Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative importance of erythropoietin (Ep) and inhibitors of erythropoiesis in the development of anemia in pediatric patients with end-stage renal disease (ESRD) was assessed in 82 patients: 41 treated with peritoneal dialysis (PD) and 41 with hemodialysis (HD). Serum Ep was determined with a sensitive radioimmunoassay. Potential serum inhibition of erythroid (CFU-E) and granulocytic (CFU-GM) progenitor cell growth was assessed using human bone marrow cell cultures. The mean Ep level for all 82 patients was 33.1 +/- 3.1 mU/ml, which was significantly higher (P less than 0.05) than the values obtained in 29 normal children (26.2 +/- 2.4 mU/ml). Serum Ep in the PD group (41.6 +/- 5.6 mU/ml) was significantly higher (P = 0.007) than that of the HD group (24.6 +/- 2.1 mU/ml). The mean hematocrit in the PD group (25.2 +/- 0.8%) was also significantly higher (P less than 0.002) than that of the HD group (22.2 +/- 0.5%). The mean serum parathyroid hormone (PTH) level as measured by a mid-terminal radioimmunoassay was not significantly different (P = 0.79) in the HD group (17,298 +/- 3,998 pg/ml) from that of the PD group (15,747 +/- 4,227 pg/ml). Neither serum Ep nor PTH concentration correlated with hematocrit or degree of inhibition of erythroid progenitor cell colony (CFU-E) formation in either group of dialysis patients, nor did the hematocrit correlate with the degree of serum inhibition of CFU-E formation. The higher level of Ep in the PD group may indicate more effective removal by PD of some enzymatic substance which reduces the immunologic and biologic activities of Ep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of different modes of dialysis on serum erythropoietin levels in pediatric patients. A report of the Southwest Pediatric Nephrology Study Group. 315 56

Accumulation of aluminum occurs in children with renal failure and can cause anemia, disabling osteodystrophy, and encephalopathy. Effects on bone mineralization are of particular concern in pediatric patients with growth potential. We measured plasma aluminum levels in 36 patients on continuous ambulatory peritoneal dialysis (CAPD) and 22 on hemodialysis under surveillance at a single pediatric center. The levels were above normal in 35 and 21 patients, respectively, and the values correlated with the oral dose of aluminum-containing phosphate-binding medications (r = 0.57; P less than 0.001). Younger and smaller children had higher plasma aluminum levels and also received larger doses of oral aluminum-containing compounds. Mean plasma aluminum levels (57.2 +/- 52.8 and 48.7 +/- 32.1 micrograms/liter, respectively) and the daily oral doses of elemental aluminum (47.3 +/- 37.6 and 39.2 +/- 26.7 mg/kg, respectively) were not statistically different in patients on CAPD and those on hemodialysis. Plasma aluminum levels did not correlate with estimated cumulative oral intake of aluminum, total duration of dialysis, serum calcium and phosphorus concentrations, N-terminal parathyroid hormone levels, or transfusion requirements. Retention of aluminum is common in children undergoing dialysis, correlates with the amount of aluminum administered orally, and results in similar elevations of plasma aluminum with CAPD and hemodialysis. Younger and smaller children are at increased risk for accumulation of aluminum. Alternative methods for control of serum phosphorus are needed in children with end-stage renal disease.
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PMID:Plasma aluminum levels in pediatric dialysis patients: comparison of hemodialysis and continuous ambulatory peritoneal dialysis. 356 Oct 41

Hypercalcemia associated with malignancy was diagnosed in a 2-year-old Thoroughbred filly admitted because of weight loss and reduced exercise tolerance of approximately 2 months' duration. Laboratory findings included hypercalcemia, hypophosphatemia, anemia, marked neutrophilia with lymphopenia and eosinopenia, and normal immunoreactive parathyroid hormone concentration. At necropsy, a 53.6-kg tumor was located in the cranioventral aspect of the abdominal cavity. Gross renal lesions were not noticed. Bone tissue appeared to be normal on gross and histologic examinations. The parathyroid glands were not grossly identified at necropsy. A specific test does not exist for detection of hypercalcemia associated with malignancy. The diagnosis of hypercalcemia associated with malignancy was made on the basis of clinical history, physical examination, radiographic interpretation, laboratory findings, histologic examination, and ruling out other causes of hypercalcemia. Hypercalcemia, increased renal phosphate excretion in the presence of hypophosphatemia, absence of bone metastases, and identifying an abdominal mesenchymal tumor that may have originated from the left ovary satisfied the basic criteria for hypercalcemia associated with malignancy from a solid tumor.
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PMID:Hypercalcemia associated with malignancy in a horse. 373 8

Although many questions still remain unanswered, it is clear that aluminum causes a microcytic hypoproliferative anemia and is one factor responsible for worsening anemia in patients with end-stage renal disease. Time course studies in a rat model have shown that the anemia is preceded by microcytosis; this has not yet been examined in man. The exact mechanism of aluminum-induced anemia is unknown, however it appears to involve inhibition of heme synthesis, either by inhibition of enzyme activity or interference with iron incorporation or utilization. The interrelationship between aluminum and iron, zinc, lead, or other metals in this anemia is also unknown, as are the effects of aluminum on erythroid colony forming units. The role of parathyroid hormone on aluminum-induced anemia has not been examined. Presently treatment of aluminum-induced anemia involves removal of the source of the aluminum, although recent studies with desferrioxamine show promise. It is unclear, however, exactly how desferrioxamine improves this anemia. It is clear, however, that aluminum in the dialysate can cause clinical problems including anemia, and that these problems can be substantially reduced if not eliminated by water treatment.
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PMID:Aluminum-induced anemia. 390 27

Numerous hemostatic abnormalities have been associated with acute and chronic renal disease. The most common abnormalities are defective platelet aggregation, decreased platelet adhesiveness, decreased platelet factor-3 availability, and prolongation of the bleeding time. Among the above platelet function tests, the bleeding time is the single test that most closely correlates with clinical bleeding. The nature of the platelet defect in uremia is still not well understood. The pathophysiologic mechanisms which have been implicated include platelet inhibition by plasma metabolites, eg, urea, guanidinosuccinic acid, phenolic acid; increased vessel wall prostacyclin; abnormal platelet arachidonic acid metabolism; increased levels of parathyroid hormone (PTH); defective binding of the Factor VIII complex to platelets or defective binding of platelets to vessel wall subendothelium by the Factor VIII complex; decreased platelet-vessel wall-interaction due to severe anemia; platelet storage pool deficiency; defective fibrinogen binding to platelets. Dialysis remains the mainstay of the prevention and treatment of uremic bleeding although it is not always immediately effective. The availability of cryoprecipitate and DDAVP offers an alternative and effective treatment for the temporary reversal of uremic bleeding in patients who require urgent invasive procedures.
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PMID:Hemostatic abnormalities in renal disease. 392 28

The survival of erythrocytes (RBC) is shortened in uremia, and it has been shown that calcium influx into RBC evoked crenation and increased their rigidity. The high blood levels of parathyroid hormone (PTH) may augment entry of calcium into RBC and hence affect their integrity. We examined the effect of PTH on osmotic fragility of human RBC and investigated the mechanisms through which PTH interacts with RBC. Both the amino-terminal (1-34) PTH and the intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH, produced significant increases in osmotic fragility. This effect was abolished by prior inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the increase in osmotic fragility. This action of PTH required calcium, was mimicked by calcium ionophore, and was partially blocked by verapamil. PTH caused significant influx of (45)Ca into RBC, which was not associated with potassium leak. The hormone did not affect water content of RBC. Scanning electron microscopy revealed that the incubation of RBC with PTH was associated with the appearance of membrane filamentous extensions, which anchor RBC together. Inhibition of glycolytic activity of RBC with NaF or inhibition of Na-K-activated ATPase with ouabain did not abolish the effect of PTH on osmotic fragility. PTH did not stimulate RBC Na-K-activated ATPase or Mg-dependent ATPase but caused marked and significant stimulation of Ca-activated ATPase. The basal activity of the RBC adenylate cyclase was low and PTH produced only a modest stimulation of this enzyme. Both cyclic AMP and dibutyryl cyclic AMP had no effect on osmotic fragility. THE DATA INDICATE THAT: (a) the RBC is a target organ for PTH, (b) the hormone increases osmotic fragility of RBC, and (c) this effect of PTH is due to enhanced calcium entry into RBC. We suggest that the increased calcium influx may affect the spectrin-actin of the cytoskeletal network of the RBC and may alter the stability and integrity of the cell membrane. This action of PTH on the RBC could be, at least in part, responsible for the shortened survival of RBC in uremia, and assign a new role for PTH in the pathogenesis of the anemia of uremia.
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PMID:Effect of parathyroid hormone on osmotic fragility of human erythrocytes. 628 9

Either primary or secondary hyperparathyroidism may be associated with anemia. The pathogenesis of this anemia remains obscure, but parathyroid hormone may directly suppress erythropoiesis or anemia may result from myelofibrosis. Previously reported in vitro studies of a direct inhibitory effect of PTH on erythroid progenitor growth were carried out with crude hormone preparations and appeared nonspecific. We have studied simultaneously the in vitro effects of pure (greater than 6000 U/mg) and crude (130 U/mg) preparations of PTH on murine and human hematopoietic progenitor growth. Increasing concentrations (2.5 to 20 U/ml) of crude PTH produced a dose-dependent inhibition of early erythroid (BFU-E) and granulocyte/macrophage progenitor (CFU-GM) growth in human and mouse marrow cell cultures. However, the biologically active N-terminal fragment containing amino acids 1-34 and the pure intact molecule of 84 amino acids failed to significantly inhibit hematopoietic colony growth. These observations demonstrate that in vitro inhibitory effects described with parathyroid gland extracts are not specific for erythropoiesis and may not be related to the circulating form of PTH.
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PMID:High levels of the circulating form of parathyroid hormone do not inhibit in vitro erythropoiesis. 631 28

In acutely uremic animals, the contractile force of the heart is consistently increased; such an increase can be dissociated from changes of afterload or catecholaminergic drive. It is associated with diminished sarcolemmal Na,K-ATPase activity in the heart which, in turn, may be related to increased levels of endogenous digitalis-like substances (endigens) that have been postulated to represent a natriuretic factor. In patients with chronic uremia, myocardial contractility is usually normal, but occasionally there may be heart failure unrelated to pre-existing hypertension, coronary heart disease, anemia, fluid overload, or other recognizable factors. So far, the experimental basis for this clinical observation is uncertain. Possible causes for the clinical syndrome include an excess of parathyroid hormone or cardiodepressor substances. There is experimental evidence of impaired cardiac response to beta adrenergic agonists, e.g., decreased isoproterenol-dependent calcium uptake, diminished inotropic and chronotropic responses. In acutely uremic rats, cardiac cyclic AMP levels are high but can be reversed by beta blockers. Heart calcium content is variable and heart weight is constantly increased in acutely uremic rats, despite decreased skeletal muscle mass. The change in heart weight is not related to anemia, to an excess of parathyroid hormone, or to sympathetic activity; its cause remains unknown. Experimental studies to date have shown a variety of abnormalities, but do not provide a uniform concept of the mechanisms or an explanation for the cardiac dysfunction so often observed in patients with uremia.
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PMID:Cardiac function in experimental uremia. 636 51

Patients with varying degrees of renal insufficiency and patients with end-stage renal disease receiving continuous ambulatory peritoneal dialysis or regular hemodialysis therapy were studied to assess the independent relationship between serum parathyroid hormone concentration, and both severity of anemia and degree of serum inhibition of erythropoiesis. In patients with renal insufficiency not receiving dialysis, a significant curvilinear relationship between serum parathyroid hormone and creatinine concentrations was present (r = 65, p less than 0.001). Serum parathyroid hormone (by radioimmunoassay) also correlated with hematocrit level (r = -0.54, p less than 0.001) and degree of serum inhibition of in vitro erythroid progenitor cell growth in fetal mouse liver cultures (r = -0.45, p less than 0.001). However, multiple linear regression analysis revealed that after controlling for the effect of creatinine, m-parathyroid hormone is no longer a significant predictor of hematocrit level or erythroid progenitor cell growth. On the other hand, when a restricted population of patients with creatinine values between 1 and 4 mg/dl was analyzed separately, controlling for the effect of creatinine, there was still a significant correlation between hematocrit level and m-parathyroid hormone, but no such relationship was seen when participants with parathyroid hormone levels of less than or equal to 1000 pg/ml were analyzed. No significant correlation was seen between hematocrit level or inhibition of erythroid colony growth and serum parathyroid hormone concentrations in patients receiving either regular hemodialysis or continuous ambulatory peritoneal dialysis. In 13 patients given regular hemodialysis studied before and after parathyroidectomy, there was no significant change in serum erythropoietin (by radioimmunoassay) or serum inhibition of erythropoiesis, although hematocrit levels increased in six of the 13 patients. The 1-34 human parathyroid hormone, 1-84 bovine parathyroid hormone, and 1,25-dihydroxycholecalciferol had no effect on in vitro erythroid burst-forming unit growth. Parathyroid hormone (8 mu/ml) inhibited and 1,25-dihydroxycholecalciferol (4.0 ng/ml) stimulated erythroid colony-forming unit growth only in the absence of exogenous erythropoietin in culture. In summary, it was not possible to demonstrate a significant relationship between serum parathyroid hormone levels and anemia or inhibition of erythropoiesis in patients with uremia either before starting dialysis or after receiving long-term dialysis treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Potential role of parathyroid hormone as an inhibitor of erythropoiesis in the anemia of renal failure. 650 97

In order to evaluate the toxicity of hypervitaminosis A in regular dialysis patients, the relationships between the plasma levels of vitamin A, retinol binding protein (RBP), prealbumin (PA), and biochemical parameters were studied in 47 patients. Plasma vitamin A levels were inversely correlated with hematocrit (r = -0.5), which was also significantly correlated with RBP/vitamin A ratio (r = 0.61). Immunoreactive parathyroid hormone (i-PTH) and very low density lipoprotein (VLDL) were inversely related to RBP/vitamin A and RBP/PA ratios. These findings suggest that a raised plasma vitamin A level in regular dialysis patients contributes to anemia and hypervitaminosis A toxicity.
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PMID:Hypervitaminosis A: a contributing factor to anemia in regular dialysis patients. 654 Aug 43


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