GLYCINURIA (glycinuria; + Greek uron wetting glycine) — one of forms of disbolism which is followed by the raised excretion of glycine with urine (more than 200 mg a Day). Secondary changes of kidneys and urinary tract can be G.'s consequence.
Can be hereditary (it is inherited on autosomal dominantly, to the type linked to a floor) and acquired — prerenalny (as «over flow») and renal (as result of disturbance of transport — a reabsorption — glycine in renal tubules).
Hereditarily of the caused primary glycinurias carry G. owing to disturbance of the specific transport mechanism of glycine to group, canalicular G. with degenerative changes of a retina, an iminoglycinuria (Joseph's syndrome), a glucoglycinuria. As the disease separately does not meet, in all cases the combined options come to light.
The glycinuria caused by disturbance of a reabsorption of glycine in renal tubules is characterized by massive excretion of glycine (to 600 mg a day). One of manifestations of this form G. is the nephrolithiasis (see. Nephrolithiasis ). At a research of chemical structure of stones dominance of calcium oxalates is revealed. 2 cases of G. with damage of eyes are described. Right after the birth at two boys the atrophy and a degeneration of a retina was noted. In the subsequent the progressing renal failure developed, and in 8 — 9 years they died from uraemia. At parents and sisters G., but less expressed was noted.
The iminoglycinuria (Joseph's syndrome) is characterized by the increased release of glycine with urine, a prolinuriya and an oksiprolinuriya. It is clinically shown by spasms, disturbance of sexual development. At a laboratory research strengthening of protein in cerebrospinal liquid is noted. The option of an iminoglycinuria is described, at Krom increase in protein in cerebrospinal liquid is not observed and there are no convulsions. Most of patients at this form of a disease somatic are healthy. Mental disorders are possible.
The glucoglycinuria along with the increased release of glycine with urine is characterized by clinic of a diabetes mellitus.
Specific methods of treatment hereditarily of the caused primary G. are not developed.
The forecast is adverse at development of uraemia. Weight of diseases is defined by extent of damage of kidneys, c. N of page and islands of a pancreas.
The glycinuria as a symptom is noted at various disturbances of transport of amino acids in proximal renal tubules. It can be hereditary caused (e.g., at Lowe's syndrome, de Tony's syndrome — Debra — Fankoni, etc.) and acquired (at a diffusion glomerulonephritis, pyelonephritis, medicamentous defeats of tubules of kidneys, etc.).
Treatment comes down to therapy of a basic disease.
Bibliography: Veltishchev Yu. E., etc. Metabolism of oxalic acid is normal also at a nephrolithiasis, Urol, and nefrol., No. 4, page 64, 1975, bibliogr.; L i-p and of i F. eed. Studio di un caso di ipergli-cinuria con calcolosi ossalica e chetoaciduria, Minerva urol., v. 24, p. 212, 1972, bibliogr.
B. P. Lebedev, M. F. Logachev.