminolevulinic dehydrase activity with increased blood porphyrins in experimental chronic renal failure.

In the absence of anemia, rats with nephrectomy-induced renal failure displayed a reduced activity of erythrocyte aminolevulinate dehydrase, increased blood porphyrin levels, and a plasma capacity to inhibit the activity of the erythrocyte aminolevulinate dehydrase in vitro. Even though it did increase hemoglobin and hematocrit levels, treatment with erythropoietin had no effect on the derangements of porphyrin metabolism. No abnormalities of the heme pathway were observed in liver tissue. Experimental chronic renal failure reproduced the same abnormalities of porphyrin metabolism usually detected in patients with end-stage renal disease.