With the industrialization of food and the increase in household income, food consumption has increased dramatically. Compared to the 1970s, the average energy intake is 500 calories/day higher, leading to a significant increase in obesity prevalence. Obesity, in turn, is a risk factor for diabetes, cardiovascular disease, and chronic kidney disease (CKD), making obesity control and nutritional therapy an integral part of CKD management. The effect of obesity on the kidney Dietary factors that increase the risk of CKD 1. sodium Because sodium can prolong the shelf life of food, processed foods often contain a large amount of sodium chloride within. Secondly, with the integration of Chinese and Western cultures, there is excessive intake of Western diet, which is higher in calories and higher in food sodium. In addition, sodium intake is 30% higher when eating out than when eating at home. Excessive sodium intake in patients with kidney disease can lead to elevated systemic blood pressure and increased blood volume, which subsequently makes blood pressure control more difficult. The impact of excessive sodium intake on kidney health is far from raising blood pressure one, but can also increase body weight, cause glomerular hypertrophy and aggravate kidney damage. Studies in animal models have shown that limiting sodium intake can reduce glomerular hypertrophy and decrease susceptibility to hypertensive injury. Excessive sodium intake can stimulate the release of NADH and NADPH from the renal cortex, aggravating oxidative stress and damaging the kidney. In addition, excessive sodium intake can also increase the expression of transforming growth factor beta, accelerating renal scarring and fibrosis. Therefore, CKD patients are recommended to have a low sodium diet and reduce the frequency of consuming fast food, processed food and eating out so as to reduce sodium intake. 2. Phosphate Compared to the daily diet, the intake of phosphate in processed foods increases by >1,000 mg. Excessive phosphate intake can cause an increase in fibroblast growth factor 23 (FGF-23) levels and promote the progression of kidney disease. In addition, elevated FGF-23 levels are associated with an increased risk of cardiovascular disease, including left ventricular hypertrophy and atrial fibrillation. 3. Protein Reasonable control of protein intake is a major modifiable risk factor for slowing the progression of CKD, especially for adult obese CKD patients. The average protein requirement (EAR) refers to the minimum protein intake to maintain zero nitrogen balance (regardless of protein quality.) The protein EAR for men (70 kg) and women (57 kg) aged 19-50 years is 0.66 g/kg/d, or 47 g/d for men and 38 g/d for women. Excessive animal protein intake may affect glomerular hemodynamics. Adjustment from low to high animal protein intake in healthy individuals increased renal blood flow and GFR by more than 30%, whereas vegetable protein intake had no effect on renal blood flow. Excessive animal protein intake in obese patients may cause dilatation of the small inlet arteries and increased intra-glomerular pressure, leading to elevated GFR or hyperfiltration and increased risk of glomerulosclerosis. Studies have shown that intake of red meat increases the risk of ESRD and that reducing red meat intake decreases the risk of ESRD; a low-protein diet (0.3 g/kg/d) may delay the progression of kidney disease compared with a low-protein diet (animal and vegetable protein, 0.6 g/kg/d). Restricting protein intake can reduce GFR, especially in patients with kidney disease due to diabetes, obesity, and hypertension, with greater benefit. However, it is important to note that restricting protein intake should take into account the patient’s physical condition, nutritional needs and dietary habits in a comprehensive manner to develop an individualized program. 4, fruits and vegetables The dietary habits of people in modern society are generally too much animal protein intake and too little fruit and vegetable intake. Too much meat intake and too little fruit and vegetable intake can trigger an imbalance of non-volatile acids (mainly from animal protein and grains) and bases (from fruits and vegetables), leading to chronic mild metabolic acidosis, stimulating endothelial cells to secrete endothelin 1, which then promotes renal fibrosis, foot cell decomposition and apoptosis. In addition, acidosis can also stimulate the secretion of angiotensin II, accelerating the progression of kidney disease. 5, dietary fiber Eating more dietary fiber-rich foods (grains, legumes, fruits and vegetables) can increase satiety and help reduce caloric intake and subsequently reduce weight. Studies have shown that more than 50% of CKD patients (GFR <60 mL/min/1.73 m2) have low dietary fiber intake (<14.5 g/d). Low dietary fiber intake in adult CKD patients is associated with elevated levels of inflammatory biomarkers, which can significantly increase the risk of death; increasing dietary fiber intake can help strengthen the intestinal barrier, reduce inflammation, delay the progression of kidney disease, and reduce mortality. The American Dietetic Association recommends a dietary fiber intake of 14 g/1000 kcal for adult CKD patients. The correlation between dietary fiber and inflammation may stem from the intestinal microbiota, as a diet with higher dietary fiber content facilitates the growth of intestinal commensal bacteria, such as bifidobacteria, which inhibit the growth of Gram-negative bacteria and subsequently reduce endotoxin levels.