1. Arterial concentration and arterial-venous differences of glutamine across the kidney, forearm, hepato—splanchnic bed and brain were measured in patients with chronic renal insufficiency and in patients with normally functioning kidneys before and during chronic ammonium chloride acidosis.
2. In chronic renal insufficiency and in chronic metabolic acidosis there is a rise in glutamine release from the muscle and a suppression of glutamine uptake by the hepato—splanchnic bed and the brain.
3. In chronic renal insufficiency arterial glutamine concentration is significantly increased in comparison with subjects with normal renal function and either normal acid-base balance or chronic metabolic acidosis.
4. In patients with chronic renal insufficiency the kidney extracts negligible amounts of glutamine, which cannot account for the renal ammonia production measured in the same patients.
Hyperammonaemic encephalopathy and severe metabolic acidosis in a patient with chronic renal insufficiency years after ureterosigmoidostomy
