Ten patients, who received cadaveric kidneys, were followed for 24 wk with serial measurements of serum erythropoietin (S‐Epo), transferrin receptor (S‐TfR) and iron variables. The mean pretransplant creatinine clearance was 8.2 (range 0–22) ml/min and the mean haemoglobin (Hb) level was 99±18.6 (range 66–124) g/l. Nine patients demonstrated a gradual increase in S‐Epo levels, which reached a peak, and was accompanied by a parallel increase in S‐TfR levels with a median lag period of 3 wk between both peaks. Hb correction followed the S‐TfR peak after a second lag period (median 7 wk). Elevated S‐Epo and S‐TfR did not result in correction of anaemia in 1 patient due to impaired graft function. Within 4 months, S‐Epo levels reached the normal range while TfR levels were higher than normal. Follow‐up of iron status demonstrated the development of iron deficiency in 5 patients, which was corrected spontaneously. Improvement in erythropoiesis after renal transplantation seems to occur by means of expansion of the erythroid marrow, as detected by increasing S‐TfR levels, subsequent to a S‐Epo peak. This expansion precedes Hb normalization. A nonuraemic environment is probably a prerequisite for the correction of anaemia but not for the increase in S‐Epo or S‐TfR levels. Iron deficiency may occur after transplantation due to an increase in iron utilization.

Gastrointestinal iron absorption was measured by an oral iron load test in patients with uremia on maintenance hemodialysis (n = 19), with iron overload (n = 9), iron deficiency (n = 10) and in healthy volunteers (n = 9). After an overnight fast, serum iron was measured before, and 1, 2, 4 and 6 h after administration of 100 mg ferrous chloride. Bone marrow iron was assessed after staining with Prussian blue. The study shows that iron absorption is impaired in uremic patients. Even uremic subjects with iron deficiency absorbed significantly less than normal subjects. Patients with iron overload and uremia absorbed even less, showing that the iron status of the patient influences absorption also in uremia.

We have studied serum erythropoietin (EPO) levels during 6 years after kidney transplantation in 16 patients. There was a serum EPO peak around 50 mU/ml after 5 weeks. After 3 months the serum EPO level stabilized at around 30 mU/ml. Patients with good transplant function had significantly higher serum EPO levels and normalized their hemoglobin (Hb) after a mean of 3 months. If transplant function was good, Hb was normalized even if the serum EPO was only slightly elevated. Patients with poor transplant function had lower serum EPO and Hb levels. We concluded that a good transplant function is the key to a normal erythropoiesis and that small amounts of EPO are needed to improve Hb.

Following successful kidney transplantation, renal anemia is gradually corrected during the first 3-4 months. Serum erythropoietin (EPO) levels are increased after the first postoperative day following grafting. In this study, the serum EPO levels in the early posttransplant phase were investigated in 8 living-donor and 7 cadaveric-kidney transplant recipients with special emphasis on the first 24 h. Despite a considerable difference in cold ischemic time of the graft in the two groups the increase in serum EPO levels was noticed at about the same time (8 h) in both groups and the first peak of serum EPO, which was observed after 24 h, reached the same level in both groups. After 9-11 days, serum EPO reached levels which usually are observed during the first months following transplantation. The EPO response seems to be blunted in relation to the degree of anemia in the early posttransplant phase.

Several indices of adrenocorticotropic (ACTH) activity were compared in order to establish the index most suitable for assay purposes, particularly of ACTH in blood. In hypophysectomized rats, the effects of ACTH on adrenal ascorbic acid, cholesterol, and steroid formation in vitro were studied. In intact rats, the effects of formalin on these variables as well as on the adrenal and plasma corticosterone levels and hypophyseal and blood ACTH activity were measured. Adrenal corticosterone as well as steroid formation in vitro increased very rapidly after stimulation by ACTH. In hypophysectomized rats, after intravenous ACTH, significant increases were observed after 5 min. In normal rats, 3 min after the injection of formalin, significant increases of steroid formation in vitro and ACTH activity were observed. The in vitro technique is suitable for the study of changes in ACTH activity. ACTH increases the fraction of corticosterone found in the total amount of corticoid secreted by rat adrenals in vitro.