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)

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

Clinical signs of hypophosphatemia, even when severe, are rare in diabetic ketoacidosis despite their high frequency in this condition. This article presents a patient with rhabdomyolysis due to severe hypophosphatemia, where the level of serum phosphorus was observed to be as low as 0.42 mg/dL on the 16th hour of ketoacidosis treatment. The patient developed acute tubular necrosis due to rhabdomyolysis, but there was no blood reaction in the urine, and the creatine kinase increased to 1200 U/L. The patient was treated without dialysis and was cured after a polyuria period of 2 months after the oliguric period.
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PMID:Rhabdomyolysis without detectable myoglobulinuria due to severe hypophosphatemia in diabetic ketoacidosis. 2164 90

Wolcott-Rallison syndrome is a rare disease presenting with insulin-dependent diabetes mellitus (DM) before 6 months old, skeletal dysplasia after 6 months old, and liver failure. Other manifestations are renal failure, microcephaly, epilepsy, central hypothyroidism, neutropenia, and dental and dermal problems. The cases were 2 patients from 2 different states of Iran (Khoozestan and Fars) who had developed DM before 6 months old. The first one was a 7-month-old infant who was healthy; in the genetic study (screening), autosomal recessive pattern and novel deletion in EIF2AK3 were reported; her sister had died at 5.5 years old due to diabetic ketoacidosis (DKA) that was associated with liver and renal failure. The second patient had developed DKA at 45 days old, which was associated with mild acute tubular necrosis and abnormal coagulation tests at onset clinical presentation, which were then resolved. He was treated with insulin, and at follow-up, the laboratory data are normal; in the genetic study, EIF2AK3 nonsense homozygous mutation was diagnosed. Genetic study of patients with insulin-dependent DM before 6 months old, especially those with DKA and associated with or without other disorders; attention to novel deletion of in EIF2AK3 gene; screening for skeletal dysplasia after 1 year old; and renal, liver, pancreatic, and thyroid function tests are recommended.
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PMID:Wolcott-Rallison Syndrome With Different Clinical Presentations and Genetic Patterns in 2 Infants. 3100 90