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)

From the above discussion it is clear that many factors have been invoked in the pathogenesis of progressive glomerular injury. Those which are most important include increased PGC, coagulation, serum lipid abnormalities, and hypertrophy. Although many hemodynamic alterations have been identified, increased PGC was noted most constantly. Furthermore, the loss of autoregulatory capability which was observed in some models with progressive glomerulosclerosis usually resulted in increased PGC. Increased PGC has been associated with augmented dietary protein and is seen in the Munich-Wistar rat made diabetic. Such an increase in PGC could cause direct mechanical injury to endothelial and epithelial cells, as well as be responsible for increased mesangial traffic of macromolecules with the potential for stimulating cellular proliferation and mesangial matrix increase. Additional support for the importance of increased PGC is provided by the protective effect of decreasing PGC with CEI therapy and anemia, and by the enhanced autoregulatory capability in both the Milan and Okamoto hypertensive rats. The significance of coagulation factors is confirmed by the formation of platelet and fibrin thrombi in the development of the glomerular lesions. The sequence of glomerular injury suggests that endothelial damage occurs with subsequent formation of platelet aggregates as a response to this injury. Formation of platelet aggregates may be associated with the production of substances potentially injurious to the endothelial cells. Although blocking the appearance of such thrombi by administration of heparin or thromboxane synthetase inhibitor prevents glomerular injury, the blood pressure lowering effect of these agents complicates the interpretation of the studies. Serum lipid abnormalities are also important factors in the progression of nonimmunologic glomerular injury. Such abnormalities are observed with increased dietary phosphorus or lipid, in the obese Zucker rat, and in rats with diabetes mellitus. Reduction in serum cholesterol by administration of clofibric acid or mevinolin diminishes glomerular injury independent of alterations in glomerular hemodynamics. The possible link between increased serum lipids and augmentation of glomerular injury is at present indirect. The importance of hypertrophy as a contributing factor to the progression of nonimmunologic glomerular injury is suggested by several lines of evidence. Hypertrophy, with increase in glomerular size and caliber of capillary loops, may amplify the effect of increased PGC by further intensifying the tension and mechanical stress on all elements of the capillary wall.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nonimmunologic mechanisms of glomerular injury. 305 12

Twelve anaemic patients on haemodialysis were treated with recombinant human erythropoietin, starting with 72 IU/kg/week. The dose was doubled after 2 weeks until an increase of 2 g/dl of haemoglobin was observed. The effects on various parameters were studied during a 3-month period. Haemoglobin increased from 6.70 +/- 0.74 to 10.49 +/- 1.04 g/dl (mean +/- SD, P less than 0.001), potassium from 5.51 +/- 0.50 to 6.06 +/- 0.65 mmol/l (P less than 0.005), phosphate from 1.78 +/- 0.40 to 2.17 +/- 0.40 mmol/l (P less than 0.001) and the calcium phosphorus product from 4.3 to 5.2 (P less than 0.001). Three patients developed marked periarticular inflammation due to calcified deposits with a high calcium-phosphorus product of 6.8. An increase in arterial blood pressure was observed in three previously well-controlled hypertensive patients, one of whom developed hypertensive encephalopathy. We conclude that recombinant human erythropoietin is very effective in treating the anaemia of end-stage renal failure on haemodialysis. Regular estimations of serum potassium and phosphate are mandatory. In hypertensive individuals a further increase in blood pressure is possible.
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PMID:Human recombinant erythropoietin in anaemic patients on maintenance haemodialysis. Secondary effects of the increase of haemoglobin. 314 24

Acute toxicity of cefodizime sodium (THR-221) was examined in mice of both sexes, rats of both sexes (including 5-day-old young), and male dogs. The LD50 values of THR-221 (mg/kg) were as follows: (1) mice: intravenous, 7200 for males and 5000 for females; intraperitoneal, 10500 for males and 11000 for females; subcutaneous, 17500 for males and 16500 for females; and oral, 28000 for males and 29000 for females. (2) rats (adult): intravenous, 7000 for males and 8200 for females; intraperitoneal, 9500 for males and 8800 for females; subcutaneous, 17000 for males and 15500 for females; oral, more than 20000 for both sexes; and intramuscular, more than 3200 for both sexes. (3) 5-day-old rats: subcutaneous, 5278 for males and 5314 for females. (4) male dogs: intravenous, more than 5000. Major changes in general conditions observed in mice and rats were decreased spontaneous activity, lying prone, respiratory changes, staggering gait, clonic or clonic-tonic convulsions, and cyanosis, and in the animals dosed orally, diarrhea or salivation was also noted. The changes in 5-day-old rats were respiratory changes, agony, loss of reflex to an external stimulus, and congestion at the injection site, and those in dogs were vomiting, dryness of the nose, and soft or mucous stools. Autopsies on the mice and rats which died revealed hemorrhage on the brain surface. In addition, the following were seen: intraperitoneal retention of fluid and dark red spots on the abdominal wall (i.p.), subcutaneous retention of fluid or jellylike material and hemorrhage at the injection site (s.c.), and retention of fluid and dark red spots on the mucosa in the digestive tract (mice p.o.). In 5-day-old rats which died, the subcutaneous tissue at the injection site showed hemorrhage macroscopically and inflammatory changes microscopically. Hematological and blood chemical tests performed in dogs showed an increase in white blood cells and changes suggesting anemia, increases in GOT, LDH and ALP activities, and slight changes in urea nitrogen and inorganic phosphorus. In one animal given a low dose of 2500 mg/kg, an increase in GPT activity was also seen. However, these changes were all transient. Microscopic findings in dogs were slight inflammatory changes in the subcutaneous tissue around the injection site.
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PMID:[Acute toxicity study of cefodizime sodium]. 317 86

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

We report two infants with pseudotumor cerebri associated with renal disease. The pathogenesis of increased intracranial pressure in this clinical setting is unclear, but may be mediated by one or more of the conditions commonly associated with pseudotumor cerebri, including sinus thrombosis, increased intravascular fluid volume, anemia, and endocrine disturbances resulting in abnormal calcium and phosphorus metabolism. The onset of pseudotumor cerebri also may be related to changes in vasopressin levels that affect brain water permeability.
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PMID:Pseudotumor cerebri associated with obstructive nephropathy. 350 95

To determine whether an anabolic steroid had any benefit in the treatment of rheumatoid arthritis 47 patients entered a parallel group study. Twenty four received nandrolone decanoate 50 mg intramuscularly every third week for two years and 23 patients received no anabolic steroids. Other therapy was unaltered. Patients attended for clinical and biochemical assessments as well as the objective assessments of elementary body composition by in vivo neutron activation analysis and measurement of the mineral content of the distal femur by single photon absorptiometry on five occasions. A modest clinical deterioration (except for grip strength) was seen in both groups. No significant changes in calcium or alkaline phosphatase were seen. There was no significant change in total body calcium, total body phosphorus, body weight, or bone index/bone width measurements in either group. Significant increases occurred in total body nitrogen, total body potassium, haemoglobin, and packed cell volume (by six months) in the group treated with nandrolone decanoate. Comparison of 10 patients in the group treated with nandrolone decanoate also receiving oral steroid therapy with 14 patients in this group not receiving oral steroid therapy showed no significant differences. The main side effect of nandrolone decanoate was hoarseness. No radiological changes were seen. Nandrolone decanoate, in a dose that produces a significant anabolic effect, has no demonstrable action on bone metabolism in rheumatoid arthritis but may improve the chronic anaemia by six months.
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PMID:A controlled trial of nandrolone decanoate in the treatment of rheumatoid arthritis in postmenopausal women. 355 59

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

The authors report the result obtained with CAPD in 20 chronic renal patients treated during 4.6 years in average. The dialysis possibilities have maintained at middle term. Nevertheless, the awaited advantages concerning anemia, calcium and phosphorus disorders, neuropathy, are transient and incomplete. The water and sodium intakes need strongly to be controlled in order to achieve normal blood pressure. Finally the use of "Y" disconnect systems dramatically reduces the peritonitis rate.
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PMID:[Continuous ambulatory peritoneal dialysis: results after more than 3 years]. 369 70

The individual and combined effects of aflatoxin and deoxynivalenol (DON) were evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial with treatments of 0 and 2.5 micrograms of aflatoxin/g of feed (ppm) and 0 and 16 micrograms of DON/g of feed. The broilers were maintained on these dietary treatments from hatching to 3 weeks of age in electrically heated batteries with feed and water available ad libitum. The aflatoxin treatment significantly (P less than .05) decreased body weight; weight gain; increased the relative weight of the spleen, liver, and kidney; induced hepatic hyperlipemia; decreased activity of lactic dehydrogenase; and decreased serum levels of protein, albumin, and phosphorus. The toxicity of DON was expressed through reduced growth rate, increased feed conversion; increased relative weight of the gizzard, anemia, decreased activity of lactic dehydrogenase, and decreased serum triglycerides. The interaction between aflatoxin and DON was characterized by reduced growth rates; increased feed conversion, increased relative weight of the proventriculus, gizzard, spleen, liver, and kidney, anemia, hepatic hyperlipemia, decreased activity of alkaline phosphatase, glutamic oxalacetic transaminase, and lactic dehydrogenase, and decreased serum levels of protein, albumin, uric acid, cholesterol, triglycerides, and calcium. These data demonstrate that both aflatoxin and DON can limit broiler performance and adversely effect broiler health. The effects of the combination of aflatoxin and DON on broiler performance and health was more severe than the individual effects of these mycotoxins; however, the interaction was not severe enough to represent toxic synergy and can best be characterized as additive toxicity.
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PMID:Individual and combined effects of aflatoxin and deoxynivalenol (DON, vomitoxin) in broiler chickens. 374 45

The question of the mechanism of the physiological anemia of childhood was reexamined; we took into consideration the fact that microcytosis is a feature of this anemia as well as the evidence suggesting that the 2,3 DPG/hemoglobin ratio may depend in part on red cell size. In a group of normal, not-iron deficient children a high inverse correlation was obtained between the MCV and the 2,3 DPG/Hb ratio; this latter ratio did not correlate with serum phosphorus levels, previously incriminated in the indirect causation of the anemia of childhood.
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PMID:The anemia of childhood revisited. 381 31


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