Glucosuria

Glucosuria 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 tubular reabsorption is impaired. Normally, nearly all filtered glucose is reabsorbed in the proximal tubule by SGLT2 transporters (with SGLT1 contributing in the distal nephron). The renal threshold for glucose is about 180 mg/dL of plasma; when plasma glucose exceeds this level, glucose appears in the urine.

Glucosuria can be classified as overflow or renal. Overflow glucosuria results from very high plasma glucose, most commonly in uncontrolled diabetes mellitus, leading to osmotic diuresis. Renal glucosuria arises from defects in renal glucose reabsorption, such as familial renal glucosuria due to SGLT2 mutations or generalized proximal tubule dysfunction (e.g., Fanconi syndrome). Medications known as SGLT2 inhibitors deliberately cause glucosuria to improve glycemic control in diabetes.

Clinical features and diagnosis vary. Glucosuria can be asymptomatic and detected incidentally on a urine dipstick. When present with hyperglycemia, patients may experience polyuria and polydipsia due to osmotic diuresis. A dipstick test indicates glucose in urine but does not quantify it; abnormal findings are followed by measurement of plasma glucose and further evaluation. If glucosuria persists without hyperglycemia, evaluation for renal tubular disorders is considered.

Management depends on the underlying cause. In diabetes, treatment targets glycemic control to reduce glucosuria and its consequences. In non-diabetic renal glucosuria, prognosis is typically favorable, with management focused on monitoring and addressing any associated conditions.