The physiology and pathophysiology of renal H+ ion excretion and urinary
buffer systems are reviewed. The main focus is on the two major conditions related to
acid-base metabolism that cause
kidney stone formation, i.e.,
distal renal tubular acidosis (
dRTA) and abnormally low urine pH with subsequent
uric acid stone formation. Both the entities can be seen on the background of disturbances of the major urinary
buffer system, NH3+ <--> NH4+. On the one hand, reduced distal tubular secretion of H+
ions results in an abnormally high urinary pH and either incomplete or complete
dRTA. On the other hand, reduced production/availability of NH4+ is the cause of an abnormally low urinary pH, which predisposes to
uric acid stone formation. Most recent research indicates that the latter abnormality may be a renal manifestation of the increasingly prevalent
metabolic syndrome. Despite opposite deviations from normal urinary pH values, both the
dRTA and
uric acid stone formation due to low urinary pH require the same treatment, i.e.,
alkali. In the
dRTA,
alkali is needed for improving the body's
buffer capacity, whereas the goal of
alkali treatment in
uric acid stone formers is to increase the urinary pH to 6.2-6.8 in order to minimize
uric acid crystallization.