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Glycosuria
Last reviewed: 23.04.2024
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Causes of the glycosuria
Increased excretion of glucose in the urine due to various reasons. In healthy individuals, glucosuria is not expressed, it cannot be determined by routine laboratory methods, and the increase in the severity of glucosuria, for example, when conducting a glucose tolerance test is transient.
Renal glucosuria is often an independent disease; it is usually discovered by chance; polyuria and polydipsia are extremely rare. Sometimes renal glucosuria is accompanied by other tubulopathies, including in the composition of Syndrome.
Among the possible causes of types 1 and 2 of renal glucosuria, mutations of one of the tubular carrier proteins that reabsorb glucose with two sodium ions are discussed. However, the distinction between these options at the genetic level is difficult, because in one family, cases of renal glucosuria of both type 1 and 2 are diagnosed.
Three types of isolated renal glucosuria are distinguished.
- In type 1 renal glucosuria, a significant decrease in glucose reabsorption in the proximal tubule is observed with relatively preserved values of glomerular filtration. The ratio of the maximum glucose reabsorption to GFR in patients with type 1 renal glucosuria is reduced.
- Type 2 renal glucosuria is characterized by a significant increase in glucose reabsorption threshold by proximal tubule epithelial cells. The ratio of maximum glucose reabsorption to GFR is close to normal.
- It is extremely rare to observe type 0 renal glucosuria, in which the ability of epithelial cells of proximal tubules to reabsorb glucose is completely absent. The development of glucosuria is associated with a mutation causing the absence or significant defect, accompanied by the complete loss of the reabsorbing function, of the canalicular proteins transporting glucose. In these patients, the magnitude of glycosuria reaches especially high numbers.
There are more rare variants of renal glucosuria. A combination of type 1 renal glucosuria with glycineuria and hyperphosphaturia has been described; however, there are no other signs of Fanconi syndrome, including aminoaciduria.
When a combination of renal glucosuria with glycineuria patients often suffer from cystic fibrosis. It is believed that this variant of tubulopathy is inherited in an autosomal dominant manner.
A mutation has been identified that causes a significant decrease in the activity of the intestinal transporter for glucose and galactose. At the same time, these patients exhibit impaired glucose reabsorption in the tubules, often similar to type 2 renal glucosuria.
Renal glucosuria is observed in pregnant women. Its development is due to a significant physiological increase in GFR with relatively stable indicators of maximum glucose reabsorption. Glycosuria of pregnant women is transient.
Causes of glycosuria
Nature of glycosuria |
The reasons |
Glycosuria overflow (with hyperglycemia) |
|
Iatrogenic |
Medications (corticosteroids) Infusion solutions (dextrose solutions) Parenteral nutrition |
Renal |
Type A Type B Type O Fanconi Syndrome Impaired absorption of glucose and galactose in the intestine (selective malabsorption of glucose and galactose) Glycosuria pregnant |
Other species |
Intracranial Hypertension Hypercatabolic states (extensive burns) Endocrine gland dysfunctions Sepsis Malignant tumors |
Diagnostics of the glycosuria
[9], [10], [11], [12], [13], [14], [15], [16],
Laboratory diagnosis of glycosuria
Renal glucosuria is diagnosed by the presence of glucose in the urine on an empty stomach with a normal level of glycemia. The renal origin of glycosuria is confirmed by the detection of glucose in at least three urine samples and the absence of changes in the glycemic curve during the glucose tolerance test.
In renal glucosuria, the amount of glucose excretion in the urine varies from 500 mg / day to 100 g / day or more, in most patients it is 1-30 g / day.
What do need to examine?
What tests are needed?