glucosurie

Glucosuria, or glucosuria, is the presence of glucose in the urine. In a healthy person, nearly all filtered glucose is reabsorbed in the proximal tubule, so urine normally contains little to no glucose. Glucosuria occurs when filtered glucose exceeds the kidney’s reabsorptive capacity or when proximal tubule function is impaired.

Most glucosuria arises from elevated blood glucose levels, as seen in diabetes mellitus or transient stress hyperglycemia, and in pregnancy. The renal threshold for glucose is about 180 mg/dL (roughly 10 mmol/L); when plasma glucose rises above this level, glucose spills into the urine. Less commonly, glucosuria reflects a proximal tubule defect (renal or euglycemic glucosuria) such as Fanconi syndrome or certain genetic conditions, where glucose reabsorption is reduced even with normal blood glucose. Drugs that block SGLT2 transporters, used to treat diabetes, can also cause pharmacologic glucosuria.

Diagnosis is usually made by urinalysis showing glucose in urine. Urine dipsticks can detect glucose but may miss low levels; confirmation with quantitative urine glucose testing and correlation with serum glucose is common. If glucosuria is detected, clinicians typically assess fasting glucose or HbA1c to evaluate for diabetes and review renal function and electrolytes. If fasting glucose is normal and glucosuria persists, evaluation for proximal tubule disorders or medication effects is warranted.

Clinical significance: glucosuria itself does not define a disease but indicates either hyperglycemia or a renal reabsorption abnormality. It is associated with an increased risk of urinary tract and genital infections due to glucose in urine and, with osmotic diuresis, dehydration.

Management depends on the underlying cause. In diabetes, glycemic control usually reduces glucosuria. In renal glucosuria, monitoring suffices. If drug-induced, adjusting or stopping the medication may be appropriate. Persistent glucosuria requires medical evaluation to identify the cause.