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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pulmonary silicoproteinosis, massive proteinuria and fatal renal failure developed in a 23 year old male sandblaster. Examination of the kidney by immunofluorescence revealed granular deposits of immunoglobulin M (IgM) and the third component of complement (C3) along the glomerular basement membrane. Light microscopy disclosed mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures. The silicon content of the kidney was 264 parts per million (ppm), but particles of silicon were not demonstrated by electron microscopy. No primary or systemic causes of renal diseases were elucidated. The renal dysfunction apparently resulted from acute renal silicon toxicity, a new complication of acute pulmonary silicoproteinosis.
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PMID:Massive proteinuria and acute renal failure in a patient with acute silicoproteinosis. 34 91

87 patients with end-stage renal failure on long-term hemodialysis, 25 not on dialysis and 37 with renal transplants have been studied. Serum ferritin was measured by immunoradiometric and radioimmuno-assay. The correlation between the two methods was excellent (p less than 0.001). In 25 patients on long-term hemodialysis a good correlation was found between serum ferritin levels and stainable iron (p less than 0.001). All patients with adequate iron stores had serum ferritin levels above 60 ng/ml, whereas only one out of 10 with decreased or absent iron stores had a higher leve (118 ng/ml). According to these criteria the iron stores were decreased in 59% of our patients on long-term hemodialysis, decreased or adequate in 14% and adequate or increased in 27%. There was no correlation between serum ferritin levels and serum iron and total iron binding capacity. The distribution pattern of the serum ferritin levels was log normal and did not significantly differ in the three groups studied, although the patients with renal transplants had nearly normal hemoglobin and creatinine levels. Elevated serum ferritin levels in patients (21%) on hemodialysis could only partly be explained by repeated transfusions or chronic infections.
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PMID:[Serum ferritin in renal insufficiency, hemodialysis and kidney transplantation]. 36 27

Quantitation of the erythropoiesis with radio-iron (59Fe) was applied to 9 patients with untreated myelomatosis. The method included blocking of the 59Fe reutilization by injection of non-radioactive iron. There was no uniform pattern in the Fe-kinetics values. The Plasma Iron Turnover (PIT) and the Red Blood Cell Iron Turnover (RBCIT) varied from subnormal to values markedly increased above upper normal limit. The calculated average Mean Red Cell Life time (MRCL) of erythrocytes was just below normal range. The mean Marrow Transit Time (MTT) was normal in the patients, despite subnormal venous haematocrit, indicating insufficient stimulation of the bone marrow. The renal function, measured as 51Cr-EDTA clearance, was found positively correlated to the RBCIT (r = 0.78, P less than 0.05). The results suggest that the previously demonstrated relationship between anaemia and renal failure in patients with myelomatosis is caused mainly by an inability of the bone marrow to produce sufficient red blood cells under the stress of anaemia related to the degree of renal impairment.
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PMID:Quantitation of erythropoiesis in myelomatosis. 47 59

Seventeen patients without renal failure and 14 patients receiving long-term hemodialysis were studied. Serum and bone marrow ferritin determinations were made at the time of bone marrow aspiration. A good correlation was found between serum ferritin levels and bone marrow iron stores, as well as between bone marrow ferritin levels and iron stores. Serum ferritin determinations appear to give an accurate estimation of bone marrow iron stores, thereby providing a reliable guide for iron replacement therapy and reducing the need for repeated bone marrow aspirations. Serum ferritin levels of less than 105 ng/ml suggest decreased iron stores, and values greater than 120 ng/ml indicate adequate or increased iron stores. Preliminary data also suggest that bone marrow ferritin determinations may be useful in quantitating bone marrow iron stores.
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PMID:Serum ferritin level. Determinant of iron requirement in hemodialysis patients. 57 60

The percentage of fat-cell areas in bone marrow particles from 22 patients with untreated myelomatosis was estimated. In only 1 patient was the mean fat cell area below 25% of the bone marrow area measured. A negative correlation was found between the area of fat cells and plasma cells, indicating a displacement of the fat cell area by the plasma cells. 28% of the patients had empty bone marrow deposits of iron. However, based on a normal iron saturation of S-transferrin and a normal sideroblast count in the bone marrow, the supply of iron to the erythropoiesis was considered sufficient. All patients but one had normoblastic bone marrows. Using a deoxyuridine suppression test in 10 patients, no biochemical defect could be demonstrated. To judge from the correlation coefficient a minor degree (9-14%) of the variation in Hb values could be predicted from the cellularity in the bone marrow while a major degree (70%) could be predicted from the renal glomerular filtration rate. The results do not support a displacement of blood-forming elements, iron deficiency, vitamin B12 or folic acid deficiency to be of general significance in the pathogenesis of anaemia, but agrees with a causal relationship between anaemia and renal failure.
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PMID:Bone marrow studies in myelomatosis. 71 78

The present study was done in order to determine whether treatment with triiodothyronine (T3) would improve the anemia of chronic renal insufficiency. Four patients with stable renal failure and anemia were treated with 75 microgram/day of T3 for a period of four weeks. The patients were not in chronic dialysis, had normochromic normocytic anemia and hypocellular bone marrow, and showed no evidence of external blood loss during the study. They had received no iron, folic acid, or androgenic steroids for at least six months prior to the study. The administered dose of T3 was adequate to depress the serum levels of thyroid-stimulating hormone (TSH); however, there was no detectable improvement in the levels of hemoglobin, hematocrit, bone marrow cellularity, serum and erythrocyte folate determinations, serum iron (Fe), 59Fe half-life, plasma iron turnover rate, percentage Fe incorporated into red blood cells, or in the ratio of surface radioactive counting over bone marrow/liver and spleen. It is concluded that the experimental observations concerning direct bone marrow stimulation by T3 in anephric rats are probably not clinically applicable for the treatment of the anemia associated with uremia.
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PMID:Effects of triiodothyronine on the anemia of chronic renal failure. 73 33

Since macrocytosis was observed in a high percentage of our renal transplant patients, a follow-up study was carried out on 36 patients with determination of the mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH) and haemoglobin concentration (MCHC). These parameters were determined monthly for periods of up to two years (16 cases) following transplantation. There was a rise in both MCV and MCH within one month. Macrooperative MCHC, however, remained normal. Anaemia was absent or mild. The bone marrow showed striking megaloblastic changes with nuclear-cytoplasmatic dissociation in both red and white cell precursors. Vitamin B 12 absorption tests were normal in all 8 patients investigated. Macrocytosis was not detectable in two patients with a low serum iron concentration. Macrocytosis disappeared in 4 patients with chronic rejection when progressive renal failure developed. It is concluded that azathioprine therapy induces macrocytosis in renal transplant patients provided renal function is satisfactory.
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PMID:[Macrocytosis in renal transplant patients (author's transl)]. 79 85

Various factors are involved in the pathogenesis of anemia in dialysis patients. Reduced erythropoiesis is mainly attributed to erythropoietin deficiency. Stimulation of erythropoiesis may be promoted by androgens. Substitution of iron is recommended in case of iron deficiency. As a rule, supplementation of vitamin B12 is not necessary, but administration of folic acid is recommended. Treatment of anemia in renal failure is rendered more effective by increased technical efficiency in hemodialysis permitting a relatively protein-rich diet. Blood transfusions are not necessary during routine treatment of dialysis. Since bilateral nephrectomy will always provoke severe anemia, it should be reserved to special cases of severe hypertension. Until now, no conservative therapy has been developed which would allow optimal treatment of anemia in dialysis patients. Successful renal transplantation still is, and will be, the best therapeutic intervention.
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PMID:[Anemia in terminal kidney failure. Pathogenesis and therapy]. 83 56

A series of patients with primary hyperparathyroidism showed a high incidence of anemia. Red cell morphology and indices, iron, folate and B12 were generally normal and reticulocyte counts inappropriately low. Focal fibrosis of the marrow space was observed in marrow biopsies from two patients, but no patient showed overt signs of a myelophthisic process. Anemia tended to occur in those with more severe hyperparathyroidism (higher serum calcium level or radiographic osteitis fibrosa cystica). Since severe hyperparathyroidism frequently compromises renal function, it is not always clear whether the anemia should be attributed to renal failure or to the metabolic disease. In nine of the 24 anemic patients, however, renal function was normal. Hyperparathyroidism may cause a hyporegenerative anemia, the mechanisms for which have not been elucidated.
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PMID:Hyporegenerative anemia in primary hyperparathyroidism. 91 Jan 74

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


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