Renal diabetes

Introduction Renal glucosuria refers to a disease of diabetes caused by a decrease in glucose function in the proximal tubules when the blood glucose concentration is normal or lower than the normal renal sugar threshold. Clinically divided into primary renal glucosuria and secondary renal glucosuria. Renal glucosuria can be associated with many tubular defects, including amino aciduria and renal tubular acidosis. If the system appears alone, and other kidney functions are normal, it is mostly autosomal dominant hereditary features, and even invisible, the isolated renal glucosuria and diabetes secondary to diabetes occur at a ratio of about 2:1000. . The maximum glucose reabsorption rate is reduced, and glucose is excreted in the urine. In addition to the rare glucose-galactose malabsorption, intestinal transport of glucose is normal.

Cause

(1) Causes of the disease

The causes of renal diabetes are divided into primary and secondary.

1. Primary renal glucosuria: also known as familial renal glycosuria, mostly autosomal recessive genetic disease, and some are dominant inheritance. The disease can be divided into two types according to the sugar titration curve:

(1) Type A: The renal sugar threshold and the maximum reabsorption rate of renal tubular glucose (TMG) are reduced. When the blood glucose is not high, the renal tubular reabsorption of glucose is also lower than normal, so it is true diabetes. It can be a barrier to glucose transport in the renal tubule alone, but often combined with other renal tubular transfusion function defects, such as Fanconi syndrome, Lowe syndrome.

(2) Type B: The renal sugar threshold is lowered and TMG is still normal, so it is pseudo renal glucosuria. It is because the reabsorption function of glucose in individual nephrons is reduced, and the maximum absorption rate of glucose in the renal tubules is not found in diabetes, that is, the renal sugar threshold is reduced, which is more common in clinical practice.

2. Secondary renal glucosuria: less common, can be secondary to chronic kidney diseases such as chronic interstitial nephritis, nephrotic syndrome, multiple myeloma or other nephrotoxic substances such as lead, cadmium, mercury, oxalic acid, cyanide Compound and other hereditary diseases Fanconi syndrome, Lowe syndrome, cystine accumulation disease, etc.

an examination

Related inspection

Bacteriological examination of urinary sediment tube type urine specimens of urinary sediments

1. Urine flow test: glucose test with sucrose oxidase test can be significantly increased. Diet with heat card 103J / kg (30cal / kg) or carbohydrates accounted for 50% of the total calories, 24h urine glucose quantitative > 500mg health search, and even more up to 100g / 24h, most in 5 ~ 30g /24h. Urine phosphorus, amino acids, uric acid hydrogencarbonate and other uric acid tests were normal.

2. A large amount of galactose can be detected.

3. The glucose tolerance test is normal or slightly fluctuating.

4. Fasting blood glucose is normal, glomerular filtration rate of chrysanthemum clearance is 148 ~ 158ml / (min · 1.73m2) sugar clearance and glomerular filtration rate is almost equal. After glucose was administered intravenously to increase the blood glucose concentration to 261-342 mg/dl (14.48-18.98 mmol/L), the blood glucose clearance rate remained unchanged.

5. Other auxiliary inspections: Regular B-ultrasound and X-ray examination.

Differential diagnosis

Need to be identified with the following symptoms:

Proteinuria: The normal glomerular filtrate contains a small amount of small molecular protein, the content of 20mg/100ml. Reabsorption through the renal tubules, and finally the protein remaining in the urine is very small, no more than 70 ~ 100 mg / 24h. It can not be detected by ordinary urine routine examination. When the protein content in the urine increases, the routine urine examination can be measured, which is called proteinuria.

Keto-urine: severely starved or untreated diabetics with low blood glucose levels lead to increased gluconeogenesis, fatty acid oxidation accelerates the production of large amounts of acetyl-CoA, while gluconeogenesis causes oxaloacetate to be depleted, while the latter is acetyl-CoA into the lemon Essential for the acid cycle, whereby acetyl-CoA is directed to the direction of the ketone body. A large number of ketone bodies appear in the blood and urine.

Diabetes: generally refers to glucose and urine. Normal people have a small amount of glucose in the urine, and the daily urine sugar content is 0.7~0.52 mmo1 (31-93 mg), and the qualitative test is negative. Daily urine sugar exceeds 0.83 IIUnol door p) is positive by qualitative test, called diabetes. The previous qualitative test of diabetes used copper sulfate reagent (Ban's L is based on the reduction of sugar, urine contains glucose, fructose sugar, maltose, pentose, non-sugar substances with reducing effect (some drugs * can be positive In recent years, glucose oxidase paper method has been used to measure urine sugar, which is specific to glucose, but can also be positive when ascorbic acid or salicylate is present.

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