S. Casati

IMPROVEMENT IN THE HAEMOSTATIC DEFECT OF URAEMIA AFTER TREATMENT WITH RECOMBINANT HUMAN ERYTHROPOIETIN

Patients with uraemia have a defect of primary haemostasis expressed as long skin bleeding times and reduced platelet adhesion to the arterial subendothelium. Transfusion of red cells shortens the bleeding time and stops bleeding symptoms in uraemia. This study investigated whether the efficacy of recombinant human erythropoietin in correcting anaemia and the improvement in haemostasis are correlated. Recombinant human erythropoietin was given to seven consecutive patients with chronic uraemia, a history of bleeding, severe anaemia (haematocrit below 23%), and long bleeding times (above 19 min). The progressive rise in haematocrit induced by increasing doses of recombinant human erythropoietin was paralleled by a pronounced shortening of the bleeding time. Platelet adhesion to the subendothelium of human umbilical arteries, very low before the study, increased greatly in all patients and became normal in six. None of the patients bled during the study period.

Benefits and risks of protracted treatment with human recombinant erythropoietin in patients having haemodialysis

Fourteen patients with uraemic anaemia and having regular haemodialysis were given human recombinant erythropoietin in increasing doses, beginning with 24 U/kg thrice weekly. One patient was dropped from the study because of recurrent thrombosis of vascular access sites. In the other 13 patients, followed up for a mean of 9.1 months (range 8-11), haemoglobin concentrations increased from 62 (SD 8) to 105 (9) g/l. No antierythropoietin antibodies were detected during the study. The correction of anaemia was associated with a tendency to hyperkalaemia and a mild increase of unconjugated bilirubinaemia. In eight previously hypertensive patients antihypertensive treatment had to be reinforced, but in normotensive patients blood pressure did not change. Thrombosis of arteriovenous fistulas occurred in two patients and a cerebral ischaemic lesion in one. Protracted treatment with human recombinant erythropoietin evidently can maintain normal haemoglobin concentrations in uraemic patients over time. Full correction of anaemia, however, may trigger some vascular problems, particularly in hypertensive patients and those with a tendency to thromboembolism.

Dopamine and Frusemide in Oliguric Acute Renal Failure

Into 24 oliguric patients with acute renal failure (ARF) for whom mannitol and high-dose frusemide had failed to promote a diuresis, dopamine (3 micrograms/kg/min) plus frusemide (10-15 mg/kg/h) were infused for 6-24 h. In 19 of the 24 patients this treatment produced significant increases in diuresis (from 11 +/- 7 to 85 +/- 51 ml/h; p less than 0.001) and natriuresis (from 45 +/- 13 to 88 +/- 22 mEq/1; p less than 0.001), without any significant modification of blood pressure, pulse rate or central venous pressure. 10 of the 24 patients required dialysis: 5 because therapy failed to promote diuresis and the other 5 because of their hypercatabolic state in spite of polyuria. 5 patients died of causes unrelated to ARF. Since all patients who responded were treated within 24 h after the onset of oliguria, it appears to be crucial to administer dopamine and frusemide early, before more severe anatomical and functional damage develops.

Treatment of Uraemic Anaemia with Recombinant Human Erythropoietin

Several factors have been involved in the pathogenesis of uraemic anaemia: inhibition of erythropoiesis and hyperhaemolysis to uraemic toxins (1); iron deficiency due to blood losses in the extracorporeal circuit (2); severe hyperparathyroidism with osteitis fibrosa (3) ; abnormally high concentrations of aluminium (4). However, there is general agreement that the main cause of uraemic anaemia is the insufficient production of erythropoietin from the diseased kidneys (5).

Peritoneal Permeability in Continuous Ambulatory Peritoneal Dialysis After the Correction of Anemia by Erythropoietin

Anemia due to insufficient production of erythropoietin is a common feature of patients with chronic renal failure undergoing dialysis [1-6]. Although anemia in patients on continuous ambulatory peritoneal dialysis (CAPD) is less frequent and severe than in hemodialysis (HD) [5] it can be a relevant clinical problem [6].