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Glucosuria
Last reviewed: 04.07.2025

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Causes glucosuria
Increased urinary glucose excretion is caused by various reasons. In healthy individuals, glucosuria is not expressed, it cannot be determined by routine laboratory methods, and an 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 observed extremely rarely. Sometimes renal glucosuria is accompanied by other tubulopathies, including those in Fanconi syndrome.
Among the possible causes of renal glucosuria types 1 and 2, mutations of one of the tubular transport proteins that reabsorb glucose together with two sodium ions are discussed. However, distinguishing these variants at the genetic level is difficult, since cases of renal glucosuria of both types 1 and 2 are diagnosed in one family.
There are three types of isolated renal glucosuria.
- In renal glucosuria type 1, a significant decrease in glucose reabsorption in the proximal tubules is observed with relatively preserved values of glomerular filtration. The ratio of maximum glucose reabsorption to SCF in patients with renal glucosuria type 1 is reduced.
- Renal glucosuria type 2 is characterized by a significant increase in the threshold of glucose reabsorption by epithelial cells of the proximal tubules. The ratio of maximum glucose reabsorption to SCF is close to normal.
- Renal glucosuria type 0 is extremely rare, in which the ability of proximal tubular epithelial cells to reabsorb glucose is completely absent. The development of glucosuria is associated with a mutation that causes the absence or significant defect, accompanied by a complete loss of the reabsorbing function, of tubular proteins that transport glucose. In these patients, glucosuria values reach particularly high figures.
There are also rarer variants of renal glucosuria. A combination of renal glucosuria type 1 with glycinuria and hyperphosphaturia has been described; other signs of Fanconi syndrome, including aminoaciduria, are absent.
When renal glucosuria is combined with glycinuria, patients often suffer from cystic fibrosis. It is believed that this variant of tubulopathy is inherited in an autosomal dominant manner.
A mutation causing a significant decrease in the activity of the intestinal transporter for glucose and galactose has been identified. At the same time, these patients have impaired glucose reabsorption in the tubules, often similar to renal glucosuria type 2.
Renal glucosuria is observed in pregnant women. Its development is due to a significant physiological increase in SCF with relatively stable indicators of maximum glucose reabsorption. Glucosuria in pregnant women is transient.
Causes of glucosuria
The nature of glucosuria |
Reasons |
Overflow glycosuria (with hyperglycemia) |
|
Iatrogenic |
Medicines (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) Glucosuria in pregnancy |
Other types |
Intracranial hypertension Hypercatabolic conditions (extensive burns) Dysfunctions of endocrine glands Sepsis Malignant tumors |
Diagnostics glucosuria
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Laboratory diagnostics of glucosuria
Renal glucosuria is diagnosed by the presence of glucose in the urine on an empty stomach with a normal glycemic level. Renal origin of glucosuria is confirmed by the detection of glucose in at least three portions of urine and the absence of changes in the glycemic curve during a 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?