Glucosuria R81

In the 18th century, the English physician Matthew Dobson was the first to observe a connection between blood and urine glucose.

For a long time, blood glucose measurement was the only method of monitoring blood glucose in diabetes mellitus. Initially, this was done by evaporating the urine, in which sugar crystals and, through yeast, the fermentation of the urine sugar could then be detected. It was not until 1941 that a copper reduction method, the Clinitest, was marketed by the Ames Company (Walker 1990).

The first glucose oxidase-based test (GOD test), the Clinistix, followed in 1956 from Ames Comp. Elkhart (Voswinckel 1993).

Glucosuria is the presence of glucose in urine beyond physiological levels, which is < 15 mg / dl in morning urine (Herold 2020) and < 25 mg / dl in fresh random urine (Liman 2021).

Glucosuria occurs when the glomerulus filters more glucose than the proximal tubule is able to reabsorb. This may be due to 2 causes, which may occur singly or in combination:

• 1. inability of the proximal tubule to reabsorb glucose...
• 2. significant increase in glucose in the circulating blood (Liman 2021).

The principle of glucosuria is used therapeutically in SGLT2- inhibitors for the treatment of diabetes mellitus (Brandes 2019).

Normally, the renal threshold for glucose is about 180 mg / dl glucose in the blood. The excretion of glucose in the urine is physiological up to 15 mg / dl (0.8 mmol / l) in morning urine and up to 25 mg / dl in random urine (Liman 2021).

The level of glucosuria behaves proportionally to blood glucose up to a value of about 150 - 180 mg / dl (8.3 - 10.0 mmol /l), after which it increases exponentially (Herold 2020 / Mehnert 2011).

Glucose is initially glomerular filtered and almost completely reabsorbed in the proximal tubule. The reabsorption occurs together with sodium via a carrier system (Mehnert 2011):

- SGLT1 at the end of the proximal tubule and in the small intestine.

- SGLT2 in the first half of the proximal tubule (Brandes 2019).

Since glucose is poorly absorbable and reabsorption of water and NaCl is decreased in the proximal tubule,increased excretion of glucose results in:

• Volume deficiency
• Hypertension
• Hypernatremia, as the sodium concentration in the urine is lower than in the blood, and thus more water is lost than sodium (Kasper 2015)

Glucosuria leads to weight loss (Kasper 2015).

Glucosuria occurs in:

• Type 1 diabetes
• type 2 diabetes
• renal glucosuria (in which the renal threshold for glucose is pathologically reduced [Herold 2020])
• alimentary glucosuria (occurs in patients with high carbohydrate consumption [Liman 2021])

• hereditary, e.g. in the case of:
  • tubulopathies (e.g. De Toni - Debré - Fanconi syndrome)
  • Disorders of the glucose carrier (Mehnert 2011) such as:
    • familial renal glucosuria
    • glucose-galactose malabsorption
    • Fanconi-Bickel syndrome (Liman 2021)
• acquired damage to the tubule such as in:
  • Pyelonephritis
  • nephrotoxicity due to pharmaceuticals (Mehnert 2011)
  • acute tubular necrosis (Liman 2021)
• by lowering the threshold for glucose (the plasma glucose concentration above which significant glucosuria occurs [Walker 1990]) such as:
  • during pregnancy
  • Hyperthyroidism
  • fever
  • physical exertion
• by various substances such as:
  • Chloride
  • Bromide
  • Sodium nitrate
• due to insufficient oxygen supply to the proximal tubule

(Liman 2021)

There may also be an increase in the renal threshold for glucose. This is found:

• in old age
• diabetic glomerulosclerosis
• chronic hyperglycemia
• heart failure

(Liman 2021)

Spontaneous urine or collected urine from precisely defined collection periods (e.g. night urine) is used for diagnosis. Urine analyses before and 2 - 3 h after a main meal can provide information on pre- or postprandial glucose values.

Urine should be analysed within 2 h after delivery, otherwise there may be a loss of glucose (up to 40 % within 24 h).

(Mehnert 2011)

The diagnosis of glucosuria is possible with:

Urine test strips

This is a glucose oxidase-peroxidase reaction, which leads to a color change of the test strip (Mehnert 2011).

The lower detection limit for glucose is about 30 mg / dl (Herold 2020). From a glucose concentration of > 250 mg / dl (14 mmol / l), differentiation is only possible to a limited extent.

Possible errors with the test strip are:

• False negative test result for:
  • Urine pH value < 5
  • Ingestion of much Vit. C
  • intake of salicylic acid > 2 g / d
• False positive test result for:
  • through incorrect cleaning of the test device with e.g. peroxides

(Mehnert 2011)

Hexokinase or glucose oxidase method

These methods allow a quantitative enzymatic determination. The measurements are very accurate. A false positive result only occurs in the case of fructosuria (very rare) (Mehnert 2011).

In addition to glucosuria there is

• Hypernatremia (see also "Pathophysiology")

(Kasper 2015)

1. Brandes R et al (2019) Human physiology with pathophysiology. Springer Verlag 409
2. Herold G et al (2020) Internal medicine. Herold Publishers 601, 730
3. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 275, 295 a
4. Liman M N P et al (2021) Physiology, Glucosuria. NCBI. StatPearls Publishing LLC. Bookshelf ID: NBK557441. PMID: 32491373
5. Mehnert H et al (2011) Diabetology in clinic and practice. Georg Thieme Verlag Stuttgart 90 - 91
6. Voswinckel P (1993) Black urine From horror to laboratory parameter: urina nigra, alkaptonuria, haemoglobinuria, myoglobinuria, porphyrinuria, melanuria. Blackwell Science 258
7. Walker H K et al (1990) Clinical methods: the history, physical, and laboratory examinations. 3rd edition. Butterworth Publishers Bookshelf ID: NBK245. PMID: 21250089