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Glycosuria

What It Is, Causes, Signs and Symptoms, Treatment, and More

Author: Emily Miao, PharmD

Editors: Alyssa Haag, Ian Mannarino, MD, MBA, Kelsey LaFayette, DNP

Illustrator: Jessica Reynolds, MS

Modified: 26 Feb 2024

What is glycosuria?

Glycosuria refers to the presence of reducing sugars (e.g., glucose, galactose, fructose) in the urine. Fructosuria (i.e., fructose in the urine) and galactosuria (i.e., galactose in the urine) can occur in the setting of an enzyme deficiency, however, these occurrences are relatively rare. Since glucose is the most common sugar found to be elevated in the urine, glycosuria is often synonymous with glucose in the urine. 

Normally, the glomerulus, which is a network of capillaries within the kidney, filters contents of blood (e.g., nitrogenous waste, electrolytes, glucose, amino acids) into the plasma filtrate of renal tubules and reabsorbs substances like electrolytes, glucose and amino acids from the proximal tubule of the renal tubules back into the bloodstream. The proximal tubule contains sodium-glucose cotransporters,  specialized sodium-potassium-ATPase transporters, which facilitate sodium and glucose reabsorption across the membranes, and back into the blood. While a trace amount of glucose in the urine is physiologic (i.e., normal or expected), more than 25 milligrams per deciliter (mg/dl) of filtered glucose is considered pathologic or abnormal. Pathologic glycosuria occurs when the amount of filtered glucose exceeds the reabsorptive capacity of the proximal tubules. 

What causes glycosuria?

Glycosuria can be caused by a variety of etiologies that either cause elevated blood sugar levels in the bloodstream or prevent glucose reabsorption in the renal tubules. Causes of elevated glucose levels include diabetes mellitus and gestational diabetes, or diabetes mellitus diagnosed during pregnancy. Glycosuria in gestational diabetes is thought to occur from a physiologic increase in renal blood flow to the kidney, resulting in excess glucose filtration and a reduction in glucose reabsorption. Glucose reabsorption is facilitated by glucose transporters (e.g., SGLT1, SGLT2, GLUT2) which are present on the membranes. Mutations in these glucose transporters may cause glucosuria. For example, a mutation in SGLT1 is associated with glucose-galactose malabsorption, and a mutation in SGLT2 is associated with familial renal glucosuria (FRG). 

Another etiology of glycosuria due to dysfunctional glucose reabsorption despite normal blood sugar levels include Fanconi syndrome (i.e., a rare form of renal glycosuria also known as type II proximal renal tubular acidosis, characterized by a defect in the proximal tubule of the kidney that prevents glucose reabsorption). Fanconi syndrome can either be inherited, such as in Wilson disease, which results in abnormal copper accumulation and deposition in the kidneys thereby causing kidney damage; or acquired, specifically medication-induced (e.g. cisplatin, aminoglycosides). Additionally, some medications can prevent glucose reabsorption and cause glycosuria as an intended effect, such as diuretics (e.g., thiazides) used in hypertension, or sodium-glucose cotransporter-2 (SGLT-2) inhibitors like canagliflozin used in type 2 diabetes mellitus.

Increased age is a risk factor due to the increased risk of developing chronic disease conditions like diabetes mellitus and hypertension with age. These chronic conditions overwhelm the kidney’s reabsorptive capacity but also increase the risk for renovascular damage, leading to subsequent leakage of glucose and proteins into the urine. 

What are the signs and symptoms of glycosuria?

Signs and symptoms of glycosuria typically reflect signs of excess blood glucose, including increased urination and frequency (i.e., polyuria), excessive thirst (i.e., polydipsia), non-specific constitutional symptoms (e.g.,  fatigue, unintended weight loss due to polyuria), and recurrent urinary tract infections. Individuals with elevated blood glucose with undiagnosed diabetes mellitus may also experience increased hunger since the body is not adequately utilizing glucose, and may also present with diabetic ketoacidosis, a medical emergency characterized by prolonged and extremely high blood sugar levels. 

How is glycosuria diagnosed?

Diagnosis of glycosuria begins with a thorough medical history and review of symptoms. Information pertaining to a family history of diabetes mellitus or Fanconi syndrome, and medication history should be elicited to identify the underlying cause of glycosuria. The diagnosis can be made using a urine dipstick test which can identify microscopic amounts of glucose, amino acids, and proteins. In cases where glycosuria is accompanied by elevated blood sugar levels on blood testing, a hemoglobin A1c blood test, which measures the average blood sugar levels over three months, can be used to assess for diabetes mellitus. 

Moreover, in Fanconi syndrome, there may be electrolyte abnormalities that can be detected with additional laboratory testing (e.g., comprehensive metabolic panel, or CMP). Due to the generalized defect of the proximal convoluted tubule in Fanconi syndrome, there may be hypophosphatemia with metabolic acidosis in the blood due to bicarbonate wasting and subsequently, phosphaturia, aminoaciduria, and glucosuria. 

How is glycosuria treated?

Management of glycosuria involves treating the underlying cause. For etiologies where glycosuria is a result of elevated blood sugar levels, strategies should be aimed at reducing glucose levels, such as lifestyle modifications like proper diet and exercise, and pharmacologic modalities such as glucose-lowering agents (e.g., insulin, metformin). In individuals with glycosuria likely due to dysfunctional glucose reabsorption capabilities, treatment consists of supportive measures such as frequent hydration with electrolyte solutions and further avoidance of nephrotoxic medications. Individuals taking medications known to cause glycosuria as a side effect should be monitored for complications related to excess glucose in the urine (i.e., urinary tract infections). If the patient and healthcare professional agree that the risks of the medication outweigh the benefits, the medication may be discontinued. 

What are the most important facts to know about glycosuria?

Glycosuria refers to the presence of reducing sugars (i.e., glucose, galactose, fructose) in the urine, but is often synonymous with glucose in the urine.  Glycosuria can be caused by elevated blood sugar levels in the bloodstream or conditions that prevent glucose reabsorption in the renal tubules. Signs and symptoms of glycosuria typically reflect signs of excess blood glucose, including polyuria, polydipsia, fatigue, and weight loss. A urine dipstick can detect glucose levels in the urine and diagnose glycosuria. Management is aimed at treating the underlying etiology, which includes optimization of blood glucose levels and maintenance of hydration in individuals with dysfunctional kidney disease that prevents glucose reabsorption. 

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