Abstract
An alteration in acid-base balance has wide-ranging effects on many systems in the body. It has long been recognized that acid-base regulation is linked to nitrogen metabolism. Ammonium (NH4 +), which is a constituent of normal urine, is excreted in greater quantities in metabolic acidosis. Earlier work showed that the rise in NH4 + excretion in acidosis coincided with a decrease in the rate of urea excretion. When it was realized that the enzyme urease was lacking in mammalian tissues, it was concluded that urea is not a direct source of urinary NH4 +. The discovery that the extraction of glutamine by the kidney contributed significantly to urinary NH4 + focused attention on the renal metabolism of glutamine. It is now well established that the extraction of glutamine by the kidney and the renal mitochondrial deamidation of glutamine are accelerated in chronic metabolic acidosis.
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