1.Nutritional control.
(1) Protein control.
Protein intake in patients with kidney disease is a problem that has not been well solved for many years. As mentioned earlier, the function and structure of the kidney will be affected when the protein intake of normal people is insufficient. Kidney patients lose a lot of protein from urine every day, and the body is in a state of protein deficiency; therefore, adequate protein intake should be given. According to the results of our research in the 60’s, the protein intake for chronic kidney patients (without hyperalgesia) should meet ① the minimum daily requirement of human body; ② replenish the daily loss in urine; ③ replenish the previous lack of body; ④ replenish the amount of application of adrenocorticotropic hormone to increase protein decomposition (30~40mg prednisone, which can make 19g protein decomposition). However, high protein diet can increase GFR and urinary protein excretion, and high protein diet can promote glomerulosclerosis. Therefore, it is incomplete to emphasize only protein deficiency and apply a high protein diet. It should be given the amount of protein that can avoid negative nitrogen balance and at the same time avoid excessive protein damage to the kidney. It has been proposed that patients with nephrotic syndrome can be given 147 kJ/kg (35kcal/kg) of calories and 1.0g/kg of high quality protein per day, while small amounts of angiotensin transaminase inhibitors can be added to avoid an increase in proteinuria.
In 1984, Bergstrom gave a more comprehensive discussion on low protein diet. At the beginning of this century, it was noted that a reduction in protein intake could reduce total urinary nitrogen and urea excretion, and in the 1920s and 1940s, it was observed that feeding experimental renal failure animals a high-protein diet could increase nitrogen retention and shorten survival; restricting protein intake could lead to severe protein deficiency in the organism. Numerous studies have been conducted to find out the appropriate protein intake and other treatments that can slow down the progression of renal failure and maintain protein nutrition, such as low protein diet with essential amino acids, keto acid, or hydroxy acid therapy. The therapeutic effect of low protein diet has been confirmed.
In 1984, Monteon et al. reported that the study of 14 cases of nitrogen balance in 5 patients with chronic renal failure (creatinine clearance 10 ml±/min) showed that most patients had a negative nitrogen balance when given 0.55-0.6 g of protein per kg per day with a heat intake of 105 kJ/kg (25 kcal/kg). If the heat intake was increased to 147kJ/kg (35kcal/kg), most of the patients had a positive nitrogen balance. This indicates that adequate caloric intake must be ensured in the treatment of low-protein diet, which is more important in the treatment of patients with acute renal failure.
Dietary nutrition plays a more important and direct therapeutic role in acute renal failure. The general caloric intake should be around 12,600kJ (3,000kcal) per day to reduce the consumption of own protein. If you do not eat enough or cannot eat, you can use total intravenous high nutrition, including high concentration of glucose, 10-20% fat emulsion and essential amino acids to improve the negative nitrogen balance and slow down the rise of blood urea nitrogen and creatinine.
During the treatment of nephrotic syndrome, drugs that promote protein synthesis and reduce protein catabolism in the body should also be sought. Over the years, the application of sex hormones such as phenylpropyl testosterone failed to have a positive effect. Animal experiments illustrated that Astragalus (the water-soluble component Astragalus polysaccharide can affect the nucleic acid metabolism of hepatocytes, inhibit the degradation of hepatocyte rRNA and promote the synthesis of albumin) and Angelica (which can increase the DNA content and liver glycogen storage in hepatocytes) can increase the plasma albumin level in rats with nephrotic syndrome. The study using tracer kinetic method further observed that Astragalus and Angelica plus high protein diet can increase the protein synthesis rate in rats with nephrotic syndrome. Using molecular biology methods it was further shown that Astragalus and Angelica can upregulate liver albumin mRNA expression in rats with nephrotic syndrome, indicating that it can promote liver albumin synthesis. These works have yet to be confirmed in clinical work.
(2) Lipid control.
Observations on dietary polyunsaturated fatty acids in the treatment of renal disease.
(1) Effects on experimental renal disease: The animal model most commonly used to observe the effects of polyunsaturated fatty acids on the process of glomerulosclerosis is the model of glomerulosclerosis resulting from major nephrectomy. Supplementation of animals with linoleic acid decreased elevated blood creatinine, reduced urinary protein excretion, decreased the incidence of glomerulosclerosis, and increased glomerular production of PGE2, the beneficial effects of which were more pronounced when combined with a low protein diet. Supplementation of accelerated anti-GBM rats with linoleic acid resulted in reduced urinary protein excretion and decreased crescent formation. Reduced urinary protein and reduced renal histological damage were also observed in animals with immune complex-mediated nephritis supplemented with linoleic acid. Fish oil supplementation in mice with lupus nephritis showed a decrease in urinary protein, reduced glomerular damage, significantly slowed down the process of nephrosclerosis, and greatly reduced mortality. η-3 and η-6 polyunsaturated fatty acids also significantly reduced glomerular damage and glomerulosclerosis in immune complex-mediated nephritis.
The effect of ② on human kidney disease: normal human intake of large amounts of linoleic acid can increase renal PGE biosynthesis and increase urinary sodium and creatinine excretion. Schaap et al. observed 15 patients with chronic kidney disease and gave a high-protein diet for 4 weeks after limiting protein intake for 4 weeks, followed by a high-protein diet with dietary supplementation of η-3 polyunsaturated fatty acids, and found that glomerular filtration rate and renal blood flow were highest after supplementation with η-3 polyunsaturated fatty acids, urinary protein excretion did not change, blood triglyceride The levels of triglycerides decreased, but total cholesterol and LDL increased. Fish oil also has a more beneficial effect on IgA nephropathy. It has an immunosuppressive effect on the transplanted kidney.
Based on the beneficial effects of η-3 and η-6 polyunsaturated fatty acids on kidney disease, a diet low in cholesterol and high in polyunsaturated fatty acids has been emphasized as a first-line treatment for nephrotic syndrome. However, different conclusions exist as to whether a low-cholesterol diet can reduce hypercholesterolemia in nephrotic syndrome. Recently Grundy suggested that the administration of a low-fat diet to correct hypercholesterolemia may elevate blood triglycerides [51].Maschio observed a large group of patients with early renal failure caused by different etiologies given low protein, low cholesterol, and high polyunsaturated fatty acid therapy and found no cholesterol or triglyceride lowering effect.Schasschmidt et al. gave experimental nephrectomized major The animals were supplemented with fish oil 5 weeks after surgery, and the experimental group showed deterioration in renal function and a high incidence of glomerulosclerosis on renal histology, failing to show the beneficial effects of fish oil. No beneficial effects were observed in mice with spontaneous lupus nephritis given linoleic acid. Thus, dietary treatment still needs a lot of clinical and experimental studies.
(3) Vitamin control.
Vitamin A: Given that vitamin A is not deficient but far beyond the normal range in patients with chronic renal failure, clinical attention should be paid to the fact that vitamin A should not be supplemented in that case.
Vitamin D: There are two main types of vitamin D, ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3), which are steroidal complexes that are metabolized to 1,25(OH)2D3 or calcitriol and become active. Vitamin D is involved in regulating calcium and phosphorus metabolism by regulating intestinal calprotectin in the mucosal cells of the small intestine. The kidney is the main organ that produces 1,25(OH)2D3, which has a half-life of 6-8 hours and a normal value of 25-50 pg/ml, and is 99% in bound form in the body. Certain foods contain vitamin D, such as fish oil, egg yolk, liver, etc. The absorption site is mainly in the upper part of the small intestine, while vitamin D in the skin is broken down into vitamin D3 by sunlight exposure and enters the blood circulation. Vitamin D is converted to 1,25(OH)2D3 in the kidney, which inhibits 1α hydroxylase activity and increases calcium and phosphorus reabsorption. 1,25(OH)2D3 also has immunomodulatory effects, causing the release of cytokines, such as interleukins and γ-interferon, and can strengthen monocyte antigenicity and enhance B-lymphocyte synthesis of immunoglobulins. In experimental studies, 1,25(OH)2D3 was found to be effective in preventing autoimmune diseases and prolonging the survival of allografts.
In severe renal failure, intestinal absorption of calcium is reduced and 1,25(OH)2D3 synthesis is decreased, leading to abnormal bone development and manifesting as rickets. In nephrotic syndrome, reduced 1,25(OH)2D3 levels in children are associated with the loss of its precursor 25(OH)D3 due to the elimination of large amounts of protein in the urine and the combination of 25(OH)D3 and vitamin D binding protein. Some of the 1,25(OH)2D3 is also bound to vitamin D binding protein and is lost in the urine. PTH levels are elevated in the early stages of renal failure, to the same extent as renal failure, and hypocalcemia is common in chronic renal failure and is an important factor in stimulating PTH secretion. In uremia, the number of 1,25(OH)2D3 receptors in parathyroid cells is reduced, resulting in a weaker inhibitory effect of 1,25(OH)2D3 on PTH secretion. 1,25(OH)2D3 deficiency stimulates PTH secretion in two ways: by decreasing intestinal calcium absorption and causing hypocalcemia, and by directly altering PTH gene transcription. Animal experiments have shown that 1,25(OH)2D3 not only reduces PTH synthesis but also inhibits parathyroid cell proliferation, so 1,25(OH)2D3 synthesis deficiency may also be an important factor in stimulating parathyroid hyperplasia.
Vitamin E: Given that chronic renal failure and dialysis patients are prone to vitamin E deficiency, vitamin E (300 mg/d) should be appropriately supplemented in order to maintain vitamin E at normal levels. However, vitamin E in the blood circulation is not easily lost in dialysis when partially combined with protein, so it should not be blindly over-supplemented, and if you can eat normally you can maintain vitamin E in your body in a normal state.
Vitamin B6: Normal adults need 2.2mg of vitamin B6 daily, and in chronic renal failure patients are prone to vitamin B6 deficiency, so it is recommended that the daily supplementation of vitamin B610mg, the amount is sufficient to correct its lack of state. In addition, supplementation of vitamin B6 has a certain effect on reducing the high oxalic acid content of patients.
Vitamin C: Vitamin C is a small molecule (98d), which is easily removed by hemodialysis. It should be decided by both vitamin C level and blood oxalic acid level, and it is better to test both, but only when vitamin C is insufficient and blood oxalic acid is not high.
Folic acid and vitamin B12: In recent years, it has been suggested that high doses of folic acid can lower cholesterol and triglycerides, thereby reducing cardiovascular complications in chronic renal failure. It is worth noting that excessive folic acid supplementation can cause fatigue, irritability, headache, insomnia and gastrointestinal symptoms such as nausea and vomiting. Therefore, a daily folic acid supplementation of 5 mg is appropriate for patients with chronic renal failure. Even if the patient’s need for folic acid increases when receiving erythropoietin therapy, 5 mg of folic acid supplementation is sufficient to meet the treatment needs.
The amount of vitamin B12 stored in the body is about 2~5mg, even if there is a long-term lack of vitamin B12 in food, it will take 3~6 years for the body to develop vitamin B12 deficiency. On the contrary, in chronic renal failure hemodialysis patients, if conventional dialyzers (copper mimic membrane or acetate membrane) are used, the level of vitamin B12 in the body is often high because of the large molecular weight of vitamin B12 which is not easily permeable (among water-soluble vitamins, it is the only one that cannot be permeated). Therefore, if not for the application of erythropoietin, chronic renal failure and dialysis patients do not need to supplement vitamin B12, but only folic acid.
2. Dietary practice guidelines.
The following are several dietary remedies.
(1) bean juice drink: black soybeans, mung beans, adzuki beans, raw rice kernel 30g each washed, 10 garlic, wheat bran 60g (cloth bag), a total of water into the boiling cooked and rotten, drink thick juice. Appetite, cure edema.
(2) clothed peanuts, red dates, adzuki beans, dulcimer, fenugreek 30g each boiled and cooked with water, drink thick juice. Tonic kidney to cure edema.
(3) U carp soup: U carp a (500g), remove the scales and viscera, into the white atractylodes, mulberry demolition to, Chen Pi, adzuki beans 15g each, white onion 5, cooked into a thick soup. Drink soup and eat fish to cure edema.
(4) astragalus 30g (gauze bag), raw rice kernel 30g, red beans 30g, red dates 7, a total of water into the boiling cooked rotten, remove the astragalus and eat. Tonic deficiency to eliminate edema.
(5) Fresh goat milk 250~500ml per day for children and 500~1000ml per day for adults can cure edema and reduce proteinuria.
(6) Mulberry seeds 30g, raw coix seeds 20g, raisins 20g plus appropriate amount of round-grained rice, cook porridge, eat twice a day, can nourish the kidney to cure edema.
(7) carp simmered garlic: carp 1, remove the viscera, garlic 1 ~ 2, peeled, filled into the belly of the fish, wrapped in paper, thread bound, outside the yellow mud wrapped, simmered in grass ash, remove the mud paper, eat fish, can cure edema.
(8) astragalus boiled hen: hen 1, cut open the abdomen to remove the viscera, into the astragalus 120g boiled, eat chicken and drink soup, tonic deficiency to eliminate edema.
(9) Duck with Cordyceps: 1 old duck, cut open the abdomen and remove the viscera, enter Cordyceps 6g, garlic 3~4, boil it. Eat the duck and drink the soup, tonic deficiency and eliminate edema.
(10) Steamed snapper with sand: 1 snapper, washed and steamed with 6g of sand, eat snapper and drink soup. Tonic deficiency to eliminate edema.
(11) steamed garlic in winter melon: 1 in winter melon, cut open at one end, incorporating 120g of garlic, peeled, 60g of adzuki beans, steamed and taken to drink its juice, cure edema.
(12) Coix seed rice soup: 60g of coix seed rice, 100g of japonica rice and 1000ml of water.