Acidosis and nutrition

Citation
Jd. Louden et al., Acidosis and nutrition, KIDNEY INT, 56, 1999, pp. S85-S88
Citations number
33
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
56
Year of publication
1999
Supplement
73
Pages
S85 - S88
Database
ISI
SICI code
0085-2538(199912)56:<S85:AAN>2.0.ZU;2-Z
Abstract
In recent years there has been increasing evidence for the deleterious effe ct of acidosis on a number of fundamental systems of the body including nut rition [1, 2]. Approximately 70 mmol of hydrogen ions are produced daily by the body, and to maintain acid-base balance there must be an equivalent ne t acid secretion by the kidney. It is remarkable that extracellular fluid ( ECF) pH is maintained within a very narrow range of 7.35-7.45 (35-45 nM), r eflecting the fundamental importance of pH on many aspects of basic cellula r function particularly proteins. It is important to differentiate between the terms acidosis and acidemia. The former is a pathophysiologic process t ending to acidify body fluids: whereas the latter occurs when the ECF hydro gen ion concentration is above the normal range. It is possible to be acido tic (with a reduced serum bicarbonate) but not acidemic because of appropri ate buffering of hydrogen ions. The major extracellular buffer is the carbo nic acid/hydrogen carbonate system with plasma proteins and hemoglobin cont ributing significantly less. The major intra; cellular buffer is protein fo llowed by bone [3]. The type of acidosis seen in patients with chronic rena l failure changes with decreasing GFR; initially a non-anion gap acidosis i s observed secondary to the loss of bicarbonate from the proximal tubule an d impaired excretion in the distal tubule. With increasing severity of rena l impairment, failure to excrete organic and inorganic acids results in an increased anion gap [4, 5].