1954
DOI: 10.1001/jama.1954.03690280001001
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The Management of Acute Renal Insufficiency

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1955
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Cited by 79 publications
(10 citation statements)
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“…These effects are short-lived (1-2 hr) and must be reinforced by exchange resins or dialysis. Other slower emergency treatments include infusion of 200 ml of hypertonic (5%) sodium chloride or 100 ml of 10% calcium gluconate (Meroney & Herndon, 1954) or most commonly infusion of hypertonic glucose together with insulin (100-200 ml 50% glucose + 20 units soluble insulin) in order to deposit glycogen with associated potassium and phosphate into the cells (Merrill et al, 1950). This last treatment is rather slow in onset (j-1 hr) but its effect may last for several hours.…”
Section: Potassiummentioning
confidence: 99%
“…These effects are short-lived (1-2 hr) and must be reinforced by exchange resins or dialysis. Other slower emergency treatments include infusion of 200 ml of hypertonic (5%) sodium chloride or 100 ml of 10% calcium gluconate (Meroney & Herndon, 1954) or most commonly infusion of hypertonic glucose together with insulin (100-200 ml 50% glucose + 20 units soluble insulin) in order to deposit glycogen with associated potassium and phosphate into the cells (Merrill et al, 1950). This last treatment is rather slow in onset (j-1 hr) but its effect may last for several hours.…”
Section: Potassiummentioning
confidence: 99%
“…13 This makes the management of acute renal failure in conditions of trauma, burns and surgery much more complicated, but failure to debride and drain will lead to disproportionate elevations of nitrogenous end products, serum potassium and phosphate.…”
Section: Managing the Catabolic Responsementioning
confidence: 99%
“…Marked hy pocalcemia, which occurred during the oliguric phase, is a well-recognized biochemical feature of this disorder, and those patients who are initially hypocalcemic, may become hypercalcemic during the diuretic phase of acute renal failure [1][2][3]. Early studies suggest that the severity of hypocalcemia varies directly with hyperphospha temia, is related with the intensity of muscle injury and may be due to the rapid deposition of calcium salts in traumatized skeletal muscle and cytoplasmic sequestra tion [I, 2], Possible explanations for hypercalcemia in clude mobilizations of calcium already sequestered in muscle [4,5], volume depletion and autonomous secre tion of parathyroid hormone (PTH) [6,7].…”
mentioning
confidence: 99%