RT Book, Section
A1 Hruska, Keith A.
A2 Lerma, Edgar V.
A2 Berns, Jeffrey S.
A2 Nissenson, Allen R.
SR Print(0)
ID 6342875
T1 Chapter 7. Disorders of Phosphate Balance: Hypophosphatemia & Hyperphosphatemia
T2 CURRENT Diagnosis & Treatment: Nephrology & Hypertension
YR 2009
FD 2009
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-144787-4
LK accessmedicine.mhmedical.com/content.aspx?aid=6342875
RD 2024/04/19
AB New  data  demonstrate  that  serum  phosphate,  similar  to  serum  calcium,  is  a  signaling  molecule.  The  mechanisms  for  sensing  serum  phosphate  signal  transduction  concentration  are  not  understood.  This  chapter  considers  serum  phosphorus  in  a  context  greater  than  mineral  and  metabolic  homeostasis.  The  bulk  of  total  body  phosphate  (85%)  is  in  the  bone  as  part  of  the  mineralized  extracellular  matrix.  This  phosphate  pool  is  accessible,  albeit  in  a  limited  fashion  through  bone  resorption.  Phosphate  is  a  predominantly  intracellular  anion  with  an  estimated  concentration  of  approximately  100  mmol/L,  most  of  which  is  either  complexed  or  bound  to  proteins  or  lipids.  Serum  phosphorus  concentration  varies  with  age,  time  of  day,  fasting  state,  and  season.  It  is  higher  in  children  than  adults.  Phosphorus  levels  exhibit  a  diurnal  variation  with  the  lowest  phosphate  level  occurring  near  noon.  Serum  phosphorus  concentration  is  regulated  by  diet,  hormones,  and  physical  factors  such  as  pH.  Importantly,  because  phosphate  moves  in  and  out  of  cells  under  several  influences,  the  serum  concentration  of  phosphorus  may  not  reflect  phosphate  stores.