Medical Nutrition Therapy for Renal Disorder And

Enteral Nutrition A. Afaghi, MPH, PhD Qazvin University of Medical Science, School of Medicine

Function Of The Kidney

• The main function of kidney is to maintain homeostatic balance with respect to fluids, electrolytes and organic solutes by continues filtration.

• The normal kidney has the ability to perform this function over a wide range of dietary fluctuations in sodium, water and various solutes . • Kidney receives 20% of cardiac output, which filtrates 1600 L/day of blood

Function Of The Kidney

• 180 L of fluid is produced in filtering this blood and through active reabsorbing certain compounds, the composition of this fluid changed to 1.5 L urine in an average day • If the waste products are not eliminated appropriately, the condition will be Azotomia • Renal failure is the consequence of inability to excretion of daily load of these waste.

azotemia

• Urea predominates in amount, depending on the protein content of the diet. Uric acid, creatinine (Cr), and ammonia are present in small amounts. If normal waste products are not eliminated appropriately, they collect in abnormal quantities in the blood, known as

azotemia.

oliguria

• The minimum urinary volume capable of eliminating a relatively fixed 600 mOsm of solute is 500 mL, assuming that the kidney is capable of maximum concentration.

• Urinary volume of less than 500 mLi day is called

oliguria;

• it is impossible for such a small urine volume to eliminate all of the daily waste.

RENAL DISEASES

• The manifestations of renal disease are significant. They can be ordered by degree of severity: (1) kidney stones, (2) acute kidney injury (AKI), (3) chronic kidney disease (CKD), and (4) end-stage renal disease (ESRD).

Kidney Stones (Nephrolithiasis)

• frequent occurrences between the ages of 30 and 50, predominance in males, and a high recurrence rate. The risk doubles in those with a family history of kidney stones • Increased frequency of obesity, diabetes, and metabolic syndrome have resulted in increasing rates of nephrolithiasis among women, decreasing the male/female ratio from 1.7: 1 to 1.3: 1

Calcium stones

• Calcium stones are the most common: 60% of stones are calcium oxalate, 10% calcium oxalate and calcium phosphate, and 10% calcium phosphate. Other stones are 5% to 10% uric acid, 5% to 10% struvite, and 1% cystine.

Type 2 diabetes and kidney stones • Uric acid stones are common in the presence of type 2 diabetes. Hyperinsulinemia may also contribute to the development of calcium stones by increasing urinary calcium excretion

Obesity and kidney stones • Obese stone formers excrete increased amount of sodium, calcium, uric acid, and citrate, and have lower urine pH.

• Obesity is the strongest predictor of stone recurrence in • first-time stone formers. • As body weight increases, the excretion of calcium, oxalate, and uric acid also increases.

• Patients with higher body mass index (BMI) have a decrease in ammonia excretion and impaired hydrogen ion buffering • With increasing BMI, uric acid stones become more dominant than calcium oxalate stones, especially in men.

Weight control in stone former

• Weight control may be considered one of the preventive modalities and in stone formers, a BMI of 18 to 25

kg/m2

is recommended.

Hypercalciuria

•

Calcium Stones.

One third to one half of patients with calcium stones are hypercalciuric. •

Hypercalciuria

describes a value of calcium in excess of 300 mg (7.5 mmol) per day in men, 250 mg (6.25 mmol) per day in women, or 4 mg (0.1 mmol)/kg/day for either in random urine collections of outpatients on unrestricted diets. Causes of hypercalciuria may include : • primary hyperparathyroidism, sarcoidosis, • excess vitamin D intake, hyperthyroidism, glucocorticoid • use, or renal tubular acidosis (RT A) • A trial of combined calcium vitamin D supplementation to prevent bone loss and fractures led to higher rates of stone formation in women

urinary calcium and urinary oxalate

• The risk in both men and women rises with increasing urine calcium and oxalate and decreases with increasing citrate and urine volume.

• Reducing dairy product intake may lead to osteoporosis, and is not recommended

Foods to Avoid for a Low Oxalate Diet • Rhubarb • Spinach • Strawberries • Chocolate • Wheat bran and whole-grain wheat products • Nuts (almonds, peanuts, or pecans) • Beets • Tea (green, black, iced, or instant) • High doses of turmeric

Data from Siener R et al: Oxalate content of cereals and cereal products, J Agric Food Chem 54:3008, 2006.

Uric Acid Stones

Uric acid is an end product of purine metabolism from food, and tissue catabolism. Approximately half of the purine load is from endogenous sources. Exogenous dietary sources provide the other half,. The solubility of uric acid depends on urine volume, the amount excreted, and urine pH. Uric acid stones form when urine is supersaturated with undissociated uric acid, which occurs at urinary pH less than 5.5.

Effect of Urine pH on Stone Formation pH <5.5

5.5-7.5 >7.5

State of Urate Likely Stone Development Undissociated urate Uric acid stones Dissociated urate Calcium oxalate stones Dissociated urate

Calcium phosphate stones

Ascorbic acid & urinary oxalate

• Ascorbic acid accounts for 35% to 55%, and glyoxylic acid accounts for 50% to 70% of urinary oxalate. In patients with CKD, excessive vitamin C intake may lead to stone formation. Oxalate synthesis is not increased with a high protein diet (Knight et aI., 2009). Because pyridoxine acts as a cofactor in the conversion ofglyoxylate to glycine, its deficiency could increase endogenous oxalate production.

Milk and oxalate absorption

• Milk appears to reduce oxalate absorption by binding it in the gut lumen as calcium oxalate , making it less absorbable. Herbal teas have much lower oxalate content of 31-75 urnol/L and are an acceptable alternative (Massey, 2007). Soft drinks and colas that contain phosphoric acid should be avoided because of their urine acidifying effect

Alkaline foods and renal acid load

• The most abundant alkaline foods are plant based foods; particularly vegetables and fruit abundant in alkalinizing micronutrients such magnesium, calcium, sodium,and potas ium. A more alkaline diet consisting of a higher fruit and vegetable intake is associated with a low potential renal acid load (PRAL) (Remer, 1995)

ACUTE KIDNEY INJURY (AKI) (ACUTE RENAL FAILURE) • is characterized by a sudden reduction in

glomerular filtration rate (GFR),

the amount of filtrate per unit in the nephrons, and altered ability of the kidney to excrete the daily production of metabolic waste. AKI can occur in association with oliguria (decreased output of urine) or normal. urine flow, but it typically occurs in previously healthy kidneys. Duration varies from a few days to several weeks.

Causes of AKI

• The causes of AKI are numerous, and can occur simultaneously. These causes are generally classified into three categories: (1) Inadequate renal perfusion (prerenal) (2) diseases within the renal parenchyma (intrinsic) (3) urinary tract obstruction (postrenal)

Medical Nutrition Therapy in AKI

•

Protein

. A range of recommended levels can be found in the literature, from 0.5-0.8 g/kg for nondialysis patients to 1-2 g/kg for dialyzed patients. With CRRT protein losses are high, and estimated protein needs increase to 1.5-2.5 g/kg. • Energy: 30 to 40 kcal/kg of dry body weight per day.

Fluid and Sodium

• Sodium is restricted, based on decreased urinary production. In the oliguric phase when the sodium output is very low, intake should be low as well, perhaps as low as 20 to 40 mg/day.

Summary of Medical Nutrition Therapy for Acute Kidney Injury

Nutrient

Protein Energy

Amount

0.8-1 glkg IBW increasing as GFR returns to normal; 60% should be HBV protein 30-40 kcallkg of body weight Potassium Sodium Fluid Phosphorus

30-50 mEq/day

phase in oliguric phase (depending on urinary output, dialysis,and serum K+level); replace losses indiuretic 20-40 mEq/day in oliguric phase (depending on urinary output, edema, dialysis, and serum Na" level); replace in diuretic phase Replace output from the previous day (vomitus, diarrhea, urine) plus 500 mL Limit as necessary •

GFR,

Glomerular filtration rate;

HBV,

high biologic value;

lBW,

ideal body weight;

K',

potassium;

Na',

sodium.

CHRONIC KIDNEY DISEASE (CKD)

• Once approximately one half to two thirds of kidney function has been lost, regardless of the underlying disease, progressive further loss of kidney function ensues • Diabetes is the leading risk factor for CKD followed by hypertension.

Medical Nutrition Therapy (CKD)

• The recommended dietary protein level for CKD patients has changed over time. Historically, these patients received diets high in protein (up to 1.5 g/kg/day) • However, studies have shown that a reduction of protein intake to as low as 0.8 g/kg/day may decrease proteinuria without adversely affecting serum albumin.

• Dietary protein has been championed as a factor that increases glomerular pressure and thus leads to accelerated loss of renal function. 50% to 60% of the protein should be from animal sources

Medical Nutrition Therapy (CKD)

• The primary objectives ofMNT are to manage the symptoms associated with the syndrome ( edema, hypoalbuminemia, and hyperlipidemia ), decrease the risk of progression to renal failure, and maintain nutritional stores. Patients are primarily treated with Statins to correct hyperlipidemia, low-sodium diets, and diuretics

Medical Nutrition Therapy (CKD)

• Patients with an established severe protein deficiency who continue to lose protein may require an extended time of carefully supervised nutritional care. The diet should attempt to provide sufficient protein and energy to maintain a positive nitrogen balance and to produce an increase in plasma albumin concentration disappearance of edema . In most cases, and sufficient intake from carbohydrate and fats are needed to spare protein for anabolism.

Disease of The Kidney • Nephrotic syndrome ( protein losses) • Nephritic Syndrome (hematuri) • Acute Renal failure (ARF) • Tubular defect • Renal stones • End stage disease (ESRD)

Nephrotic syndrome

• Common manifestation is loss of glomerular barrier to protein. • Large protein losses in the urine lead to hypo albuminemia which consequent edema, hypercholesterolemia, hypercoagulability and abnormal bone metabolism.

Cause of Disease

• More than 90% of the cases of nephrotic syndrome stem from 3 systemic disease: Diabetes mellitus, systemic lupus erythematosus and amyloidosis and four disease primarily of the kidney (minimal change disease )

Nutritional Care

• The primary objective is to manage the symptoms associated with the syndrome: Edema hypoalbuminemia hyperlipidemia • Decrease the risk of progression to renal failure, and maintain nutrition stores

End-stage renal disease (ESRD)

• Reflects the kidney's inability to excrete waste products, maintain fluid and electrolyte balance, and produce hormones. As renal failure slowly progresses, the level of circulating waste products eventually leads to symptoms of uremia

End-stage renal disease (

Uremia

)

•

Uremia

is a clinical syndrome of malaise, weakness, nausea and vomiting, muscle cramps, itching, metallic taste in the mouth, and neurologic impairment that is brought about by an unacceptable level of nitrogenous wastes in the body.

Medical Treatment ( ESRD)

• dialysis, • transplantation, • or medical management progressing to death

Medical Nutrition Therapy (ESRD, Dialysis)

• • Protein: Dialysis is a drain on body protein, so protein intake must be increased accordingly. Protein losses of 20 to 30 g can occur during a 24-hour

Peritoneal dialysis (PD)

, with an average of 1 g/hour.

• Those receiving PD need 1.2 to 1.5

g/kg

of body weight. At least 50% should be HBV protein.

Patients who receive HD three times per week require a daily protein intake of 1.2 weight

g/kg

of body

Energy,

Fluid and Sodium Balance • Depending on the patient's nutrition status and degree of stress, between 25 and 40 kcal/kg of body weight should be provided, with the lower amount for transplantation and

Peritoneal dialysis (PD)

patients and the higher level for the nutritionally depleted patient

Fluid and Sodium Balance • The vast majority of dialysis patients need to restrict sodium and fluid intakes. Excessive sodium intake is responsible for increased thirst, increased fluid gain, and resultant hypertension. Even those patients who do not experience these symptoms but produce minimal amounts of urine will benefit from a reduced sodium intake to limit their thirst and prevent large intradialytic fluid gains.

Fluid and Sodium Balance • In the patient who is maintained on HD, sodium and fluid intake are regulated to allow for a weight gain of 4 to5 lb (2 to 3 kg) from increased fluid in the vasculature between dialyses. The goal is a fluid gain of less than 4% of body weight . A sodium intake of 87 to 130 mEq (2 to 3 g) daily and a limit on fluid intake (usually about 750 mLiday

Fluid and Sodium Balance • The fluid contained in solid foods is not included in the 750 mL limit . Solid foods in the average diet contribute approximately 500 to 800 mLiday of fluid . This fluid in solid food is calculated to approximately replace the 500 mL/day net insensible water loss.

Lipid

• Atherosclerotic cardiovascular disease is the most common cause of death among patients maintained on long-term Dialysis • Treatment of hyperlipidemia with diet or pharmacologic agents remains controversial.

Lipid

• Epidemiologic evidence demonstrating increased incidence of atherosclerotic coronary disease is balanced by studies that demonstrate that patients with clearly defined clinical evidence of atherosclerosis at the initiation of dialysis are at no increased risk for a cardiovascular event. Although routine treatment appears unwarranted, a good case can be made for dietary and pharmacologic treatment of patients with ESRD with underlying lipid disorders and evidence of atherosclerosis

Iron and Erythropoietin

• The anemia of chronic renal disease is caused by an inability of the kidney to produce EPO, the hormone that stimulates the bone marrow to produce red blood cells, an increased destruction of red blood cells secondary to circulating uremic waste products; and blood loss with dialysis or blood sampling. A synthetic form of EPO, recombinant human EPO (rHuEPO), is used to treat this form of anemia

Vitamins

• Water-soluble vitamins are rapidly lost during dialysis. In general, ascorbic acid and most B vitamins are lost through dialysate at approximately the same rate they would have been lost in the urine (depending on the type and duration of treatment), with the exception of folate, which is highly dialyzable . Patients who still produce urine may be at increased risk of loss of water-soluble vitamins. Folate is recommended to be supplemented at 1 rug/day based on extra losses . Because vitamin B12is protein-bound, losses of this B12 vitamin during dialysis are minimal

Blood Test BUN Dialysis patient ’s guide to blood values function diet normal value mg/dl 4-22 dialysis value mg/dl <100 Uric acid Creatinine 40-85 0.7-1.5

same 10-15 protein waste meat 3ser/d purine waste no change waste no change of muscle dialysis breakdown controls

Nutrition support

• Nutrition support is the delivery of formulated enteral or parenteral nutrients for the purpose of maintaining or restoring nutritional status. Enteral nutrition (EN) refers to the provision of nutrients into the gastrointestinal tract (GIT) through a tube or catheter . In certain instances EN may include the use of formulas as oral supplements or meal replacements. Parenteral nutrition (PN) is the provision of nutrients intravenously.

Enteral and parenteral nutrients

• PN should be used in patients who are or will become malnourished and who do not have sufficient gastrointestinal function • EN decreases the incidence of hyperglycemia when compared with PN.

ENTERAL NUTRITION

• By definition,

enteral

implies using the GIT, primarily via "tube feeding." When a patient has been determined to be a candidate for EN, the location of nutrient administration and type of enteral access device is selected.

ENTERAL NUTRITION Nasoenteric Routes and tube placement • Nasogastric (Cervical pharyngostomy or esophagostomy, Gastrostomy) • Nasoduodenal (Gastrostomy) • Nasojejunal (Jejunostomy) (duodenum, jejunum, ileum are 3 sections of small intestine)

Nasogastric tubes (NGTs)

• • are the most common way to access the GIT. They are generally appropriate only for those requiring short-term EN, which is defined as 3 or 4 weeks. Typically, the tube is inserted at the bedside by a nurse or dietitian. The tube is passed through the nose into the stomach.

Patients with normal gastrointestinal function tolerate this method, which takes advantage of normal digestive, hormonal, and bactericidal processes in the stomach. Rarely, complications can occur

Factors to Consider When Choosing an Enteral Formula

• Ability of the formula to meet the patient's nutritional requirements • Caloric and protein density of the formula (i.e., kcal/mL, g protein/mL, kcal :nitrogen ratio) • Gastrointestinal function of the patient • Presence of lactose, which may not be tolerated • Sodium, potassium, magnesium, and phosphorus content of the formula, especially in cardiopulmonary, renal, or • hepatic failure • Type of protein, fat, carbohydrate, and fiber in the formula tolerable for the patient's digestive and absorptive capacity • Viscosity of the formula related to tube size and method of feeding

Monitoring the Patient Receiving Enteral Nutrition

• Abdominal distention and discomfort • Fluid intake and output (dail ) • Gastric residuals (every 4 hr) if appropriate • Signs and symptoms of edema or dehydration (daily) • Stool output and consistency (daily) • Weight (at least 3

times/wk)

• Nutritional intake adequacy (at least 2

times/wk)

• Serum electrolytes, blood urea nitrogen, creatinine, (2-3 times/wk) • Serum glucose, calcium, magnesium, phosphorus,(weeklyor as ordered)

Macronutrients, vitamins, minerals, fluids • 30% to 85% of Energy as CHO • 15% and 30% of the total kilocalories of standard formulas are provided by lipids • 15% Energy as protein

MCT (Medium chain triglyceride) • MCTs can be added to enteral formulas because they do not require bile salts or pancreatic lipase for digestion and are absorbed directly into the portal circulation. Most formulas provide 0% to 85% of fat as MCTs. • MCTs do not provide the essential linoleic or linolenic acids; they must therefore be provided in combination with long-chain triglycerides.

• MCT is available naturally in milk and coconut oil

Omega-3

• Formulas contain a combination of (omega-3 fatty acids and (omega-6 fatty acids. The (omega-3 fatty acids include eicosapentaenoic acid and docosahexanoic acid. These are considered advantageous compared with (omega-6 fatty acids because of their anti inflammatory effect

Vitamins, Minerals, and Electrolytes

• Most, but not all available formulas are designed to meet the dietary reference intakes

(DRls)

for vitamins and minerals if a sufficient volume is taken.

Fluid

• Fluid needs for adults can be estimated at 1 mL of water per kilocalorie consumed, or 30 to 35 mL/kg of usual body weight Without an additional source of fluid, tube fed patients may not get enough free water to meet their needs, particularly when concentrated formulas are used.

• Standard (1 kcallmL) formulas contain approximately 85% water by volume, but concentrated (2 kcallmL) formulas contain only approximately 70% water by volume .

• All sources of fluid being given to a patient receiving EN, including feeding tube flushes, medications, and intravenous fluids, should be considered when determining and calculating a patient's intake. Additional water can be provided through the feeding tube as needed

Energy, protein requirements

• Metabolic basal:1 kcal/kg/h (for men), 0.9 kcal/kg/h (for women) • Extra energy is required for activity (300 1000 kcal) • Protein 0.8 g/kg/B/weight

Traditional & formulated foods

Whole Milk or yogurt, 240 ml=150 kcal,12g CHO,8g protein Fresh Fruit juice (apple), 240 ml= 120 kcal Filtered Soup, 240 = 100 kcal Canned fruit, 240 = 150 kcal Coconut oil, 1 g = 9 kcal, MCT

Ensure

( gluten free, lactose free ), • 400 g Can = 1724 kcal, 62 g protein, 64 g fat • 100 g = 431 kcal, 15.5 g protein, 14 g fat • 54.5 g (6 spoon+190ml=230ml) =230 kcal,

1 ml=1 kcal

• 400 g (1 Can) = 7 and half meals of 230 ml