glycosurias

Glycosuria is the presence of glucose in the urine. It occurs when the amount of glucose filtered by the kidneys exceeds the proximal tubule’s capacity to reabsorb it, or when proximal tubular reabsorption is impaired. Under normal conditions, glucose filtered by the glomerulus is almost completely reabsorbed in the proximal tubule via SGLT2 and SGLT1 transporters, with a renal threshold of about 180 mg/dL. When plasma glucose surpasses this threshold, or when tubular reabsorption is defective, glucose appears in the urine.

Causes can be broadly categorized as overflow (hyperglycemia-driven) glycosuria and renal glycosuria due to tubular dysfunction. The most common cause in adults is hyperglycemia from diabetes mellitus. Other causes include physiological glycosuria in pregnancy, renal glycosuria from SGLT2 transporter mutations, Fanconi syndrome (a generalized proximal tubule disorder), and drug-induced glycosuria (notably SGLT2 inhibitors). Less commonly, severe stress or alcohol use can contribute.

Clinical features vary; glycosuria may be detected incidentally on urinalysis or dipstick testing, and in diabetes may accompany polyuria and polydipsia. In renal tubular disorders, glycosuria often occurs with other solute losses such as amino acids or bicarbonate.

Evaluation typically starts with confirming glycosuria on urine testing and measuring plasma glucose or HbA1c to assess glycemic status. If glucose is elevated, workup focuses on diabetes. If plasma glucose is normal, assess renal tubule function and consider causes like Fanconi syndrome or genetic renal glycosuria.

Management targets the underlying cause: glycemic control for diabetes, monitoring and pregnancy-related considerations in gestational cases, and supportive care or investigation for renal tubulopathies. In asymptomatic renal glycosuria, no specific treatment is usually required.