GLYCOSURIA (glycosuria; grech, sweet + uron wetting glykys; synonym glucosuria) — release of glucose with urine. Normal in urine only the traces of glucose which are usually not revealed by the methods applied in a wedge, laboratories can be found (not always).
Emergence of glucose in urine can be caused by various reasons. Comes at disturbance of a reabsorption of glucose in tubules of kidneys in connection with decrease in intensity of processes of phosphorylation and dephosphorylation of glucose. It is observed at a hyperglycemia of a different origin (see. Hyperglycemia ), when concentration of glucose in blood exceeds a renal threshold for glucose. The renal threshold, i.e. concentration of glucose in blood, at a cut appears G., fluctuates within 160 — 200 mg of %. It can be observed also at normal concentration of glucose in blood, usually in connection with disturbance of enzymatic processes in tubules of the kidneys causing a reabsorption of glucose.
Experimentally reflex hyperglycemia from the subsequent G. was found by K. Bernard «a sugar prick» in a bottom of the fourth cerebral cavity. In the latest researches the important role of some hormones is revealed (AKTG, glucocorticoids, a glucagon, etc.) in implementation of effect of «a sugar prick», and also reflex impacts on c. N of page. Experimentally G. can be caused also administration of somatotropic and adrenocorticotropic hormones, glucocorticoids, a glucagon, and also mesoxalyl urea which selectively strikes beta cells of islets of Langerhans (so-called alloxan diabetes). Renal G. can be reproduced administration of vegetable glucoside of the floridzin blocking processes of phosphorylation in cells of an epithelium of renal tubules.
Forms of a glycosuria
Allocate the following Forms. Alimentary glycosuria results from consumption of excessive amounts of the carbohydrates with food (e.g., saccharobiose) which are especially quickly soaked up after their splitting in intestines that leads to the increase in a sugar content in blood exceeding a threshold of a reabsorption of glucose in kidneys. At alimentary G. the content of glucose in urine is usually small; In these cases it is observed during 2 — 4 hours after meal.
Reflex glycosuria (or central, nervous) results from an overstrain of the subcrustal centers regulating carbohydrate metabolism (see) that can come at various emotional and stressful conditions of an organism.
Group of hormonal forms of a glycosuria includes G. of a diabetic, pituitary and adrenal origin, and also thyrogenic G., edges meets very seldom.
Diabetic glycosuria (the most frequent of hormonal) is result of substantial increase of concentration of glucose in blood owing to absolute or relative insulyarny insufficiency (see a diabetes mellitus). Loss or weakening of the regulating effect of insulin on carbohydrate metabolism (see. Insulin ) leads to delay of transport of glucose from blood and intercellular spaces in cells of fabrics, and also to acceleration of a glyukozoobrazovaniye from not carbohydrate substances in a liver and a bast layer of kidneys (gluconeogenesis). Is a consequence of excess of glucose in a blood channel. At a severe form of diabetes concentration of glucose in blood can exceed 1000 mg of %, and release at the same time of glucose kidneys can be more than 100 g per day.
Pituitary. it is observed at the tumors of a hypophysis which are followed by strengthening of an inkretion of somatotropic (STG) and adrenocorticotropic (AKTG) of hormones. STG stimulates an inkretion glucagon (see), processes the gluconeogenesis and and at long supersecretion slows down formation of insulin. The strengthened inkretion of AKTG leads to increase in products of glucocorticoids (see. Glucocorticoid hormones ), stimulating a gluconeogenesis and strengthening of a glyukozoobrazovaniye in a liver and kidneys. Can arise at tumors of a medulla of adrenal glands (see. Pheochromocytoma ) owing to strengthening of secretion catecholamines (see), stimulating fosforolitichesky splitting of a glycogen in a liver and intake of glucose in blood.
Renal glucosuria arises at normal concentration of glucose in blood owing to dysfunction of the enzymatic systems providing the return absorption of glucose from primary urine in renal tubules. Renal G. — genetically determined disease, apparently, caused by the single dominant gene which is not connected with a floor.
However renal G. can arise at toxicoses of pregnancy and diseases of kidneys (a glomerulonephritis, a nephrosis, etc.), at some bacterial intoxications.
It is very rare hepatic a glycosuria, caused by functional inability of a liver to regulate a homeostasis of glucose in blood.
The glycosuria at children
With urine of the healthy child is allocated per day to 16 — 130 mg of glucose which are not found usual qualitative tests. A renal threshold of a plant louse of glucose (190 — 230 mg of %) and assimilatory border of glucose (amount of glucose in grams on 1 kg of body weight, a cut the child is capable to transfer without G.'s development) are inversely proportional to age of children and is much higher, than at adults.
The alimentary glycosuria is inherent to newborns and children of chest age, especially premature, owing to enzymatic insufficiency of system of regulation of assimilation of glucose. Arises in 30 — 60 min. after loading glucose and proceeds slightly longer, than at adults (to 5 hours). Alimentary G. is observed at dyspepsias (see), exudative diathesis (see. Exudative and catarral diathesis ) and some other states. Conditionally carries to alimentary G.'s category hereditary y the glucose acquired disturbance in system allocation caused by decrease in a renal threshold of its reabsorption.
Reflex glycosuria (central, nervous). Children have mechanical, traumatic, chemical and toxic irritations of a nervous system quicker and easier, than at adults, cause. Inclusion of system a hypothalamus — a hypophysis — bark of adrenal glands through final metabolic effect of hormones at children strengthens glycolysis (see) and a gluconeogenesis, privodishchy to a compensatory hyperglycemia and it is consecutive to a glycosuria. Reflex G. is usually short. It accompanies acute patol. to processes (bacterial and viral infections, meningitis, encephalitis, etc.), it is noted at asphyxia and craniocereberal hemorrhages at birth trauma, a hyperthermia, an anesthesia, etc., and also at patol, processes in c. N of page (tumors of a brain, craniocereberal injury, residual phenomena of damages of a brain, etc.).
Hormonal a glycosuria it is observed in the early childhood at a hypernephroma, in more senior — at a thyrotoxicosis, Cushing's syndrome, a hyperpituitarism, a pheochromocytoma.
Separately allocate diabetic G. though at children she is less than at adults, generally at a diabetes mellitus (see. a diabetes mellitus, at children ); feature of this form are sharp fluctuations of G. within a day and frequent lack of dependence of G. on the content of glucose in blood. Conditionally carry G. at children of pubertal age to hormonal; include G. at a number of exchange diseases in the same group (e.g., obesity).
The renal glycosuria at children, as well as at adults is connected with disturbance of a resorption of glucose in tubules, but is observed much more often in the form of the hereditary or acquired renal diabetes (see. Diabetes renal ). Carry secondary renal G. to them at hron, diseases of kidneys, Albright's syndrome — Laytvuda (see. Laytvuda — Albright a syndrome ), a nefrotichny glikozurichesky nanism with gipofosfatemichesky rickets of Fankoni and dr. and cyclic (intermittent) G. — a row from them is inherent only in children.
Hepatic a glycosuria are connected with lability of glikopeksichesky function of a liver and meet much more often than at adults.
To establish an origin of a glycosuria at adults: and children usually easily. At renal G. the content of glucose in blood remains within norm. Leads the use of excessive amount of carbohydrates with food to alimentary G.; such G. quickly disappears. As a result of a long and constant hyperglycemia confirms an average or severe form of diabetes. Any form G. is established by definition of availability of glucose in urine along with the analysis of content of glucose in blood; in some cases this research needs to be conducted against the background of peroral standard loading glucose. At patients with diabetes results of analyses of G. (and its changes per day) and a glycemia allow to judge weight of a state and to carry out control of efficiency of treatment (see. Altgauzena method , Benedikta methods , Gorodetsky methods , Carbohydrates ).
Bibliography: Genes S. G. Diabetes mellitus, MTjT 1963, bibliogr.; Diabetes, under the editorship of R. Rkuilyams, the lane with English, M., 1964; At-to about in about to and y M. A. Children's endocrinology, M., 1971; Ilyin V. S. Mechanism of action инс^ина, Vestn. USSR Academy of Medical Sciences, No. 8, page 3, 196 of $; ** L of e y with about N L. G. Sakhar of blood, Regulyatsiya4 of a sugar content in blood at animals and. the person, M. — L., 1962; The Multivolume guide to pathological physiology, under the editorship of H. N. Si-rotinina, t. 3, page 617, M., 1966, bibliogr.; Multivolume guide to pediatrics, sprout. Yu. F. Dombrovskoy, t. 10, page 87, M., 1965, iibliogr.; The guide to endocrinology, under r1ed. B. V. Alyoshina, etc., M., 1973, bibliogr.; Wu Yi of l to and N with L. Diagnosis and treatment of endocrine disturbances at detoky and youthful age, the lane with English, M., 1963; In about d a n s k at M. and. In about-d a n s k at O. of Biochemistry of disease, N.Y., 1957; James R. Page of a. Chase G. R. Evaluation of some commonly used semiquanti-tative methods for urinary glucose and ketone determinations, Diabetes, v. 23, p. 47 |, 1974; Joslin E.P. Diabetes iheHitus, Philadelphia, 1971.
V. S. Ilyin; A. V. Kartelishev (ped.).