Renal glucosuria

　　The etiology of renal glucosuria is divided into primary and secondary.

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

　　Type A: Both the renal glucose threshold and the maximum reabsorption rate of glucose in the renal tubules (TMG) are reduced. Even when blood glucose levels are not high, the reabsorption of glucose in the renal tubules is also lower than normal, hence it is true glucosuria. It can be due to the renal tubules' sole impairment in glucose transport, but it often combines with other renal tubular transport function defects, such as Fanconi syndrome and Lowe syndrome.

　　Type B: The renal glucose threshold is reduced while TMG is still normal, hence it is called pseudo-renal glucosuria. This is due to the reduced reabsorption function of glucose in individual renal units, where glucosuria occurs before blood glucose reaches the maximum reabsorption rate of glucose in the renal tubules, that is, the renal glucose threshold is reduced, which is relatively common in clinical practice.

　　Secondary renal glucosuria is relatively rare and 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, and other genetic diseases, including Fanconi syndrome, Lowe syndrome, cystinosis, and others.

　　The pathogenesis of this disease is unknown and may be related to the following factors:

　　1, The ratio of the surface area of the proximal renal tubules to the glomerular filtration membrane area decreases, leading to tubuloglomerular imbalance.

　　2, The transport system function of glucose reabsorption in the renal tubules is unbalanced.

　　3, The accumulation function of renal tubular cells for glucose at different concentrations is reduced, with a decrease in the number of glucose reabsorption transporters or changes in affinity or gradient disorders.

　　4, The permeability of renal tubular cell membranes to glucose is reduced. In addition, there is also a barrier to the absorption of glucose in the intestines.

　　Renal glucosuria can be complicated by dehydration, malnutrition, hypoglycemia, and diabetes-related lesions. Diabetes-related lesions include foot disease (gangrene, amputation), kidney disease (renal failure, uremia), eye disease (blurred vision, blindness), brain disease (cerebrovascular lesions), and heart disease, which are the main factors leading to the death of diabetic patients.

　　Renal glucosuria includes primary renal glucosuria and secondary renal glucosuria, with specific symptoms as follows:
　　Primary renal glucosuria is caused by genetic factors and is a disorder of glucose reabsorption in the proximal renal tubules. Clinically, there are two diseases: intestinal glucose-galactose malabsorption syndrome and benign familial renal glucosuria.
　　1, Intestinal glucose-galactose malabsorption syndrome is a congenital defect in the transport of galactose and glucose by the jejunal and renal tubular epithelial cells. The main manifestation is intestinal absorption disorder, with watery diarrhea at birth, dehydration, and malnutrition. Large amounts of galactose can be detected in the stool, and the condition can be cured by feeding fructose. Renal lesions are relatively mild and are only seen in homozygous individuals.
　　2, Benign familial renal glucosuria is an autosomal dominant genetic disease, which can be divided into two types: Type A, where the renal glucose threshold and MTG both decrease, and may have Fanconi syndrome; Type B, where only the renal glucose threshold decreases, with varying degrees of glucosuria among individuals, with the most severe cases having almost no glucose absorption in the renal tubules.
　　3, Primary renal glucosuria patients, in addition to having a family history, usually lack the common symptoms of diabetes such as polydipsia, polyuria, and pyuria. Most are discovered through routine urine analysis, with onset at birth, generally asymptomatic, and without affecting development, with a good prognosis. This may be due to compensatory hyperphagia, which supplements the loss of urinary glucose. A few pediatric cases may also exhibit hypoglycemic symptoms due to excessive urinary glucose, but generally do not transform into metabolic diabetes. A few cases may have the 'three pluses' symptoms of polydipsia, polyuria, and polyphagia, often with persistent glucosuria, and the amount of urinary glucose is generally...

　　There are no special preventive measures for renal diabetes. If it is a case of malabsorption syndrome of glucose-galactose in the small intestine, switching to fructose can effectively prevent this condition; secondary renal diabetes mainly focuses on the treatment of the primary disease, preventing damage to the kidney glomeruli by nephrotoxic substances to protect the normal function of the kidney glomeruli.

　　Routine renal diabetes examination includes B-ultrasound and X-ray examination, other examinations include:

　　1, Urine flow examination: The urine glucose can be significantly increased by using the sucrose oxidase experiment, under the condition that the diet contains 103 J/kg (30 cal/kg) or carbohydrates account for 50% of the total calories, the quantitative glucose in 24h urine is more than 500 mg, and even up to 100g/24h, most of which are 5-30g/24h, and the urine phosphorus, amino acids, uric acid, bicarbonate, and other acidification tests are all normal.

　　2, Large amounts of lactose can be detected in the stool.

　　3, Normal or slightly fluctuating glucose tolerance test.

　　4, Fasting blood glucose is normal, the glomerular filtration rate of uric acid clearance is 148-158 ml/(min·1.73m2), the glucose clearance rate is almost equal to the glomerular filtration rate, after intravenous administration of glucose to raise blood glucose concentration to 261-342 mg/dl (14.48-18.98 mmol/L), the glucose clearance rate does not change.

　　Patients with renal diabetes can adopt the following food therapy recipe:

　　1, Astragalus congee. 30-60 grams of raw Astragalus, 60 grams of sticky rice, 10 grams of dried tangerine peel powder. First, decoct the Astragalus into a decoction and remove the residue, then add the sticky rice to cook into congee, and add the dried tangerine peel powder when the congee is done. This recipe can improve kidney function, eliminate proteinuria, and enhance physical fitness.

　　2, Euryale ferox and银杏congee. 30 grams of euryale ferox, 10 white bitter almonds, 30 grams of glutinous rice. Shell the white bitter almonds and cook them with the euryale ferox and glutinous rice in a pot with water to make congee. This recipe can treat kidney disease due to spleen deficiency and dampness, cloudy urine, and a large amount of protein excreted in urine, and can be eaten long-term.

　　3, Black soybean braised pork. 50 grams of black soybean, 100 grams of lean pork. First, bring the pork to a boil in water, then add the black soybean to simmer together. Add appropriate seasonings after it is cooked, and eat the meat and drink the soup. This recipe has the effects of kidney-tonifying, diuresis, and spleen-tonifying.

　　4, Carassius auratus congee. One Carassius auratus (skin and internal organs removed), 6 grams of leontopodium, 50 grams of rice. Boil the ingredients together to make congee. Remove the leontopodium and eat the congee with the fish. It has the effects of diuresis and protein supplementation.

　　5. Goji berry congee. Take 30 grams of goji berries and 50 grams of glutinous rice. Cook them together into congee and eat them in the morning and evening. It has the effects of kidney and spleen tonification and elimination of proteinuria.

　　At the same time, patients with nephrogenic diabetes should eat the following foods in their diet:

　　1. Starchy staple foods include rice, flour, corn flour, sorghum flour, buckwheat flour, millet, etc;

　　2. Vegetables include cabbage, rapeseed, clover seedlings, mustard greens, radishes, pumpkins, luffa, winter melon, cucumbers, zucchinis, etc;

　　3. Fruits include watermelons, myrtles, kiwifruits, strawberries, etc;

　　4. Fish and meat include lean meat, eggs (using egg whites), turtle, eel, crucian carp, bream, etc., which can be taken in moderate combinations;

　　5. Choose vegetable oil as the main fat source, such as rapeseed oil, sesame oil, corn oil, cottonseed oil, etc.

　　In addition, patients with this disease should avoid the following foods:

　　1. Limit fat intake. Because fat can exacerbate atherosclerosis, kidney disease itself is a manifestation of renal atherosclerosis. The daily intake of vegetable oil should also be controlled below 60 grams.

　　2. Control the intake of plant proteins. Diabetics should control the intake of carbohydrates and often use plant proteins as a supplement to nutrition. Plant proteins often contain a large amount of purine bases, and excessive consumption will increase the burden on the kidneys. Therefore, soybeans, mung beans, soy milk, etc. should also be limited in consumption, and fish, shrimp, sea cucumber, and lean meat should be used instead.

　　3. Reduce salt intake and avoid eggs. When kidney disease causes edema and hypertension, the amount of salt intake should be limited, and the general daily salt intake should be 2-4 grams; the protein in eggs produces a lot of uric acid during metabolism, and when kidney function is impaired, it will accumulate metabolic products in the body and increase the burden on the kidneys, so eggs should be avoided when kidney function failure occurs.

　　4. Limit high-purine foods. The metabolism of a large amount of purines in the body will increase the burden on the kidneys. Various broths, pork head meat, sardines, and animal internal organs all contain a large amount of purines, and the intake should be strictly controlled.

　　Nephrogenic diabetes is a genetic disease. It is currently believed that no special treatment is needed. Patients who may experience hypoglycemia and ketosis should receive glucose supplementation. To prevent hypoglycemia, patients should be provided with sufficient carbohydrates, avoid long periods of fasting, and pay attention to nutritional reinforcement during pregnancy, and eat meals more frequently. Secondary nephrogenic diabetes is mainly treated by treating the underlying disease.