TmP/GFR and Ionized Calcium in the Management of Severe Hypophosphataemia

Coyle, Sallyeana; Masters, P W; Barnard, D. L.

doi:10.1177/000456329202900516

Cited by 16 publications

(8 citation statements)

References 6 publications

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“…The mean renal threshold phosphate concentrations were similar between thermally injured and multiple trauma patients which is within the anticipated normal range of 2.5 mg/dL to 4.2 mg/dL. 38 When combined with the urinary excretion data, these data indicate that our thermally injured patients did not have a defect in renal tubular reabsorption. We also examined urinary phosphorus clearance, which describes the relationship between urinary phosphorus excretion and serum phosphorus concentration.…”

supporting

confidence: 66%

A Comparison of Renal Phosphorus Regulation in Thermally Injured and Multiple Trauma Patients Receiving Specialized Nutrition Support

Dickerson¹,

Gervasio²,

Sherman³

et al. 2001

J Parenter Enteral Nutr

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supporting

confidence: 66%

A Comparison of Renal Phosphorus Regulation in Thermally Injured and Multiple Trauma Patients Receiving Specialized Nutrition Support

Dickerson¹,

Gervasio²,

Sherman³

et al. 2001

J Parenter Enteral Nutr

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“…At very low serum phosphate levels, most cells, including renal tubular cells, become phosphate depleted. This results in low intracellular adenosine triphosphate (ATP) concentrations and subsequently in impaired tubular reabsorption of phosphate (Coyle, Masters, & Barnard, 1992). Thus, in cases of severe phosphate depletion, TmP/GFR can be very low, whatever the primary cause.…”

Section: Discussionmentioning

confidence: 99%

Reversible tubular dysfunction that mimicked Fanconi's syndrome in a patient with anorexia nervosa

Alexandridis

Liamis

Elisaf

2001

Intl J Eating Disorders

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Patients with anorexia nervosa exhibit acid-base and electrolyte disturbances. Hypophosphatemia is commonly found in these patients during nutritional recovery. However, marked, possibly, life-threatening hypophosphatemia associated with proximal tubular dysfunction has not been previously described. We report a case of anorexia nervosa complicated by a nonacidotic proximal tubulopathy, which was manifested by renal glycosuria, as well as inappropriate phosphaturia and uricosuria resulting in hypophosphatemia and hypouricemia.

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“…Another suggested mechanism is depletion of intracellular phosphate in renal tubular cells, potentially interfering with reabsorption of urinary phosphate [15]. …”

Section: Case Presentationmentioning

confidence: 99%

Hyperphosphatemia during spontaneous tumor lysis syndrome culminate in severe hypophosphatemia at the time of blast crisis of Phneg CML to acute myelomoncytic leukemia

et al. 2012

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Extreme swing of phosphor from severe hyperphosphatemia to severe hypophosphatemia in a patient with blast crisis of myeloid origin was the result of imbalance between massive apoptosis of leukemic cells in the context of spontaneous tumor lysis syndrome and massive production of leukemic cells with only 1% of blast in peripheral blood. The mutated p53 protein suggested acting as oncogene in the presented case and possibly affecting phosphor status.

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TmP/GFR and Ionized Calcium in the Management of Severe Hypophosphataemia

Cited by 16 publications

References 6 publications

A Comparison of Renal Phosphorus Regulation in Thermally Injured and Multiple Trauma Patients Receiving Specialized Nutrition Support

A Comparison of Renal Phosphorus Regulation in Thermally Injured and Multiple Trauma Patients Receiving Specialized Nutrition Support

Reversible tubular dysfunction that mimicked Fanconi's syndrome in a patient with anorexia nervosa

Hyperphosphatemia during spontaneous tumor lysis syndrome culminate in severe hypophosphatemia at the time of blast crisis of Phneg CML to acute myelomoncytic leukemia

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