Renal threshold for glucose

As early as 1904, the detection of glucose in urine in euglycemia was described by Folin.

The concept of the "renal threshold" originated from Sindoni and Shannon in the 1930s and 1940s (Wolf 2009).

The renal threshold is the tubular transport maximum for glucose (Wolf 2009), i.e. the value of blood glucose at which glycosuria occurs (Wiehl 2014).

The renal threshold for glucose is normally about 180 mg / dl glucose in the blood in adults (Herold 2020). Above this value, the tubular transport mechanisms can no longer ensure complete reabsorption of glucose from the primary urine and glucose appears in the urine (Wolf 2009).

Physiological glucosuria is 15 mg / dl, the lower detection limit of a test strip is about 30 mg / dl (Herold 2020).

But there are deviations from this:

• Pregnancy:

In pregnancy, the renal threshold for glucose is < 150 mg / dl (Herold 2020).

To diagnose gestational diabetes, an oral glucose tolerance test (oGTT) should always be performed as screening, since glucosuria can identify on average only 10% of gestational diabetics (Herold 2020).

• Children and adolescents:

In children and adolescents, the capacity limit of the renal tubules for reabsorption of glucose varies, so that the renal threshold has a margin between 140 mg / dl - 160 mg / dl blood glucose (Danne 2014).

• Diabetic nephropathy:

In patients with diabetic nephropathy, the threshold can be much higher at up to about 300 mg / dl. Thus, no glucosuria is found in these patients despite hyperglycemia. Therefore, test strips are not always meaningful and a normoglycemic therapy goal cannot be controlled by urine sugar self-testing.

For the early diagnosis of diabetes mellitus, it is therefore better to determine the fasting blood glucose value (NBZ) (Herold 2020).

• Glucosuria in normoglycemia:

The reversed case of glucosuria in normoglycemia is also possible. This is the rare clinical picture of renal diabetes mellitus with tubular partial dysfunction or the use of SGLT2 / (1) inhibitors(gliflozines such as empagliflozin [Menche 2020]), which lower the renal threshold for glucose by inhibiting the sodium-glucose cotransporter (Kessing 2014; Herold 2020).

• Cortisol / ACTH:

Both cortisol and ACTH can lower renal threshold (Weissbecker 2013).

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