Hyperglycinuria is a benign autosomal dominant disorder caused by mutations in one of the neutral amino acid transporters (SLC36A2, SLC6A20, SLC6A19).
Bröer S et. al. (2008) Iminoglycinuria and hyperglycinuria are discrete human phenotypes resulting from complex mutations in proline and glycine transporters.[^]
Oberiter V et. al. (1978) Hyperglycinuria with nephrolithiasis.[^]
Greene ML et. al. (1973) Familial hyperglycinuria. New defect in renal tubular transport of glycine and imino acids.[^]
Tancredi F et. al. (1970) Renal iminoglycinuria without intestinal malabsorption of glycine and imino acids.[^]
None (1968) Renal tubular transport of proline, hydroxyproline, and glycine. 3. Genetic basis for more than one mode of transport in human kidney.[^]
Adams CW et. al. (1967) Persistent tachycardia, paroxymal hypertension, and seizures: association with hyperglycinuria, dominantly inherited microphthalmia, and cataracts.[^]
DE VRIES A et. al. (1957) Glycinuria, a hereditary disorder associated with nephrolithiasis.[^]