glycosuria

Glycosuria is the excretion of glucose in urine. It most commonly results when blood glucose exceeds the kidney’s reabsorptive capacity, but it can also occur when proximal tubule glucose reabsorption is impaired.

Two main mechanisms are recognized: osmotic or overflow glycosuria from hyperglycemia (as in diabetes mellitus or pregnancy-related hyperglycemia), and renal glycosuria from defects in proximal tubule transport (genetic or acquired conditions such as Fanconi syndrome). Medications that promote glycosuria, notably sodium-glucose cotransporter 2 (SGLT2) inhibitors used to treat diabetes, can also cause this condition.

Clinical presentation ranges from asymptomatic to symptoms of osmotic diuresis, including polyuria and dehydration, when glycosuria accompanies significant hyperglycemia. Renal glycosuria with normal plasma glucose is usually mild or clinically insignificant.

Diagnosis starts with detection of glucose in urine, commonly by dipstick testing, followed by measurement of plasma glucose to determine whether hyperglycemia is present. If plasma glucose is elevated, the glycosuria is typically diabetes-related. If plasma glucose is normal, renal causes should be considered. Additional evaluation may include testing for other features of proximal tubule dysfunction (bicarbonate loss, phosphaturia, aminoaciduria), assessment of renal function, review of medications, and, when indicated, genetic testing for inherited renal glycosuria.

Management targets the underlying cause. Diabetes-related glycosuria is addressed with glycemic control. Renal glycosuria and related disorders may require monitoring and treatment of associated electrolyte disturbances. In isolated renal glycosuria, prognosis is generally benign.