Glucosuria Nutritional

Nutritional glucosuria should be considered as an early clinical manifestation of more serious metabolic disorders, manifested by impaired carbohydrate metabolism, as well as hyperglycemia, but without confirmation by laboratory indicators. This is one of the pressing and intractable problems of clinical medicine, caused by the body’s inability to use glucose as effectively as other carbohydrates. The reasons for the disruption of such processes can be hereditary or acquired, but they have one thing in common - they are based on metabolic changes at the cellular level.

Clinical analysis showed an increase in fasting blood glucose levels to 7.5-8.0 mmol/l and 2 hours after meals to 8.9 mmol/l, which indicates a pronounced tendency to develop manifest carbohydrate disorders. When examining a biochemical blood test, disorders of lipid and protein metabolism were revealed, such as dysproteinemia due to an increased level of beta-lipoproteins in combination with an increased content of cholesterol and triglycerides. The presence of low-normal levels of glycosylated hemoglobin indicated chronic hyperglycemia. In order to resolve the issue of the causes of congenital glycosuria, nutritional examinations of parents and their health status were carried out the necessary instrumental studies. They included non-invasive ultrasound examination of the abdominal cavity, liver, kidneys with assessment of their size, structure and function, consultation and examination by an endocrinologist. For a more accurate conclusion, a course of treatment by a pediatric nutritionist specializing in childhood diabetes was recommended. It is also recommended to conduct an annual assessment of the status of all indicators of carbohydrate, lipid and protein metabolism, including studies of platelets and platelet aggregation. The presence and nature of the severity of affect should be considered as a criterion for prescribing preventive treatment or pharmacotherapy.

Glucosuric deficiency Nutritional diabetes is characterized by chronic insufficiency of endogenous insulin secretion based on the principle of depletion of the insular pool of cells. Such patients, as a rule, have diabetic ketoacidosis and fasting hyperglycemia, decreased body weight, and early complications such as gangrene of the fingers, secondary neuropathic defect (nephropathy, polyneuropathy), characteristic changes in the fundus, and neuropsychiatric disorders.