Acid–base metabolism: implications for kidney stosne formation

Abstract

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, ${{\rm NH}}_{{{\rm 3}}} {\hbox{ + H}}^{{\hbox{ + }}} {\hbox{ }} \leftrightarrow {\hbox{ NH}}^{{\hbox{ + }}}_{{{\rm 4}}}$. 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 ${{\rm NH}}^{{\hbox{ + }}}_{{{\rm 4}}}$ 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.