STUDY - Technical - New Dacian's Medicine
Diet
Therapy (3)
Translation Draft
We continue previous posts with diet in case of chronic kidney failure. Dietary therapy plays an essential role in the treatment of all stages of renal failure, but is of particular importance in the terminal stage of kidney disease. Patients with chronic renal failure are particularly susceptible to malnutrition due to inadequate intake and alteration of nutrient metabolism.
In the absence of surgery, vitamin D deficiency can lead to decreased calcium absorption, hyperparathyroidism and osteodystrophy. Dialysis itself removes nutrients, and dialysis patients pose a risk for vitamin B6, vitamin C and folate deficiency (increased plasma levels of vitamin A and disorders in carnitine metabolism may occur). Excessive protein intake increases glomerular filtration and can accelerate the loss of kidney function (i.e., protein restriction in the diet can delay the progression of kidney disease).
Energy intake should be adequate (35 kcal/kg daily) to spare the proteins consumed and to reduce the catabolism of endogenous proteins, but also to reduce the risk of developing malnutrition. Patients with progressive renal impairment may benefit from a diet that provides 0.55-0.6 g of protein/ kg daily, including 0.35g/kg/day of high biological value proteins (animal proteins such as meat, eggs and fish). If diets with very limited protein intake (0.28 g protein/ kg daily) are tried in patients with severe renal impairment, supplementation with amino acids and ketoacids is required to prevent malnutrition.
Reduction of phosphorus in the diet (5-10 mg/ kg daily) is a trait inherent in hypoprotein diets. More severe restriction of dietary phosphorus is only necessary if serum phosphorus levels are increased. Potassium restriction in the diet is not usually necessary in patients without dialysis, but if hipposemia is present, restriction of potassium intake may be used. Sodium intake is limited to 1,000-3,000 mg/ day, usually this level is sufficient to control hypertension and edema from renal failure. Dialysis patients, as well as non-dialysis patients, often have increased plasma levels.
It is advisable to introduce dietary restriction of total fats (less than 30% of total energy intake), saturated fats (less than 10%) cholesterol (below 300 mg/day), although the reduction in lipid levels or mortality by this method has not been sufficiently documented. Patients with dialysis terminal renal disease should benefit from a protein supplement in the diet (1 - 1.4g/kg in hemodialysis patients and 1.2 - 1.4g/ kg in patients with peritoneal hemodialysis), associated with adequate energy intake (approximately 35 kcal/kg daily), to compensate for the catabolic effects of dialysis. Indeed, hemodialysis patients who consume large amounts of protein (0.93 to 1.29 g/ kg daily) may have a lower mortality rate than those with lower protein intake (0.65 g/kg or less daily).
Patients treated outpatiently, permanently or episodically, by peritoneal dialysis lose large amounts of protein in dialysis, while glucose, which is absorbed from peritoneal dialysis, should be included in the calculations of energy intake. Phosphorus retention with hyperphosphatemia occurs in the terminal stage of renal disease, and treatment of hemodialysis or peritoneal dialysis patients usually requires phosphoric restriction (less than 18 mg/ day) and administration of phosphorous chelating compounds. To maintain calcium balance, dialysis patients need 1,400 to 1,600 mg calcium/ day from diet and supplements. In order to prevent hyperkalemia, potassium intake should be limited to 1,500 to 2,700 mg/ day in patients taking hemodialysis.
In general, patients on peritoneal dialysis do not have elevated levels of serum potassium, so dietary potassium restriction is rarely required. Sodium restrictions (1,000 - 1,500 mg/ day) and liquids (700 - 1,500 ml/ day) are often necessary for hemodialysis patients, as they are usually oligurian or anuric, but achieving such a degree of restriction is difficult for most patients. Increased sodium and fluid intake (up to 6,000 to 8,000 mg sodium/ day and 3,000 ml/ day) is allowed for patients with peritoneal hemodialysis, as dialysis can be adjusted to remove excess. Finally, supplementation with hydrosoluble vitamins and active vitamin D metabolites is necessary in terminal renal disease, due to the likelihood of a deficiency achieved through the diet of restriction, excessive loss and metabolic disorders.
Changes in protein and mineral ration in the dietary treatment of chronic renal failure can be "illustrated" by the following diet: 1. protein dietary factor a. predialysis 0.55 - 0.6 g/kg/day, (0.35 g/kg/day protein with high biological value), b. hemodialysis 1 - 1.4 g/kg/day and c. peritoneal dialysis 1.2 - 1.4 g/kg/day, 2. calcium 1,400 - 1,600 mg/day (regardless of stage), 3. phosphorus a. predialysis 5-10 mg/day, b. hemodialysis and peritoneal dialysis less than 18 mg/kg/day, 4. sodium a. predialysis 1,000 - 3,000 mg/day, b. hemodialysis 1,000 - 1,500 mg/ day (in peritoneal dialysis excess is removed with dialysis) and 5. potassium a. in predialysis is necessary only in case of hyperkalemia, b. in hemodialysis 1,500 - 2,700 mg/ day and c. in peritoneal dialysis is rarely necessary.
To switch to gastrointestinal disorders. Gastrointestinal disorders are almost always associated with alteration of nutritional intake or absorption. These conditions have multiple "forms" and I will address the most "significant" of these.
Let's start with lactose intolerance. Approximately 25% of adults have lactose intolerance, manifested by abdominal distension, flatulence and diarrhoea, occurring after eating medium or large amounts of lactose-containing foods. This disorder is treated by restricting the consumption of these foods. Dairy products are the main source of lactose in the diet, but matured cheese (due to its very low lactose content), yogurt with the addition of active cultures, dairy products with added bacterial enzymes that degrade lactose are well tolerated by most patients. Indeed, most patients experience negligible symptoms when consumption is limited to the equivalent of a milk carton (approximately 12g of lactose) daily or chir less.
Symptomatic treatment of diarrhoea requires the replacement of fluid losses with isotone saline solutions, restriction of lactose intake (less than 5g per meal), fats (less than 40 g/ day) and fibre. Very restrictive regimens such as banana-based diet, rice, apple juice, tea and toast are not recommended, as extreme dietary restriction can compromise the recovery of the intestinal mucosa. A vicious cycle of malabsorption and diarrhea may occur, especially in patients with compromised immunity.
In the case of constipation, diets with high fibre content, especially those with bread, containing whole or partially ground grains, and those with cereals are very useful in treatment and prevention. The typical diet provides around 15g fiber daily, while a high-fiber diet brings 20 to 35g fibre per day, fibre from products containing whole grains, fine fruits and vegetables. Very high intake of fibre from dietary products (greater than 35 g/day) can cause gas distension and increase the risk of intestinal obstruction (also can lead to micronutrient malabsorption).
In the case of gastroesophageal reflux, dietary adjustments may be useful. Because it decreases the tonicity of the lower esophageal sphincter, chocolate, fatty foods and carminatives (e.g. mint) should be avoided. Orange juice, tomato juice and coffee are direct irritants of the mucosa, so you should avoid it. Weight loss in obese patients, drugs such as omeprazole, the 3-hour interval between food intake and switching to clinostatism are measures that can help.
For irritable bowel syndrome, excessive intake of food, drinks sweetened with fructose or sorbitol, or foods with increased lactose content may lead to the appearance of symptoms suggestive of irritable bowel syndrome or may worsen this syndrome if it is already present. If constipation is present, the high-fiber diet may help, although studies evaluating the therapeutic effects of fiber (from diet or supplements) have shown inconsistent results. Close follow-up to each patient of the ratio between different foods and the appearance of symptoms allows the establishment of an individual diet that controls symptoms and ensures adequate nutritional intake.
In inflammatory bowel disease, weight loss is significant in 65-75% of patients with Crohn's disease and in 18-62% of patients with ulcer-hemorrhagic colitis. Reduced dietary intake is the major cause of weight loss due to anorexia and postprandial pain. Establishing an individualized regimen can improve the nutrition status of these patients. Enteropathy with loss of protein and malabsorption of fats, fat-soluble vitamins, vitamin B12 and minerals may occur in patients with inflammatory bowel disease, associating with intestinal loss of some nutrients (such as iron in hemorrhages or zinc in diarrhea). Interactions between food and drugs are also important, for example, sulfasalazine is a competitive inhibitor of folate absorption, and glucocorticoids decrease calcium absorption, causing osteopenia, and promote protein catabolism.
Dietary changes useful in the treatment of these conditions include low lactose intake (if intolerance is suggested by anamnesis) and fats (less than 70g/day or depending on the patient's tolerance, especially if steatorea is present) and sufficient energy and protein intake of tissue repairs. The intake of fibre sofa in the diet should not be limited unless intestinal subocclusion is present.
Dietary preparations useful in inflammatory bowel disease contain predigested proteins up to amino acids, carbohydrates and essential nutrients. It makes sense to reduce the exposure of the damaged intestine to contact with intact proteins that can induce a secondary immune response, but at the same time nutrients and energy must be brought in adequate amounts. In practice, liquid diets evaluated in these conditions contain short chain peptides and moderate amounts of lipids (shredded foods may be useful). Although a reduction in symptoms has been observed in some studies, enteral nutritional support is inferior to treatment with glucocorticoids in remission induction in patients with Crohn's disease. Intolerance to preparations, especially those taken orally, limits their effectiveness in some patients.
We continue in the upcoming post!
We continue previous posts with diet in case of chronic kidney failure. Dietary therapy plays an essential role in the treatment of all stages of renal failure, but is of particular importance in the terminal stage of kidney disease. Patients with chronic renal failure are particularly susceptible to malnutrition due to inadequate intake and alteration of nutrient metabolism.
In the absence of surgery, vitamin D deficiency can lead to decreased calcium absorption, hyperparathyroidism and osteodystrophy. Dialysis itself removes nutrients, and dialysis patients pose a risk for vitamin B6, vitamin C and folate deficiency (increased plasma levels of vitamin A and disorders in carnitine metabolism may occur). Excessive protein intake increases glomerular filtration and can accelerate the loss of kidney function (i.e., protein restriction in the diet can delay the progression of kidney disease).
Energy intake should be adequate (35 kcal/kg daily) to spare the proteins consumed and to reduce the catabolism of endogenous proteins, but also to reduce the risk of developing malnutrition. Patients with progressive renal impairment may benefit from a diet that provides 0.55-0.6 g of protein/ kg daily, including 0.35g/kg/day of high biological value proteins (animal proteins such as meat, eggs and fish). If diets with very limited protein intake (0.28 g protein/ kg daily) are tried in patients with severe renal impairment, supplementation with amino acids and ketoacids is required to prevent malnutrition.
Reduction of phosphorus in the diet (5-10 mg/ kg daily) is a trait inherent in hypoprotein diets. More severe restriction of dietary phosphorus is only necessary if serum phosphorus levels are increased. Potassium restriction in the diet is not usually necessary in patients without dialysis, but if hipposemia is present, restriction of potassium intake may be used. Sodium intake is limited to 1,000-3,000 mg/ day, usually this level is sufficient to control hypertension and edema from renal failure. Dialysis patients, as well as non-dialysis patients, often have increased plasma levels.
It is advisable to introduce dietary restriction of total fats (less than 30% of total energy intake), saturated fats (less than 10%) cholesterol (below 300 mg/day), although the reduction in lipid levels or mortality by this method has not been sufficiently documented. Patients with dialysis terminal renal disease should benefit from a protein supplement in the diet (1 - 1.4g/kg in hemodialysis patients and 1.2 - 1.4g/ kg in patients with peritoneal hemodialysis), associated with adequate energy intake (approximately 35 kcal/kg daily), to compensate for the catabolic effects of dialysis. Indeed, hemodialysis patients who consume large amounts of protein (0.93 to 1.29 g/ kg daily) may have a lower mortality rate than those with lower protein intake (0.65 g/kg or less daily).
Patients treated outpatiently, permanently or episodically, by peritoneal dialysis lose large amounts of protein in dialysis, while glucose, which is absorbed from peritoneal dialysis, should be included in the calculations of energy intake. Phosphorus retention with hyperphosphatemia occurs in the terminal stage of renal disease, and treatment of hemodialysis or peritoneal dialysis patients usually requires phosphoric restriction (less than 18 mg/ day) and administration of phosphorous chelating compounds. To maintain calcium balance, dialysis patients need 1,400 to 1,600 mg calcium/ day from diet and supplements. In order to prevent hyperkalemia, potassium intake should be limited to 1,500 to 2,700 mg/ day in patients taking hemodialysis.
In general, patients on peritoneal dialysis do not have elevated levels of serum potassium, so dietary potassium restriction is rarely required. Sodium restrictions (1,000 - 1,500 mg/ day) and liquids (700 - 1,500 ml/ day) are often necessary for hemodialysis patients, as they are usually oligurian or anuric, but achieving such a degree of restriction is difficult for most patients. Increased sodium and fluid intake (up to 6,000 to 8,000 mg sodium/ day and 3,000 ml/ day) is allowed for patients with peritoneal hemodialysis, as dialysis can be adjusted to remove excess. Finally, supplementation with hydrosoluble vitamins and active vitamin D metabolites is necessary in terminal renal disease, due to the likelihood of a deficiency achieved through the diet of restriction, excessive loss and metabolic disorders.
Changes in protein and mineral ration in the dietary treatment of chronic renal failure can be "illustrated" by the following diet: 1. protein dietary factor a. predialysis 0.55 - 0.6 g/kg/day, (0.35 g/kg/day protein with high biological value), b. hemodialysis 1 - 1.4 g/kg/day and c. peritoneal dialysis 1.2 - 1.4 g/kg/day, 2. calcium 1,400 - 1,600 mg/day (regardless of stage), 3. phosphorus a. predialysis 5-10 mg/day, b. hemodialysis and peritoneal dialysis less than 18 mg/kg/day, 4. sodium a. predialysis 1,000 - 3,000 mg/day, b. hemodialysis 1,000 - 1,500 mg/ day (in peritoneal dialysis excess is removed with dialysis) and 5. potassium a. in predialysis is necessary only in case of hyperkalemia, b. in hemodialysis 1,500 - 2,700 mg/ day and c. in peritoneal dialysis is rarely necessary.
To switch to gastrointestinal disorders. Gastrointestinal disorders are almost always associated with alteration of nutritional intake or absorption. These conditions have multiple "forms" and I will address the most "significant" of these.
Let's start with lactose intolerance. Approximately 25% of adults have lactose intolerance, manifested by abdominal distension, flatulence and diarrhoea, occurring after eating medium or large amounts of lactose-containing foods. This disorder is treated by restricting the consumption of these foods. Dairy products are the main source of lactose in the diet, but matured cheese (due to its very low lactose content), yogurt with the addition of active cultures, dairy products with added bacterial enzymes that degrade lactose are well tolerated by most patients. Indeed, most patients experience negligible symptoms when consumption is limited to the equivalent of a milk carton (approximately 12g of lactose) daily or chir less.
Symptomatic treatment of diarrhoea requires the replacement of fluid losses with isotone saline solutions, restriction of lactose intake (less than 5g per meal), fats (less than 40 g/ day) and fibre. Very restrictive regimens such as banana-based diet, rice, apple juice, tea and toast are not recommended, as extreme dietary restriction can compromise the recovery of the intestinal mucosa. A vicious cycle of malabsorption and diarrhea may occur, especially in patients with compromised immunity.
In the case of constipation, diets with high fibre content, especially those with bread, containing whole or partially ground grains, and those with cereals are very useful in treatment and prevention. The typical diet provides around 15g fiber daily, while a high-fiber diet brings 20 to 35g fibre per day, fibre from products containing whole grains, fine fruits and vegetables. Very high intake of fibre from dietary products (greater than 35 g/day) can cause gas distension and increase the risk of intestinal obstruction (also can lead to micronutrient malabsorption).
In the case of gastroesophageal reflux, dietary adjustments may be useful. Because it decreases the tonicity of the lower esophageal sphincter, chocolate, fatty foods and carminatives (e.g. mint) should be avoided. Orange juice, tomato juice and coffee are direct irritants of the mucosa, so you should avoid it. Weight loss in obese patients, drugs such as omeprazole, the 3-hour interval between food intake and switching to clinostatism are measures that can help.
For irritable bowel syndrome, excessive intake of food, drinks sweetened with fructose or sorbitol, or foods with increased lactose content may lead to the appearance of symptoms suggestive of irritable bowel syndrome or may worsen this syndrome if it is already present. If constipation is present, the high-fiber diet may help, although studies evaluating the therapeutic effects of fiber (from diet or supplements) have shown inconsistent results. Close follow-up to each patient of the ratio between different foods and the appearance of symptoms allows the establishment of an individual diet that controls symptoms and ensures adequate nutritional intake.
In inflammatory bowel disease, weight loss is significant in 65-75% of patients with Crohn's disease and in 18-62% of patients with ulcer-hemorrhagic colitis. Reduced dietary intake is the major cause of weight loss due to anorexia and postprandial pain. Establishing an individualized regimen can improve the nutrition status of these patients. Enteropathy with loss of protein and malabsorption of fats, fat-soluble vitamins, vitamin B12 and minerals may occur in patients with inflammatory bowel disease, associating with intestinal loss of some nutrients (such as iron in hemorrhages or zinc in diarrhea). Interactions between food and drugs are also important, for example, sulfasalazine is a competitive inhibitor of folate absorption, and glucocorticoids decrease calcium absorption, causing osteopenia, and promote protein catabolism.
Dietary changes useful in the treatment of these conditions include low lactose intake (if intolerance is suggested by anamnesis) and fats (less than 70g/day or depending on the patient's tolerance, especially if steatorea is present) and sufficient energy and protein intake of tissue repairs. The intake of fibre sofa in the diet should not be limited unless intestinal subocclusion is present.
Dietary preparations useful in inflammatory bowel disease contain predigested proteins up to amino acids, carbohydrates and essential nutrients. It makes sense to reduce the exposure of the damaged intestine to contact with intact proteins that can induce a secondary immune response, but at the same time nutrients and energy must be brought in adequate amounts. In practice, liquid diets evaluated in these conditions contain short chain peptides and moderate amounts of lipids (shredded foods may be useful). Although a reduction in symptoms has been observed in some studies, enteral nutritional support is inferior to treatment with glucocorticoids in remission induction in patients with Crohn's disease. Intolerance to preparations, especially those taken orally, limits their effectiveness in some patients.
We continue in the upcoming post!
Love, Gratitude and
Understanding!!!
Dorin, Merticaru