S B Baker1, L I G Worthley. 1. Department of Critical Care Medicine, Flinders University of South Australia, Adelaide, South Australia.
Abstract
OBJECTIVE: To review the components of calcium, phosphate and magnesium metabolism that are relevant to the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported on calcium, phosphate and magnesium disorders in the critically ill patient. SUMMARY OF REVIEW: Calcium, phosphate and magnesium have important intracellular and extracellular functions with their metabolism often linked through common hormonal signals. A predominant portion of total body calcium is unionised within bone and serves an important structural function. Intracellular and extracellular ionised calcium changes are often linked and have important secretory and excitatory roles. The extracellular ionised calcium is carefully regulated by parathyroid hormone and vitamin D, whereas calcitonin is secreted largely in response to hypercalcaemia. Phosphorous is needed for bone structure although it also has an important role in cell wall structure, energy storage as ATP, oxygen transport and acid-base balance. Ionised calcium, in as far as it controls PTH secretion, indirectly controls urinary phosphate excretion. When plasma phosphate increases, tubular reabsorption also increases up to a maximum (TmPO4), thereafter phosphate is excreted. The minimum oral requirement for phosphate is about 20 mmol/day. Magnesium is a predominantly intracellular ion that acts as a metallo-coenzyme in more than 300 phosphate transfer reactions and thus has a critical role in the transfer, storage and utilisation of energy within the body. Extracellular magnesium concentrations are largely controlled by the kidneys with the renal tubular maximum reabsorption (TmMg) controlling the plasma magnesium concentration. CONCLUSIONS: In the critically ill patient calcium, magnesium and phosphate metabolism, are often disturbed with an alteration in intake, increased liberation from bone and damaged tissue and reduced excretion (e.g. during renal failure), causing alterations in extracellular concentrations and subsequent disordered organ function.
OBJECTIVE: To review the components of calcium, phosphate and magnesium metabolism that are relevant to the critically ill patient in a two-part presentation. DATA SOURCES: A review of articles reported on calcium, phosphate and magnesium disorders in the critically ill patient. SUMMARY OF REVIEW: Calcium, phosphate and magnesium have important intracellular and extracellular functions with their metabolism often linked through common hormonal signals. A predominant portion of total body calcium is unionised within bone and serves an important structural function. Intracellular and extracellular ionised calcium changes are often linked and have important secretory and excitatory roles. The extracellular ionised calcium is carefully regulated by parathyroid hormone and vitamin D, whereas calcitonin is secreted largely in response to hypercalcaemia. Phosphorous is needed for bone structure although it also has an important role in cell wall structure, energy storage as ATP, oxygen transport and acid-base balance. Ionised calcium, in as far as it controls PTH secretion, indirectly controls urinary phosphate excretion. When plasma phosphate increases, tubular reabsorption also increases up to a maximum (TmPO4), thereafter phosphate is excreted. The minimum oral requirement for phosphate is about 20 mmol/day. Magnesium is a predominantly intracellular ion that acts as a metallo-coenzyme in more than 300 phosphate transfer reactions and thus has a critical role in the transfer, storage and utilisation of energy within the body. Extracellular magnesium concentrations are largely controlled by the kidneys with the renal tubular maximum reabsorption (TmMg) controlling the plasma magnesium concentration. CONCLUSIONS: In the critically ill patientcalcium, magnesium and phosphate metabolism, are often disturbed with an alteration in intake, increased liberation from bone and damaged tissue and reduced excretion (e.g. during renal failure), causing alterations in extracellular concentrations and subsequent disordered organ function.
Authors: Sneha Gupta; Arijit Biswas; Mohammad Suhail Akhter; Christoph Krettler; Christoph Reinhart; Johannes Dodt; Andreas Reuter; Helen Philippou; Vytautas Ivaskevicius; Johannes Oldenburg Journal: Sci Rep Date: 2016-07-25 Impact factor: 4.379
Authors: Bahare Salehi; Javad Sharifi-Rad; Ana M L Seca; Diana C G A Pinto; Izabela Michalak; Antonio Trincone; Abhay Prakash Mishra; Manisha Nigam; Wissam Zam; Natália Martins Journal: Molecules Date: 2019-11-18 Impact factor: 4.411