By use of the fetal mouse liver cell assay, serum erythropoietin (SEp) concentration was measured in 135 patients at various stages of chronic renal failure and in 59 healthy subjects. In patients with creatinine clearances (CCr) ranging from 2 to 40 ml/min/1.73 sq m, endocrine renal function was found to deteriorate in parallel to excretory renal function. The known negative correlation between SEp and hematocrit (Hct) was not apparent, probably because of the loss of renal mass accompanying progress of anemia and renal insufficiency. In contrast, in patients with minimal variation of residual excretory renal function, as in individual patients investigated repeatedly within a short period of time, changes of Hct were always accompanied by opposite changes of corresponding SEp concentrations. Thus, patients with chronic renal failure have a sustained regulatory feedback mechanism between Hct and SEp, which probably works at a lower level.

Serum erythropoietin (SEP) concentration was measured on two occasions in 42 patients with terminal renal failure (1) immediately before the first hemodialysis, and (2) 3 to 27 months following the onset of regular hemodialysis treatment. Although the hematocrit (Hct) showed an increase in every patient, the SEP concentration decreased in every patient. The mean Hct rose frm 21.7 to 28.6% (volume per volume) P < 0.001), and the SEP dropped from 509 to 182 mU/ml (P < 0.001). This shows that anemia improvement is not a consequence of increased erythropoietin production but that it is most likely due to elimination of an inhibitor of the bone marrow by hemodialysis treatment. The decrease of SEP concentration has to be interpreted as a response to the improved tissue oxygenation that correlates with the hjigher hematocrit or as a consequence of further reduction of renal mass with progress of the renal disease.

In 13 bilateral nephrectomized patients serum erythropoietin (SEp) activity could be measured quantitatively by use of the highly sensitive fetal mouse liver cell assay. SEp concentration in the majority of the cases was below the mean of normal controls. There was a significant positive correlation between SEp levels and hematocrits, suggesting erythropoietin (Ep) deficiency to be a causative factor in the anemia of the anephric state. Androgen therapy stimulated extrarenal Ep production in all of 5 anephric patients studied.

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