Glükoosiuria

Glükoosiuria, or glycosuria, is the presence of glucose in the urine. Normally, the kidneys reabsorb almost all filtered glucose in the proximal tubules, so urine contains little to no glucose. Glucose appears in the urine when the filtered glucose load exceeds the reabsorptive capacity, or when proximal tubule transport is impaired. The renal threshold for glucose is typically around 180 mg/dL but varies among individuals.

Common causes and forms include: renal glycosuria, due to mutations or dysfunction of the renal glucose transporters (such as SGLT2) or broader proximal tubule disorders (Fanconi syndrome); gestational glycosuria, which can occur in pregnancy due to increased filtration and altered reabsorption; and glycosuria secondary to hyperglycemia from diabetes mellitus or other states of high blood glucose. Drugs that inhibit SGLT2, used to treat type 2 diabetes, intentionally induce glycosuria as part of their mechanism. Infections or dehydration can exacerbate symptoms when glucose is present in urine.

Clinical features often include polyuria and polydipsia if glycosuria reflects significant hyperglycemia; otherwise glycosuria may be asymptomatic and detected by urine testing. Diagnosis usually begins with a urine dipstick test showing glucose, followed by confirmatory quantitative measurements and assessment of blood glucose and diabetes markers (fasting plasma glucose, HbA1c). In pregnancy, evaluation for gestational diabetes is recommended if glycosuria is detected.

Management focuses on the underlying cause: glycemic control in diabetes, monitoring and treating urinary tract infections if present, and addressing renal tubule disorders when identified. Glycosuria itself is typically not harmful, but persistent or significant glycosuria signals an underlying condition that may require treatment.