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].