Renal glucosuria

Glycosuria is the presence of glucose in the urine at high levels. Glucose is fully reabsorbed at the level of the nephrons, the functional units of the kidney where blood clearance occurs. However, when blood glucose levels exceed a threshold, a figure around 180 mg / dl of glycemia, the nephron allows glucose to be excreted in the urine to compensate for glycemic overload that is not compensated for by insulin.

How is it produced?

Two types of glucosuria must be differentiated:

• Glycosuria associated with elevated blood glucose levels, that is to say, of glucose in blood; This is what happens in diabetes mellitus: in the absence of insulin, glycemic levels exceed the reabsorption threshold and glucose is lost in the urine.
• Glycosuria associated with normal blood glucose levels; in this case the problem is an alteration of the mechanisms of glucose reabsorption in the kidney, hence the glycemic levels are correct.
• In the case of, the glucosuria associated with it occurs due to the high levels of glucose that appear in the blood, since they cannot be normalized by insulin. Upon reaching levels above 180 mg / dl, the nephrons allow glucose to not be reabsorbed and pass into the urine.

Types

Isolated glycosuria is a hereditary disease due to the alteration of a gene that is on chromosome 6. This alters a protein that is responsible for transporting glucose for reabsorption at the level of the tubules of the nephrons, being able to alter both the maximum glucose transport capacity and the glycemic threshold from which glucose is excreted in the urine. , so that glucose recovery is impaired. There are three different types of isolated glycosuria:

• Type A, in which both the glycosuria threshold and the maximum glucose transport capacity have been lowered
• Type B, in which the glycosuria threshold has decreased but the maximum glucose transport capacity remains stable
• Type O, very rare, in which there is no glucose transport

There is an alteration of the proximal tubules known as the, in which the reabsorption of various substances, including glucose, is hindered, which is why it is also a cause of glucosuria. Other substances that are lost through the urine in this syndrome are amino acids, phosphates, potassium and bicarbonate. Fanconi syndrome is usually primary but is sometimes associated with other diseases, such as multiple myeloma, Sjögren's syndrome, amyloidosis, or in some cases kidney transplantation.

Symptoms

• In the case of glycosuria associated with diabetes mellitus, the symptoms of this entity: increased appetite, thirst and daily volume of diuresis, which we know respectively as polyphagia, polydipsia and polyuria.
• In the case of isolated glucosuria of renal origin, exist polydipsia and polyuria, but in general the patients do not present any symptoms except, at most, a poor tolerance to fasting.
• With respect to fanconi syndrome, there may also be an increase in the sensation of thirst and the volume of urine production and sometimes there may be proteinuria. Due to the loss of phosphates, bone changes occur, such as rickets in children and bone lesions in adults, as well as muscle weakness and constant fatigue.

Diagnosis

Before a polyuria and polydipsia clinic, blood and urine tests should be performed. If glucosuria is seen, with levels between 5 and 30 grams in 24 hours, the blood analysis and the glycemic levels will allow to differentiate between a glycosuria secondary to a possible diabetes mellitus or a glucosuria of renal origin. In glucosuria of renal origin, in addition, it will be seen that glycosuria varies when modifying the diet and that carbohydrates are metabolized normally.

In the case of Fanconi syndrome, other alterations in urine analysis, with high levels of amino acids, phosphorus, potassium and bicarbonate, as well as poorly concentrated urine. Occasionally, there may be hemolytic anemia, due to rupture of the red blood cells, and alteration of leukocytes or platelets.

Treatment

The treatment of glucosuria associated with diabetes mellitus will be the correction of this disease, either with oral antidiabetic drugs or with insulin.

Glycosuria of isolated renal origin does not require any treatment. In the case of Fanconi syndrome, glucosuria will not be treated, but bone defects secondary to phosphorus loss will be treated, for which phosphates and vitamin D are administered.

Precautionary measures

There are no preventive measures for renal glucosuria. At most, periodic monitoring of both urine and blood glucose levels should be performed.