Glycosuria or glucosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria.
When glycosuria occurs with a normal plasma glucose, a primary defect of proximal tubule reabsorption needs to be considered. In this setting, glycosuria may coexist with additional manifestations of proximal tubular dysfunction, including phosphaturia (leading to hypophosphatemia), uricosuria, renal tubular acidosis, and aminoaciduria. This constellation is called the Fanconi syndrome and may result from a variety of disorders, including multiple myeloma, heavy metal exposure, and treatment with certain medications including tenofovir, lamivudine, cisplatin, valproic acid, and aminoglycosides. Glycosuria with normal plasma glucose may also be seen in patients receiving sodium-glucose cotransporter 2 inhibitors, a novel class of oral hypoglycemic agents. Glycosuria may also be an isolated defect (isolated renal glycosuria) associated with genetic mutations affecting renal glucose transport.
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