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)

Aluminium intoxication in renal failure occurred over weeks or months when dialysis fluid or parenteral solutions were heavily contaminated and over many years when the main source was oral administration of aluminium-containing phosphate binders. Encephalopathy was common during subacute intoxication but in slow aluminium poisoning the main brunt was borne by the bones. However, in both tempos of intoxication several organs or systems were involved. Encephalopathy was usually accompanied by bone disease, bone disease by parathyroid suppression and both by anaemia. The heart and the lymphocytes are probably damaged by aluminium overload. Among the many questions left unanswered 15 years after the incrimination of aluminium as the cause of this multi-system illness are: (1) does low level aluminium overload in renal failure cause gradual deterioration in cerebral function? And, if so, (2) does it resemble Alzheimer's disease or a slow-onset version of dialysis encephalopathy? The evidence we review suggests that the answer to (1) is 'yes' and to (2) 'probably the latter'.
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PMID:Aluminium intoxication in renal disease. 149 Apr 19

Aluminum intoxication is common in patients with chronic renal failure because of absorption of aluminum during dialysis from aluminum-containing dyalysate water and ingestion of phosphate binders containing aluminum. Aluminum accumulation in the body is followed by bone disease, encephalopathy and anemia. Bone diseases can be recorded in 44% of the patients treated with long-term dialysis. Two early histologic types of retarded bone turnover can be seen, i.e. osteomalacia and aplastic bone disease. In dialyzed patients, osteomalacia is usually followed by low PTH level in human serum. On the contrary, studies on uremic rats have shown that previous parathyroidectomy can prevent aluminum intoxication, because hyperparathyroidism in an early phase of chronic renal failure increases aluminum absorption from the gut and its accumulation in the body. As the pathogenesis of aluminum-induced alterations is unclear, the prevention of bone disease should be provided through lowering the aluminum intake in dialyzed patients. Bone biopsy is unavoidable for the early detection and diagnosis of the disease. Promising results in the treatment of aluminum intoxication have been obtained using deferoxamine, a chelating agent.
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PMID:[Aluminum poisoning]. 267 63

Hyperphosphataemia in haemodialysis patients is associated with secondary hyperparathyroidism and more importantly with an increased cardiovascular mortality in dialysed patients. Removal of phosphate during dialysis is less than net intestinal uptake. This imbalance results in a positive phosphate balance. To control serum phosphate concentration oral phosphate binders have to be taken to reduce net intestinal uptake. The use of classical phosphate binders such as calcium carbonate, calcium acetate and aluminium-containing phosphate binders is limited by their side effects. Hypercalcaemia aggravates vascular calcification and cardiovascular risk. Aluminium intoxication causes aluminium osteopathy, anaemia and encephalopathy. Therefore, the development of calcium- and aluminium free phosphate binders has become a challenge to clinical nephrology. Polyallylamine hydrochloride (sevelamer) is one of the new alternative compounds which has been shown to effectively bind phosphate in dialysis patients. A promising approach in the development of alternative phophate binders are trivalent-iron (Fe(III)) containing phosphate binders. They were not only successfully tested in experimental animals but have also been shown to reduce urinary phosphate excretion and serum phosphate concentrations in patients with preterminal failure and those on maintenance haemodialysis. This review outlines the experimental and clinical data on Fe-III based phosphate binders providing evidence that they will be as effective and safe as phosphate binders without the major side effects of classical phosphate-binding compounds.
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PMID:Compounds in development to combat hyperphosphataemia. 1177 14

In patients with chronic kidney disease, erythropoietin resistance is common, costly, and has implications beyond the management of anemia because the presence of erythropoietin resistance portends mortal outcomes. Exploring the provenance of erythropoietin resistance may be facilitated by the consideration of the pathogenetic triad of iron-restricted erythropoiesis, inflammation, and bone marrow suppression. Challenging to diagnose because of difficulty in interpreting tests of iron deficiency, iron-restricted erythropoiesis should be considered in patients who require high doses of erythropoietin, have low transferrin saturation (eg, <20%-25%), and do not have very high ferritin (eg, <1,200 ng/mL); a therapeutic trial of intravenous iron may be worthwhile. Aluminum intoxication is a rare cause of iron-restricted erythropoiesis that may manifest as microcytic hypochromic anemia. A decrease in serum albumin concentration may signal the presence of inflammation, which may be manifest (such as because of a recent illness or infection) or occult; the latter include clotted synthetic angioaccess, failed renal allograft, dialysis catheter, periodontal disease, underlying malignancy, or uremia per se. Marrow hyporesponsiveness may be improved by increasing the delivered dialysis dose, using ultrapure dialysate, maintaining adequate vitamin B12 and folate stores, or by treating hyperparathyroidism. In summary, improving the outcomes of erythropoietin-resistant patients will require complete patient assessment that goes beyond considerations of iron and erythropoietin dose alone. Given that erythropoietin dose is associated with mortality, mitigating erythropoietin resistance has the potential to improve patient outcomes.
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PMID:Hyporesponsiveness to erythropoietin: causes and management. 1923 68