1977
DOI: 10.1056/nejm197709292971307
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Hyperphosphatemia in Lactic Acidosis

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Cited by 68 publications
(26 citation statements)
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“…22,27 Because dehydration and prerenal azotemia frequently develop in cows with an RDA or AV, 26 we would expect exacerbation of hypochloremia Moreover, lactic acidemia, resulting from increased anaerobic glycolysis, has been shown to be associated with hyperphosphatemia in other species. 28,29 The weak correlation between serum [Pi] and AST activity in data set 1 could not be reproduced in data set 2, possibly because of the smaller number of animals. This weak correlation may be due to muscle weakness in dehydrated animals with an RDA or AV, which leads to a higher risk of muscle trauma and recumbency.…”
Section: Discussionmentioning
confidence: 96%
“…22,27 Because dehydration and prerenal azotemia frequently develop in cows with an RDA or AV, 26 we would expect exacerbation of hypochloremia Moreover, lactic acidemia, resulting from increased anaerobic glycolysis, has been shown to be associated with hyperphosphatemia in other species. 28,29 The weak correlation between serum [Pi] and AST activity in data set 1 could not be reproduced in data set 2, possibly because of the smaller number of animals. This weak correlation may be due to muscle weakness in dehydrated animals with an RDA or AV, which leads to a higher risk of muscle trauma and recumbency.…”
Section: Discussionmentioning
confidence: 96%
“…Although it is well established that some acidoses result in the liberation of phosphorus from organic com pounds within cells [17 ,18], these studies have not included acute observations and have not evaluated the effects of several physiologically important acidifying agents. In this regard, exaggerated hyperphosphatemia was described recently in patients with lactic acidosis [19], and normal or slightly elevated levels have been reported in patients with diabetic ketoacidosis [20], while other data suggest that NH iCI-induced acidosis is not associated with increases in plasma phosphorus [7,21].…”
Section: Experimental Studiesmentioning
confidence: 91%
“…However, presumably the meals consumed by the patients contain potassium as well as carbohydrates, so the effect of glucose, while it plays an important modu lating role, may be offset by the concomitant ingestion of potassium. Recent consumption of a large meal contain ing phosphorus might also acutely modulate serum phos phate levels, as these patients experience phosphate reten tion, and intracellular shift may be impaired by metabolic acidosis [23][24][25][26] and by the fact that while the K+-lowering effect of insulin remains relatively intact in renal fail ure [27], the glucose-lowering effect in response to insulin is impaired [28], As glucose uptake plays a role in intracel lular shift of phosphate [5], this may also tend to accen tuate and prolong increases in serum phosphate following a meal. Patients on the evening shift may thus not have had time to accomplish this redistribution of potassium and phosphate following a large meal which is blunted in the end-stage renal disease patient, and hence they might tend to have higher predialysis potassium and phosphate levels as compared with patients dialyzed on earlier shifts who are likely to eat a smaller meal prior to dialysis or perhaps nothing and have had the overnight period to shift more potassium and phosphorus intracellularly.…”
Section: Discussionmentioning
confidence: 99%