We have analyzed some parameters of porphyrin metabolism in 60 patient
s with end-stage renal failure, 20 of them on CAPD and the remaining o
n HD. In comparison with 56 control subjects, both groups of patients
showed the three following findings: low erythrocyte aminolevulinate d
ehydrase activity, inhibition ability for the activity of this enzyme
when their plasma was incubated in vitro with normal erythrocytes, and
increased plasma porphyrin levels. Like anemia, these abnormalities w
ere more remarkable in patients on HD who also exhibited increased ery
throcyte protoporphyrin levels and compensatory porphobilinogen deamin
ase activities. Mean weekly porphyrin removal through dialysate was hi
gher in CAPD (90.8 mug) than in HD patients (30.4 mug). Dialysate and
plasma porphyrins were correlated in both circumstances (r = 0.714, P
< 0.01 and r = 0.637, P < 0.05, respectively). The less pronounced por
phyrin abnormalities found in CAPD patients with respect to HD patient
s may be due to the more efficient capability of peritoneal dialysis f
or removing from plasma protein-bound substances, as porphyrins and in
hibitors of aminolevulinate dehydrase or other enzymes involved in ery
thropoiesis. Since no close relationship was found between these abnor
malities of porphyrin metabolism and hematocrit values, the anemia of
uremia cannot be merely considered as a direct consequence of altered
heme biosynthetic pathway.