What type of aminoaciduria is characterized by excess amino acids due to defective renal tubular transport?

Renal-type aminoaciduria is characterized by an inability of the renal tubules to reabsorb specific amino acids, leading to their excess in the urine. This condition arises from defects in the renal tubular transport mechanisms responsible for reabsorbing amino acids filtered through the glomerulus. As a result, despite normal serum levels of amino acids, these substances accumulate in the urine due to the impaired reabsorption at the renal tubule level.

In contexts where amino acids are present in normal or elevated amounts in the blood, such as in overflow-type aminoaciduria, the renal tubules are unable to handle the increased load, but that differs from renal-type aminoaciduria where the issue is strictly due to impairment within the renal tubules irrespective of blood levels. In primary inherited aminoacidurias, specific genetic defects lead to a total lack of transport capabilities for particular amino acids, while secondary-acquired aminoaciduria could arise from various conditions affecting reabsorption but is typically not as directly tied to the inherent tubular transport mechanisms as renal-type aminoaciduria.