Hyperuricaemia is defined as a serum urate concentration greater than 0.42 mmol/L in the male and 0.36 mmol/L in the female. The plasma urate concentration reflects the balance between urate production and excretion and high value may occur during periods of increased production, or decreased excretion, or both.
Diabetic ketoacidosis cause hyperuricaemia by decreasing renal excretion of urate (a condition known as organic acidaemia). Diabetic ketoacidosis results from an absolute shortage of insulin; in response the body switches to burning fatty acids and producing excessive acidic ketone bodies which will be excreted through urine. The ketone bodies (organic acid anions) like acetoacetate and β-hydroxybutyrate, are competitive inhibitors of tubular urate secretion and hence can result in renal urate retention, causing hyperuricaemia.
Furthermore, excessive alcohol ingestion is often associated with hyperuricaemia, not only because of increased urate production but also because of decreased renal urate excretion. This later effect may be due to the ketoacidosis which can be associated with alcohol abuse.
Hyperuricemia or the increase of uric acid in the blood is not that common in DKA. Alcohol and fructose intake can increase this risk. The kidney will try and release the uric acid and the ketone, leaving the body with increased levels in both
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Hyperuricaemia is defined as a serum urate concentration greater than 0.42 mmol/L in the male and 0.36 mmol/L in the female. The plasma urate concentration reflects the balance between urate production and excretion and high value may occur during periods of increased production, or decreased excretion, or both.
Diabetic ketoacidosis cause hyperuricaemia by decreasing renal excretion of urate (a condition known as organic acidaemia). Diabetic ketoacidosis results from an absolute shortage of insulin; in response the body switches to burning fatty acids and producing excessive acidic ketone bodies which will be excreted through urine. The ketone bodies (organic acid anions) like acetoacetate and β-hydroxybutyrate, are competitive inhibitors of tubular urate secretion and hence can result in renal urate retention, causing hyperuricaemia.
Furthermore, excessive alcohol ingestion is often associated with hyperuricaemia, not only because of increased urate production but also because of decreased renal urate excretion. This later effect may be due to the ketoacidosis which can be associated with alcohol abuse.
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Hyperuricemia or the increase of uric acid in the blood is not that common in DKA. Alcohol and fructose intake can increase this risk. The kidney will try and release the uric acid and the ketone, leaving the body with increased levels in both
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