Investigations on spontaneous and glucocorticoid induced glucosuria in the bovine animal

Abstract

The pathologic excretion of glucose in urine is encountered in a number of diseases in which either the glucose concentration in primary urine, due to an elevated blood glucose level, exceeds the reabsorption capacity of the kidney (e.g. diabetes mellitus and in other conditions where the so-called anit-insular hormones predominate), or the renal threshold is pathologically lowered (e.g. mercury and chromate intoxication) - so-called renal glucosuria. Some of these cases have already been described in the ruminant. Central nervous disorders (e.g. rabies) can also lead to glucosuria - presumably due to stimulation of the cerebral glucose regulatory center. Transient glucosurias were observed following therapeutic glucose infusions, glucocorticoid therapy, and after transport.
In 1977, during routine examination of bovine patients upon admission to the II. Medizinische Tierklinik at the University of Munich Veterinary School, it was discovered, using quick-test-sticks, that 9% of the animals had glucosuria. Similar observations were made by MEHLS in the Klinik fur Rinderkrankheiten at the Veterinary College Hannover. In both clinics it was observed that tests for glucosuria had become negative after two days.
Since the test sticks were originally intended for monitoring human diabetics, they have a lower limit of detection of around 50 mg/dl (2.78 mmol/1) urine glucose, as higher concentrations are considered pathologic in humans. These observations led the present investigation to ask whether a physiologic glucosuria can be expected in adult bovines, and whether application of trade name glucocorticoids in recommended dosages can lead to significant loss of glucose via the kidneys.