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Under normal circumstances, glucose is readily filtered by glomeruli and the filtered glucose is reabsorbed by the proximal tubule; essentially no glucose is normally excreted in the urine. However, the capacity for the proximal tubule to reabsorb glucose is limited; if the filtered load exceeds the proximal tubule's reabsorptive capacity, a portion of the filtered glucose will be excreted in the urine. Thus, elevated serum glucose concentrations (as seen with diabetes mellitus) may result in an increase in filtered load of glucose and may overwhelm the tubules' reabsorptive capacity resulting in glucosuria. Glucosuria occurs when the renal threshold for glucose is exceeded (typically >180 mg/dL). This is most commonly, although not exclusively, seen in diabetes.
Additionally, conditions which adversely affect proximal tubule function may also result in decreased reabsorption of glucose, and increased urinary glucose concentration, even in the presence of normal plasma glucose concentrations. Some of these conditions include Fanconi syndrome, Wilson disease, hereditary glucosuria, and interstitial nephritis. These conditions are relatively rare, and most causes for elevated urine glucose concentrations are due to elevated serum glucose levels.
An indicator of abnormal proximal tubule function
Limited usefulness in the screening or management of diabetes mellitus
Elevated urine glucose concentration reflects either the presence of hyperglycemia or a defect in proximal tubule function.
As a screening test for diabetes mellitus, urine glucose testing has a low sensitivity (though reasonably good specificity).
Urine glucose monitoring for the management of diabetes mellitus has essentially been replaced by more accurate and reliable blood glucose determinations.
< or =15 mg/dL
Tietz Textbook of Clinical Chemistry, Third edition. Edited by CA Burtix, ER Ashwood. Philadelphia, WB Saunders Company, 1999