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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The management of patients with chronic renal failure is complicated and demanding for both physician and patient, but is frequently rewarding. When specific treatment of the underlying cause is not possible, therapy is aimed at making the maximum use of existing nephrons and preventing further loss of nephrons through hypertension and infection. Careful attention to salt and water balance is necessary, and all patients and all drugs prescribed must be considered with care. Special problems exist with regard to anaemia, bone disease, pericarditis and hyperkalaemia. An important aspect of care at this time is the education of patients about the next major phase of management, dialysis and transplantation.
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PMID:The conservative management of chronic renal failure. 93 26

Patients with chronic renal failure who were on maintenance haemodialysis, were given monthly 600 mg iron intravenously as iron-dextran complex to a body replacement total of 5-6 g iron. Those patients who had been on maintenance haemodialysis for a long period and had received numerous blood transfusions failed to show a rise in haemoglobin levels. Those patients who received iron from the commencement of maintenance dialysis, and who had not received blood transfusions, showed a significant increase in haemoglobin concentrations which has been maintained for more than 18 months after iron therapy ceased, despite a concurrent decrease in serum iron concentrations. Pre-treatment and post-treatment levels of serum iron are not of predictive value for the success of iron treatment, neither for the haemoglobin nor the serum iron response. A body replacement dose of iron given intravenously over a year benefits the majority of patients on maintenance haemodialysis and is recommended for the treatment of their anaemia.
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PMID:Haemoglobin and serum iron responses to periodic intravenous iron-dextran infusions during maintenance haemodialysis. 94 Jun 18

Twelve anephric patients on maintenance haemodialysis received treatment with oral enteric coated cobalt chloride 25 to 50 mg daily. The change in haemoglobin concentration, and packed cell volume, are recorded and discussed with special reference to possible toxicity and mechanism of action of cobalt. Six of eight patients who completed the first course with cobalt chloride 50 mg daily for 12 weeks showed a significant rise in haemoglobin concentration of 26 to 70 per cent and a fall to near pre-therapeutic levels when cobalt was withdrawn. Evidence of a response was present within two months of starting treatment. Four patients showed a diminution in their blood transfusion requirements and three patients experienced a definite sense of increased well-being during treatment. One patient suffered from side effects of the drug and failed to complete the study because of gastrointestinal disturbance. The improvment in haemoglobin concentration was reproducible in four patients who were given second, and in one case third courses courses with varying doses of cobalt over differing periods of time. Serum cobalt levels tended to stabilize after two months continuous treatment to the therapeutic range of 40-100 mumg per 100 ml. A rapid fall in serum cobalt was seen on cessation of treatment. It is suggested that therapy with enteric coated cobalt chloride at a dose of between 25 and 50 mg per day has a definite place in the treatment of the refractory anaemia of chronic renal failure.
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PMID:The treatment of refractory anaemia of chronic renal failure with cobalt chloride. 94 Sep 22

Serum total free phenols are elevated in chronic renal failure, acute renal failure and hepatic coma. Being partly protein-bound, phenols behave during dialysis in a similar manner to considerably larger molecules which are not protein-bound. In view of their potential toxicity they should be considered as an alternative to 'middle molecules'. Patients on regular hemodialysis have retention of phenols if their post-dialysis serum creatinine is above 6-7 mg/dl. Patients on short time dialysis have high pre-dialysis neutral phenol levels. Such levels are sufficiently high to suggest a role in the genesis of neurological symptoms, anemia and bone disease. Certainly pre-dialysis free phenols reflect adequacy of dialysis.
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PMID:Free phenols in chronic renal failure. 95 43

Failing kidneys can play havoc with other parts of the body. Specific treatment of these associated problems may help ward off uremia and preserve whatever renal function remains. Sodium levels may drop if too much water is mistakenly given to counteract kidney failure. Hyperkalemia can lead to cardiac arrest if potassium levels aren't reduced without delay. Acidosis also may reach life-threatening proportions, especially if diarrhea occurs. Almost all patients with chronic renal failure have a bleeding tendency and anemia, with the hematocrit dipping as low as 20 percent. Over half have decreased tolerance to carbohydrares, although severe hyperglycemia is rare. Disorders of calcium metabolism also are common, ranging from asymptomatic hypocalcemia to osteomalacia. The kidneys' impaired filtration ability should be kept in mind when drugs are prescribed. Dosages may need to be cut to avoid an adverse reaction.
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PMID:Conservative management of chronic renal failure. 95 17

The diminished erythropoiesis in the anemia of chronic renal disease has been attributed to three possible factors: (1) decreased erythropoietin production, (2) inhibition of erythropoietin activity, and (3) decreased bone marrow response to erythropoietin. In this report we isolated and evaluated these parameters in 19 patients with chronic renal disease, nine patients with iron-deficiency anemia, and seven control subjects. The results in patients with chronic renal failure were as follows: (1) erythropoietin enhanced heme synthesis in bone marrow cell cultures by 88 +/- 12 per cent in renal failure, as compared to 65 +/- 7 per cent in the control group; (2) plasma erythropoietin activity did not increase appropriately for the degree of anemia; and (3) erythropoietin inhibitor activity in renal failure was not greater than in a control group. In conclusion, the relative failure of erythropoiesis in chronic renal disease appears to be due primarily to decreased production of erythropoietin and not to diminished marrow response to erythropoietin.
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PMID:Erythropoiesis in chronic renal disease. 96 7

Bone marrow cells of patients with chronic renal failure were studied in short-term in vitro cultures to determine erythropietin responsiveness. Seven normals and fourtheen patients on hemodialysis were studied. Bone marrow cells of normal subjects and of patients with chronic renal failure responded similarly to erythropoietin. Total heme synthesis was significantly lower in cultures prepared with uremic serum than normal serum. We conclude that there is a substance in the serum of uremic patients which suppresses general heme synthesis and that this "uremic toxin" may be responsible, in part, for the clinically severe anemia seen in these patients.
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PMID:The anemia of chronic renal failure: in vitro response of bone marrow to erythropoietin. 116 90

During investigation of splenomegaly in a boy with chronic renal failure and osteodystrophy, bone marrow aspirates resulted in "dry taps," whereas biopsied material provided evidence that the marrow had been replaced by fibrous tissue. In a study of six other children with chronic renal failure, similar changes were observed. These findings suggest that the anemia of chronic renal failure may in part be a result of myelofibrosis, and the resulting reduction of functional bone marrow may limit the tolerance to immunosuppressive agents in patients who undergo renal transplantation.
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PMID:Myelofibrosis in children with chronic renal insufficiency. 118 35

Cardiac output, total peripheral vascular resistance, renal, extrarenal, forearm muscle and skin hemodynamics and an indicator of the splanchic vascular resistance were estimated in 20 subjects with chronic renal disease without signs of chronic renal failure and without anemia. The data were compared with a group of subjects with essential hypertension. The high blood pressure of chronic renal disease of mild or moderate severity was maintained in the first place by a high cardiac output, this being due to a rise of the stroke volume, while the heart rate was only slightly increased. The total peripheral vascular resistance was within the normal range in most of the subjects. The vascular resistance in the skin was slightly raised, that in the splanchnic area and muscle unchanged in renal hypertension. The possible pathogenic mechanisms are considered.
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PMID:General and regional hemodynamics in hypertension in chronic renal disease. 119 19

In the pathogenesis of anemia in patients on intermittent hemodialysis is a frequently mentioned factor. To evaluate the red blood cell trauma caused by the hemodialyser, free hemoglobin was determined in the plasma before and after various types of hemodialysis. We investigated 22 patients with chronic renal failure in the age range from 18 to 54 years who were hemodialysed with various types of shunt (Cimino, Scribner or Thomas shunt) and hemodialysers (Kiil or Rhone-Poulenc). Determinations of hemoglobin in the plasma before and after 8-h hemodialysis were performed by the method of RICHTERICH. A significant increase in the initial normal values for hemoglobin in the plasma were found, but without any correlation between rate of hemolysis and type of hemodialyser. The presumed mechanical destruction of erythrocytes during hemodialysis can be determined by the free hemoglobin in the plasma. The small extent of intravascular hemolysis does not correlate with the type of hemodialyser.
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PMID:[Proceedings: Plasma hemoglobin in patients with intermittent hemodialysis with special reference to various dialysis procedures]. 121 71


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