<unk>  involves excretion of urinary glutamate and aspartate, resulting from the incomplete reabsorption of anionic amino acids from the glomerular filtrate in the kidney. This affects a diseased individual's amino acid pool, as they will have to spend additional resources to replenish the amino acids which would have otherwise been present. Additionally, glutamate transporters are responsible for the synaptic release of the glutamate (neurotransmitter) within the interneuronal synaptic cleft. This hindrance of functionality in individuals with<unk>  may be related to growth retardation, intellectual disability, and a tendency toward fasting hypoglycemia and ketoacidosis.<unk>  is diagnosed by finding the increased presence of glutamate and aspartate in the urine.
Dicarboxylic aminoaciduria
Hawkinsinuria
Aspartylglucosaminuria
Essential fructosuria
Alkaptonuria
Homocystinuria
Alpha-aminoadipic and alpha-ketoadipic aciduria
Urocanic aciduria