Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 3 patients on maintenance hemodialysis who developed a fulminant, disseminated and fatal form of mucormycosis. The diagnosis was made by microscopy and culture in 1 case, yielding Rhizopus rhizopodiformis, and by post-mortem microscopy in the two other cases. These patients were receiving desferrioxamine (DFO) for aluminum overload and had no iron-overload. Ten similar patients, all (with only one possible exception) receiving DFO, have been reported from American centers. The mechanism by which DFO could precipitate mucormycosis is unsettled. The explanation might be that DFO acts as a siderophore to the Mucorales fungi. High serum levels of DFO in renal failure could enhance this mechanism. Epidemiological data, provided from an inquiry in 25 Flemish dialysis centers, support the association between DFO treatment and dialysis-associated mucormycosis.
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PMID:The role of desferrioxamine in dialysis-associated mucormycosis: report of three cases and review of the literature. 329 56

Only rather recently has the biologic and pathogenetic relevance of aluminum, this most common metal come under serious scientific scrutiny. Various laboratory findings of accumulations of aluminum in the brain, kidney, liver, parathyroid glands, skeletal muscle, heart, lungs, pancreas and spleen as well as stainable aluminum in bone have spurred widespread interest in aluminum absorption and toxicity and in the mechanisms involved in the metabolism of aluminum. Since the kidney is the major excretory organ for aluminum, this report focuses on the abnormalities occurring with aluminum accumulation in the bone of patients with renal failure to determine the metabolic interrelationships of aluminum, parathyroid hormone, vitamin D, iron, and calcium. This editorial presents an overview of the most recent investigations of aluminum accumulation in humans, experimental animal models, and at the cellular level, presents the metabolic relationships known to exist as well as those strongly suggested in documented studies, and identifies those aspects of aluminum-related bone disease awaiting study in this increasingly important field of inquiry. The study outlines the metabolism of aluminum, the pathogenesis, prevalence, morbidity and mortality of aluminum-related bone disease, the histopathology of bone with aluminum accumulation, the recognized difficulties inherent in the diagnosis of aluminum-related bone disease, and the current understanding as relates to prevention and therapy.
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PMID:Aluminum-related bone disease. 334 41

Nine patients with duodenal pseudomelanosis are described: seven had endstage renal failure while one other patient had undergone renal transplantation. Eight of the nine had been on oral iron supplements. The pigment stained positively with Perls' stain for iron in five patients, positively with the Masson-Fontana method normally used to identify melanin in one, and positively with both methods in three. Electron probe x-ray analysis of the pigment on samples from six patients showed iron to be present in all six, while sulphur was present in five. Varying sulphur content of the pigment in different patients could account for differences in histochemical characteristics. Iron was also shown in the duodenal biopsies of 34 of 48 uraemic patients on oral iron supplements, but was present in only 22 of 120 patients endoscoped for miscellaneous conditions (p less than 0.001). We postulate that the pigment of duodenal pseudomelanosis is derived from iron absorbed from the lumen.
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PMID:Clinical and ultrastructural studies in duodenal pseudomelanosis. 342 96

Hemorrhage values and the amount of iron entering the body with drugs and blood transfusions were determined in 107 patients with the terminal CRF stage. Of them 59 received regular hemodialyses. The level of serum iron and ferritin as well as iron reserves in the body were investigated at the start and end of the study. In the end a histochemical study of the content of hemosiderin in the bone marrow, liver and spleen was performed. A close interrelationship of iron reserves determined with a modified desferal test and the level of serum ferritin (r = 0.94) was established. The highest iron reserves were revealed in the patients receiving blood transfusions and parenteral iron drugs. Criteria for the assessment of iron reserves in patients with renal failure were determined by means of the modified desferal test and investigation of serum ferritin. Normal ferritin reserves in such patients corresponded to serum ferritin values within the range of 50-400 micrograms/l and indices of the modified desferal test ranging from 0.4 to 2.0/0.5 g of desferal. Of a degree of hemosiderosis one could judge on the basis of a histochemical investigation of tissue hemosiderin only. Iron drugs per os were proposed for the prevention of disorders of iron balance in patients with renal failure.
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PMID:[Iron reserves in patients with chronic renal insufficiency]. 368 52

Repeated intraperitoneal injections of ferric nitrilotriacetate (Fe-NTA) induce nephrotoxic features such as proximal tubular necrosis and renal failure, an unexpected phenomenon for a ferric compound. The mechanism of Fe-NTA toxicity was investigated by electron microscopy and respiration studies of renal cortical mitochondria in rats. Four hours after a single intraperitoneal injection of Fe-NTA, 5 mg iron/kg body wt, loss of microvilli, increased number of cytoplasmic vacuoles, electron-dense cytoplasmic deposits, mitochondrial swelling, karyorrhexis, and rupture of cytoplasmic membrane were observed in proximal tubular epithelia. At 24 hours, an increased number of cells had become necrotic. Polarographic studies of mitochondria from renal cortex 4 hours after Fe-NTA treatment showed a significant decrease in State 3 respiration and DNP-uncoupled respiration, whereas little change was observed in State 4 respiration and ADP/O.
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PMID:Nephrotoxicity of ferric nitrilotriacetate. An electron-microscopic and metabolic study. 370 95

Acute iron poisoning is most common in children below the age of 5 years. While there is no doubt that it may be fatal, recent surveys show that death occurs in only a very small percentage of cases and that iron salts are responsible for a small minority of fatalities due to overdosage with drugs. Similarly, the proportion of severe cases seems to have fallen over the last thirty years, possibly due to earlier and more aggressive treatment but more probably due to an increase in the number of minor exposures reported. Iron salts are directly toxic to the gastrointestinal tract causing vomiting, diarrhoea, abdominal pain and occasionally significant blood loss. They also cause metabolic acidosis by interfering with intermediary metabolism and producing shock and reduced tissue perfusion. The clinical course of acute iron poisoning is divided into 4 phases. Features of acute gastrointestinal irritation dominate the period up to 6 hours after ingestion and most patients do not develop other features or progress beyond this stage. Rarely, blood loss may be sufficient to cause hypotension. Severe poisoning is characterised by impairment of consciousness, convulsions and metabolic acidosis. The second phase, 6 to 12 hours after ingestion, is one of remission of features. Phase 3 comprises the period 12 to 48 hours from ingestion and is reached only by a small minority of patients. Recurrence or development of shock, and metabolic acidosis are usual and renal failure and features of extensive hepatocellular necrosis may develop. The last (fourth) phase, 2 to 6 weeks after ingestion, is only likely to develop in young children and is characterised by recurrence of vomiting due to gastric or duodenal stenosis caused by healing of iron-induced mucosal ulcers. Acute iron poisoning in humans has not been adequately studied and is unlikely to be so now because of the infrequent and sporadic occurrence of cases. The evidence for many conventional aspects of management is therefore unsatisfactory. Assessment of severity of poisoning is an essential prerequisite to optimum management but is difficult. The amount of elemental iron ingested is unacceptable since it is seldom known with accuracy and absorption is unpredictable because of vomiting and diarrhoea. The commonly encountered clinical features are also unreliable although it is generally accepted that coma, shock and metabolic acidosis indicate severe poisoning.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Management of acute iron poisoning. 378 42

Nitrilotriacetate (NTA), an effective metal-chelating agent, has been used as a substitute for polyphosphates in household laundry detergents. Nephrotoxicity and renal tumorigenicity have been reported in experimental animals that received high doses of NTA po for 4 weeks to 2 years. Since NTA exists in water as a variety of NTA-metal complexes, it was important to investigate the biological effects of NTA in a complexed form. In this study, acute and subchronic toxicity of a ferric iron chelate of NTA (Fe-NTA) was investigated in rats. When Fe-NTA was given ip, acute tubular necrosis and renal failure occurred following a single injection of 15 mg iron/kg. Repeated injections of sublethal doses produced degeneration and necrosis of the proximal tubular epithelium and was associated with polyuria, glucosuria, aminoaciduria, and azotemia. After 9 days of treatment, regeneration of the tubular epithelium with atypical cells was observed. Except for a parenchymal iron deposit, no marked changes were observed in other organs. None of these effects were observed in animals given noncomplexed NTA. In conclusion, the toxicity observed following high doses of NTA given po may be the result of an absorbed metal-NTA chelate.
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PMID:Acute renal failure and glucosuria induced by ferric nitrilotriacetate in rats. 397 99

The possibility that supplemented, very-low-protein diets may slow the progression of CRF increases the importance of that type of diet therapy (1). If the results are confirmed in large numbers of patients, it is likely that the supplements will become commercially available and will be used widely to treat patients with progressive renal failure. Adequate vitamin and mineral supplementation will be necessary in order to maintain good nutritional status. On the basis of previously reported data and the present results, supplemental thiamin, riboflavin, niacin, vitamin B-12, folic acid, pyridoxine, calcium, and possibly iron and zinc are recommended for patients treated with these very-low-protein diets. These recommendations are preliminary and may be altered as more long-term data are collected on the vitamin and mineral status of CRF patients.
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PMID:Very-low-protein diets in chronic renal failure: nutrient content and guidelines for supplementation. 404 81

A patient with renal failure developed widespread calcification in the thighs after the injection of iron-dextran (Imferon). This is considered as an example of calciphylaxis, a process in which calcium is laid down in parts of the body following the administration of a "challenger." Iron-dextran is a known challenger, and should be used with caution in uraemic subjects, who may be sensitized by high serum parathyroid hormone levels. Contributing factors may have been a high calcium/phosphate product, steroids, and the patient's immobility.
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PMID:Calciphylaxis in man. 578 25

The differential ferrioxamine test measures the amount of body iron as ferrioxamine (Fv) chelated by a standard dose of desferrioxamine.Five patients with untreated, uncomplicated idiopathic haemochromatosis and one with transfusion haemosiderosis gave Fv in the range 1,948 to 2,462 mug./kg. (normal 110 to 500). One case of transfusion haemochromatosis with haemolytic anaemia and renal failure gave an Fv value of 8,019 mug./kg. Four patients with idiopathic haemochromatosis after therapeutic venesection gave Fv values of 212 to 885 mug./kg. One relative with a value for Fv of 776 mug./kg. was shown to have early cirrhosis by liver biopsy. Serial Fv measurement after venesection in this patient provided a preliminary assessment of the relationship between Fv values and available iron stores up to about 2,000 mg. iron. This relationship applies only when red cell survival is normal. Approximate figures for the range of available storage iron in 31 healthy men are deduced, namely, 200 mg. to 1,000 mg. (3 to 14 mg./kg.). The test should prove useful in the diagnosis of iron overload, in the screening of relatives for early haemochromatosis, and in the management of iron storage diseases.
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PMID:Differential ferrioxamine test in idiopathic haemochromatosis and transfusional haemosiderosis. 590 97


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