Glucosuria results from the glomerular filtration of more glucose than the renal tubule can absorb. It occurs in all normal individuals in amounts up to 25 mg/dl. Abnormally increased glucosuria [more than 25 mg/dl in random fresh urine], results from either an elevated plasma glucose, an impaired renal glucose absorptive capacity, or both. Glucosuria leads to osmotic diuresis and dehydration.
Renal glucosuria is a rare condition in which the simple sugar glucose is eliminated (excreted) in the urine despite normal or low blood glucose levels.
Studies have demonstrated the mutations in the gene expressing SGLT2 transmembrane transporter responsible for most cases of renal glucosuria. These inhibitors are beneficial in reducing cardiovascular morbidity, mortality and the progression of diabetic renal. One of the proposed mechanisms underlying these cardiovascular beneficial effects is reduced weight and BP values.
In some cases, glucosuria may be pronounced enough to result in excessive urination (polyuria), excessive thirst (polydipsia), and other associated symptoms.
Glucosuria
