Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, the survival rate of high risk infants has markedly increased. The role of such medical management as fluid, electrolyte and nutritional therapy have assumed a greater importance in assuring optimal quality of the survivors. The very low birth weight infants, particularly those with respiratory distress syndrome and perinatal asphyxia, are at highest risk. The inefficient renal function, unique characteristic of body fluid composition and/or presence of severe clinical illness often make the management of fluid and electrolytes in this group of infants difficult. The numerous factors that influence insensible water loss make calculation of fluid management in the high risk infant even more challenging. Systematic collection of data such as daily body weight, intake, output, urine specific gravity and serum electrolyte is essential to appropriately maintain fluid and electrolytes balance in these infants. Respiratory distress syndrome is a common problem in premature infants and the fluid and electrolyte management in these infants will require similar attention to details as described for the fluid and electrolytes of very low birth infants. Perinatal asphyxia often results in oliguria or anuria because of possible development of inappropriate ADH secretion or acute tubular necrosis. It is essential that fluid restriction be done on the first day or two of life to avoid fluid overload.
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PMID:Renal function and fluid therapy in high risk infants. 304 69

Heme proteins transport oxygen and facilitate redox reactions. Heme, however, may be dangerous, especially when free in biologic systems. For example, iron released from hemoglobin-derived heme can catalyze oxidative injury to neuronal cell membranes and may be a factor in post-traumatic damage to the central nervous system. We have shown that heme catalyzes the oxidation of low density lipoproteins which can damage vascular endothelial cells. The endothelium is susceptible to damage by oxidants generated by activated phagocytes, and this has been invoked as an important mechanism in a number of pathologies including the Adulte Respiratory Distress Syndrome (ARDS), acute tubular necrosis, reperfusion injury and atherosclerosis. Because of its highly hydrophobic nature, heme readily intercalates into endothelial membranes and potentiates oxidant-mediated damage. This injury is dependent on the iron content of heme and is completely blocked when concomitant hemopexin is added. Ferrohemoglobin, when added to cultured endothelial cells, is without deleterious effects, but if oxidized to ferrihemoglobin (methemoglobin), it greatly amplifies oxidant damage. Methemoglobin, but not ferrohemoglobin, releases its hemes which can then be incorporated into endothelial cells. Cultured endothelial cells, when exposed to methemoglobin but not ferrohemoglobin, cytochrome c or metmyoglobin, potentiate this oxidant injury. Stabilization of the methemoglobin by cyanide, haptoglobin or capture of the heme by hemopexin abrogates this effect. Paradoxically, more prolonged exposure of endothelium to heme or methemoglobin renders them remarkably resistant to oxidant challenge. Endothelium defends itself from heme by induction of the heme degrading enzyme heme oxygenase and the concomitant production of large amounts of the iron binding protein ferritin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heme and the vasculature: an oxidative hazard that induces antioxidant defenses in the endothelium. 808 43