Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether amino acid hyperalimentation sensitizes the kidney to ischemic renal injury. Sprague-Dawley rats were infused with a control infusate or control infusate plus 15 essential and nonessential amino acids (FreAmine III, 2 mg of amino acids/kg/min). After 1 hr, bilateral renal ischemia was induced (15 min pedicle cross clamp). GFR, urine flow, and renal blood flow (RBF) were measured before and for 0 to 2 hr postischemia. None of these parameters were statistically different between the two groups of rats prior to renal ischemia. However, the decrease in GFR following renal ischemia was twice as great in the amino acid versus the nonamino acid treatment group (decreases 73 +/- 4% vs. decreases 36 +/- 4%, respectively; P less than 0.001). The postischemia urine flow rate was also significantly less (P less than 0.01) with amino acid treatment. RBF did not differ between the two groups. Renal histology confirmed greater tubular injury with amino acid treatment (P less than 0.001). In conclusion, infusion of therapeutic doses of amino acids can exacerbate early functional and histologic parameters of ischemic renal injury and thus, may sensitize the kidney to ischemic acute renal failure.
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PMID:Potentiation of ischemic renal injury by amino acid infusion. 666 84

Postoperative phosphate dynamics were studied in 30 patients who underwent radical surgery for thoracic esophageal cancer and who were postoperatively nourished by total parenteral nutrition. There was a significant fall in the serum phosphate level on the 2nd and 3rd postoperative days in all patients. Postoperative hypophosphatemia was due to an increase in urinary phosphate excretion which was indicated by the fall in TRP% and TmPO4/GFR. A highly significant positive correlation was observed between the increase in urinary phosphate loss and the enhanced secretion of parathyroid hormone which was possibly triggered by surgical stress, a decrease in the serum level of calcium, the action of phosphate buffer or diuretics. All the patients except for those with postoperative pulmonary complications responded to the drop in serum phosphate by renal conservation of phosphate. A slight decrease in the serum level of phosphate was also found on the 6th postoperative day in most patients who were receiving parenteral hyperalimentation. The second fall in phosphate was due to transcellular shifts of phosphate. It is concluded that patients with postoperative pulmonary complications develop severe hypophosphatemia which should be prevented by replacement therapy with phosphate in the immediate postoperative period.
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PMID:[Postoperative hypophosphatemia in patients with cancer of the thoracic esophagus]. 846 25