1. Describe methods of parenteral nutrition administration, i.e. continuous, cyclic, central, peripheral.
2. Discuss labs for monitoring parenteral nutrition.
3. Describe the possible complications of parenteral nutrition.
4. Identify each part of the nephron and discuss its function.
5. Identify and discuss metabolic abnormalities associated with renal failure.
6. Discuss goals of nutrition therapy in patients with renal failure.
Parenteral Nutrition Information
ROUTES OF INFUSION
Parenteral nutrition, total parenteral nutrition (TPN) or peripheral parenteral nutrition (PPN) is the administration of nutrient (i.e. glucose, amino acids, fat, vitamins and minerals) intravenously either by central or peripheral vein. Indications for use are only when oral or enteral feeding is inadequate or contraindicated. If the gut works, use it first. Solutions vary and depend on calorie, protein, mineral, vitamin, and fluid requirements of the individual.
The components of a parenteral feeding formulation will determine its osmolarity and infusion route. Parenteral nutrition (PN) may be prepared for peripheral venous infusion or infusion through a central venous access device. PN may also be prepared as a total nutrient admixture (TNA) or a “2-in-1” solution. 2-in-1 solutions contain all necessary IV macronutrients and micronutrients in the same container except intralipids, which may be infused separately. Parenteral formulations are hypertonic to body fluids, and, if administered inappropriately, may result in venous thrombosis, thrombophlebitis, and extravasation. Specifically, the osmolarity of a parenteral feeding formulation is dependent primarily on the dextrose, amino acid, and electrolyte content. The maximum osmolarity of PN through a peripheral line is 900 mOsm/L.
Central Parenteral Nutrition
Central Parenteral Nutrition (CPN) is often referred to as “total parenteral nutrition” (TPN) because the entire nutrient needs of the patient may be delivered by this route. A complete, balanced formulation includes dextrose, amino acids, intravenous fat emulsion (IVFE), electrolytes such as potassium, magnesium, and phosphorus, vitamins, and multiple trace elements such as zinc, copper, manganese, chromium, and selenium. CPN is delivered into a large-diameter vein such as the superior vena cava adjacent to the right atrium. The rate of blood flow in these large vessels rapidly dilutes the hypertonic parenteral feeding formulation to that of body fluids. CPN may be concentrated to provide adequate calories and protein for those patients requiring a fluid restriction. CPN is preferred for use in patients who require PN support for longer than 7 to 14 days.
Peripheral Parenteral Nutrition
Peripheral Parenteral Nutrition (PPN) has a similar composition as CPN, but lower concentrations of nutrient components are necessary to allow peripheral venous administration. It has a lower dextrose dose of 150 to 300 g/d (5-10% final concentration) and amino acid (50-100 g/d, or 3% final concentration) content compared to CPN. PPN is usually an undesirable option for patients with a fluid restriction because concentrating the solution frequently results in a hyperosmolar solution that is not suitable for peripheral administration. PPN may be used in patients with mild to moderate malnutrition to provide partial or total nutrition support when they are not able to ingest adequate calories orally or enterally, or when CPN is not feasible. However, this therapy is typically used for short periods (up to 2 weeks). Patients considered for PPN must meet two criteria: (1) have good peripheral venous access, and (2) be able to tolerate large volumes (2.5-3 L) of fluid. They should require at least 5 days but no more than 2 weeks of partial or total PN. The use of PPN is controversial, with many believing that the risk of complications outweighs any potential benefit because candidates for this therapy have only minor, if any, nutritional deficits. IVFE may be used to increase the caloric density of the peripheral parenteral feeding formulation without increasing the osmolarity, and the addition of IVFE has also been reported to improve peripheral vein tolerance of PPN. Contraindications for peripheral parenteral nutrition include:
• Significant Malnutrition
• Severe Metabolic Stress
• Large Nutrient or Electrolyte Needs
• Fluid Restriction
• Need for Prolonged Parenteral Nutrition
• Renal or Liver Compromise
Indications for PN were derived from A.S.P.E.N guidelines and defined as patients with:
• Intestinal hemorrhage
• Intestinal obstruction
• Intractable Vomiting
• Paralytic Ileus
• Severe pancreatitis
• Stool output greater than 1 L/day
• High output fistula
• Short bowel syndrome
• Bone Marrow recipients having nausea, vomiting, and severe mucositis lasting longer than 3 days.
Other circumstances where PN has been shown to be of benefit include: perioperative support of patients with moderate to severe malnutrition, acute exacerbation of Crohn’s disease, and critical care patients who will be NPO for prolonged periods of time who are unable to utilize their gut. PN is costly and may result in serious complications when used inappropriately. The therapy should only be used in those patients who will benefit.
Considerations for PN use
1. Patients who are candidates for PN support cannot, should not, or will not eat adequately to maintain their nutrient stores. These patients are already, or have the potential, of becoming malnourished.
2. PPN may be used in selected patients to provide partial or total nutrition support for up to 2 weeks in patients who cannot ingest or absorb oral or enteral tube-delivered nutrients, or when central-vein PN is not feasible.
3. CPN support is necessary when parenteral feeding is indicated for longer than 2 weeks, peripheral venous access is limited, nutrient needs are large, or fluid restriction is required, and the benefits of PN support outweigh the risks.
Use CPN when:
1. Patient has failed EN trial with appropriate tube placement (postpyloric).
2. EN is contraindicated or the intestinal tract has severely diminished function due to underlying disease or treatment. Possible applicable conditions are as follows:
• Paralytic Ileus
• Mesenteric ischemia
• Small bowel obstruction
• GI fistula except when enteral access may be placed posterior to the fistula or volume of output (less than 200 mL/d) supports a trail of EN.
3. As occurs in postoperative nutrition support, the exact duration of starvation that can be tolerated without increased morbidity is unknown. Expert opinion suggests that wound healing would be impaired if PN is not started within 5 to 10 days postoperatively for patients unable to eat or tolerate enteral feeding.
4. The patient’s clinical condition is considered in the decision to withhold or withdraw therapy. Conditions where nutrition support is poorly tolerated and should be withheld until the condition improves are severe hyperglycemia, azotemia, encephalopathy and hyperosmolality, and severe fluid and electrolyte disturbances.
Carbohydrate- is used in the form of dextrose, which provides 3.4 kcal/g. Dextrose is commercially available in multiple concentrations ranging from 2.5% to 70%. Higher dextrose concentrations (greater than 10%) are generally reserved for central venous administration because of the propensity to cause thrombophlebitis in peripheral veins. Another carbohydrate energy substrate used less frequently is glycerol, a sugar alcohol which provides 4.3 kcal/g. Glycerol, or glycerin, is contained in certain pre-mixed PN formulations marketed for peripheral administration.
IVFE- is used to provide energy as well as essential fatty acids for PN formulations. IVFE components include soybean oil or 50:50 mixes of soybean and safflower oils, egg yolk phospholipid as an emulsifier, glycerin to render the formulation isotonic, vitamin K, and sodium hydrozide to adjust the final pH. IVFE is commercially available in 10% (1.1 kcal/mL), 20% (2 kcal/mL), and 30% (3 kcal/ML) concentrations. The IVFE 30% formulation is only approved for compounding of TNA, not for direct IV administration.
Because of enhanced microbial growth potential with infusion of IVFE separate from dextrose and amino acid formulations, the Centers for Disease Control and Prevention (CDC) recommends a 12-hour hang-time limit for IVFE. However, an admixture containing IVFE, dextrose, and amino acids in the same container may be administered over 24 hours. The hang time and infusion of this formulation is extended when compared with infusion of IVFE alone because bacterial growth is inhibited at a reduced pH and there is an increased total osmolarity when the three substrates are combined in one container. Whether infused separately from amino acids and dextrose or as a TNA, the IVFE infusion rate should not exceed 0.11 g/kg/h. Greater infusion rates are associated with an increased risk of side effects such as hypertriglyceridemia and infectious complications.
Protein- is used in the form of crystalline amino acids in PN formulations and yield 4 kcal/g. Nitrogen content varies; however, for nitrogen balance calculations amino acid products are generally assumed to be 16% nitrogen (6.25 g of protein = 1 g of nitrogen). Concentrations are available ranging from 3% to 20%.
Electrolytes- maintenance and therapeutic amounts, are added to PN formulations depending upon the patient’s requirements. The six major electrolytes are sodium, potassium, magnesium, calcium, phosphate, and chloride, all of which have an active role in the metabolic processes of the body. Potassium, phosphate, and magnesium are the major intracellular electrolytes, where as sodium and chloride are located predominantly in the extracellular compartment. When refeeding severely malnourished patients or when using high levels of dextrose in the TPN formulation, the requirement for the intracellular electrolytes increases.
The electrolyte content of TPN solutions is dependent on individual patient requirements, taking into consideration maintenance requirements; gastrointestinal and urinary losses; renal, cardiac, nutritional and endocrine status; and the nutrient composition of the TPN solution. Appropriate prescription of electrolytes requires regular monitoring of serum values. The composition of the electrolyte profile in patients receiving TPN depends on their acid-base balance.
Bicarbonate buffers are not compatible with TPN solutions; however, acetate is used in place of bicarbonate as a buffer precursor. There are a number of commercially available electrolyte solutions that facilitate the preparation of TPN. Most of the premixed electrolyte solutions do not contain calcium and phosphate for compatibility reasons. Calcium and phosphate have a tendency to form insoluble precipitates that can result in catheter occlusion or embolus formation. Electrolytes are also added to some of the commercially prepared amino acid solutions in standard amounts.
Vitamins- are commercially available in single vitamin products and multivitamin products that contain both fat-soluble and water-soluble vitamins. Vitamins should be given as a standard daily dose in parenteral nutrition. Delaying IV multivitamin therapy until development of clinical signs of vitamin deficiency is inappropriate. Certain situations may warrant special attention. Patients receiving PN and warfarin therapy need close monitoring of the desired anticoagulation level because of the inclusion of vitamin K in the parenteral multivitamin preparation. PN supplementation with additional thiamin is reasonable in PN patients with a history of alcohol abuse, especially if the patient did not receive thiamin upon hospital admission.
Trace Elements- that are commonly used in PN formulations include zinc, copper, chromium, manganese, and selenium. They are commercially available as single-entity products and in various multiple trace element combinations with concentrations for adults, pediatrics, and neonates. Some formulations may also contain electrolytes. Other trace elements that may be supplemented in PN include molybdenum, iodine, and iron.
Disease-Specific Formulations and Specific Nutrients
Renal failure formulations are composed primarily of essential amino acids based upon the theory that nonessential amino acids can be physiologically recycled from urea, while essential amino acids must be provided from the diet. These formulations are relatively dilute (5.2%-6.5%) and offer no significant advantage over the standard formulations and may result in metabolic complications; therefore, indications for these formulations are limited.
Hepatic encephalopathy formulations contain increased amounts of branched chain amino acids (BCAA) and decreased amounts of aromatic amino acids (AAA) compared with standard amino acid formulations. Altered metabolism in patients with hepatic failure can result in a high serum ratio of AAA to BCAA. This imbalance is thought to cause an increased transport of AAA into the brain, where they serve as precursors to neurotransmitters that may be responsible for altered mental status. Indications for these formulations are very limited.
Metabolic stress, trauma, thermal injury, and/or hypercatabolic state formulations are based on the theory that higher BCAA amounts are beneficial during severe metabolic stress because of increased skeletal muscle catabolism; therefore, significantly increased amounts of leucine, isoleucine, and valine are provided in these products. While the use of BCAA-enriched formulations slightly improves nitrogen balance in certain population groups, clinical evidence does not support improved outcomes.
Parenteral Nutrient Preparation: Admixtures- Dextrose-Amino Acids versus TNA
PN admixtures may be prepared for administration in either of two formats- the traditional or dextrose-amino acids (2-in-1) formulation, or the TNA system which is also referred to as a 3-in-1 or all-in-one admixture. The dextrose-amino acids format incorporates the dextrose and amino acid base solutions alone with the prescribed electrolytes, minerals, vitamins, and trace elements in one or multiple containers each day. IVFE is administered separately as a piggyback infusion. In contrast, the TNA system incorporates dextrose, amino acids, and IVFE along with the prescribed micronutrients together in the same container for final administration. There are advantages and disadvantages of each.
Advantages and Disadvantages of the Total Nutrient Admixture System
All components are aseptically compounded by the pharmacy
Preparation is more efficient for pharmacy personnel
Less manipulation of the system during administration
Less risk of contamination during administration
Inhibited or slower bacterial growth if contamination does not occur compared to separate IVFE
Less nursing time needed
Less supply and equipment expense for only one infusion pump and IV tubing
More convenient storage, fewer supplies, and easier administration in home care settings
Dextrose and venous access tolerance may be better in some situations
Possible applications in fluid restricted patients because IVFE 30% is restricted for use in TNA
May be more cost-effective
Fat clearance may be better when IVFE is administered over more than 12 hours
Large particle size of admixed IVFE precludes use of 0.22 micron (bacteria-eliminating) filter, and requires larger pore size filter of 1.2 microns.
Admixed IVFE is less stable and more prone to separation of the lipid components
Formulations are more sensitive to destabilization with certain electrolyte concentrations
Formulations are more sensitive to destabilization with low concentrations of dextrose and amino acids.
Lower pH amino acid formulations may destabilize the IVFE-portion of admixture
Formulation may be unstable when the final concentration of IVFE is low
Difficult to visualize precipitate or particulate material in the opaque admixture
Certain medications are incompatible with the IVFE portion of the admixture
Catheter occlusion is more common with daily IVFE
Less stable over time than dextrose-amino acid PN formulations with separate IVFE
Either system may be infused via a central venous access device. If PN is to be administered via a true peripheral line, certain criteria are important to decrease risk of thrombophlebitis and damage to peripheral vein(s). Osmolarity should generally be kept below 900 mOsm/L, calcium and potassium concentrations should be kept low, and IVFE is generally given daily to provide adequate kcals and decrease osmolarity. In a dextrose-amino acids system for PPN, the IVFE is usually piggybacked into the same line and infused over 24 hours, replacing the IVFE bag at 12 hours to adhere to the 12-hour hang-time limit. It has been speculated that using daily IVFE along with the dextrose-amino acids formulation may confer a modest protective effect on venous tolerance by dilution of the PPN formulation and/or by some buffering action in the vein. There has been some success in reducing or preventing thrombophlebitis through the addition of heparin and/or small amounts of hydrocortisone or the use of a nitroglycerin patch at the venous insertion site.
Central versus Peripheral Access
Central or peripheral access is not defined by the initial point of entry into the vascular system, but rather by the position of the distal catheter tip. A peripheral catheter is defined as one whose tip position is outside of the central vessels, the inferior and superior vena cava. Peripheral catheters include standard peripheral cannulas, midline catheters, and midclavicular catheters. Midline catheters are catheters with the tip terminating in the proximal portion of the upper extremity.
Central Venous Access
Central venous access is defined as a catheter whose distal tip lies in the distal vena cava or right atrium. The most common sites of venipuncture for central access include the subclavian, jugular, femoral, cephalic, and basilic veins. CVCs provide access for infusion as well as blood aspiration for laboratory monitoring. The primary indications for central venous access are chemotherapy, antibiotics, and PN. Central venous infusions are not limited by drug pH, osmolarity, or volume. CVADs can be grouped into three broad categories: nontunneled, tunneled, and implanted.
Nontunneled CVADs are most commonly used in the acute care setting for therapies of short duration. Advantages of nontunneled catheters include decreased placement costs, ease of removal, and the ability to exchange these catheters over a guidewire.
• Peripherally inserted CVC (PICC) is defined as a catheter inserted via a peripheral vein whose tip lies in the vena cava. These catheters are classified as nontunneled CVCs. PICCs are common means for securing central vascular access in both acute care and home settings.
Tunneled catheters decrease the risk of catheter infection by separating the exit and venipuncture sites. Tunneled catheters have been demonstrated to be safe and effective in long-term therapies ranging from months to years. Advantages to these catheters include ease of self-care by the patient, decrease risk of dislodgement, and the ability to repair the external lumen in the event of catheter breakage.
Implanted catheters consist of a silicone elastomer catheter attached to a plastic or titanium disk with a self-sealing silicone elastomer septum. The port is placed into a subcutaneous pocket that is most often located in the anterior chest. Ports can be accessed up to 1000 to 2000 times. Advantages to these include minimal alteration in body image and ease of self-care. Implanted systems do not require routine site care when not in use and often are maintained with a monthly routine heparin flush. Ports are ideal for those who require infrequent IV therapies, such as intermittent chemotherapy. Lower rates of infection and thrombosis have been demonstrated.
Hyperglycemia- is the most common complication associated with PN administration and can be caused by various factors such as stress-associated hyperglycemia and excess carbohydrate administration. PN should be initiated at half of the estimated energy needs or approximately 150 to 200 g for the first 24 hours. Lesser carbohydrate delivery (approximately 100-150 g of dextrose) is warranted in the hyperglycemic patient requiring insulin therapy or a hypoglycemic agent. Carbohydrate administration should not exceed a rate of 4 to 5 mg/kg/min or 20-25 kcal/kg/d. Blood glucose concentrations can be controlled with regular insulin therapy, which may be given subcutaneously or added directly to the PN solution. An insulin drip provides a more consistent and safe glucose control. Uncontrolled hyperglycemia may result in hyperosmolar hyperglycemic nonketotic dehydration, coma, and death secondary to osmotic diuresis.
Hypoglycemia- can occur from excess insulin administration via the PN solution, IV drip, or subcutaneous injection. Treatment includes initiation of a 10% dextrose infusion, administration of an ampule of 50% dextrose, and/or stopping any source of insulin administration. Abrupt discontinuation of PN solutions has been associated with rebound hypoglycemia. To reduce the risk in susceptible patients, a 1- to 2-hour taper down of the infusion may be necessary. If PN is discontinued quickly, 10% dextrose should be infused for 1 to 2 hours following PN discontinuation to avoid possible rebound hypoglycemia.
Essential Fatty Acid Deficiency- may result from IVFE-free PN, depending on the length of the PN therapy and the patient’s nutritional status. Intravenous fat emulsion is generally provided as a source of essential fatty acids and as a nonprotein calorie source. Although the incidence is low, there are several complications associated with IVFE use, such as infusion related adverse reactions and allergy to the IVFE components. Two polyunsaturated fatty acids, linoleic and alpha-linolenic, cannot be synthesized by the body and are considered essential. To prevent EFAD, 1% to 2% of daily energy requirements should be derived from linoleic acid and about 0.5% of energy from linolenic acid. This translates into approximately 500 mL of a 10% IVFE or 250 mL of 20% IVFE administered over 8 to 10 hours, twice weekly. Alternatively, 500 mL of a 20% IVFE can be given once a week. A trial of topical skin application or oral ingestion of oils to alleviate biochemical deficiency of EFAD may be given to patients who are intolerant to IVFE.
Hypertriglyceridemia- can occur with dextrose overfeeding or with rapid administration of IVFE (greater than 110 mg/kg/h). Hyperlipidemia may impair immune response, alter pulmonary hemodynamics, and increase the risk of pancreatitis. Reducing the dose and/or lengthening the IVFE infusion time will help minimize these effects. IVFE intake should be limited to less than 30% of total calories or 1 g/kg/d and be provided slowly over no less than 8 to 10 hours if administered separately. Serum triglyceride concentrations should be measured before IVFE administration in any patient with a known history of hyperlipidemia. Pancreatitis due to IVFE-induced hyperlipidemia is rare unless serum triglyceride concentrations exceed 1000 mg/dL. IVFE is considered safe for use in patients with pancreatitis without hypertriglyceridemia. However, IVFE should be withheld from the PN regimen if serum triglyceride concentrations exceed 400 mg/dL.
Azotemia- excessive protein administration results in an increased metabolic demand on the body for disposing of the byproducts of protein metabolism. Prerenal azotemia can result from dehydration, excess protein, and/or inadequate nonprotein calories. Increased blood urea nitrogen (BUN) may occur as a result of intolerance to the protein load. Patients with hepatic or renal disease are prone to developing azotemia because of the impaired ability to metabolize and eliminate urea. When urea clearance is impaired, dialysis may be required to assist with the elimination of urea and allow for adequate intake of protein.
Refeeding Syndrome- refers to the metabolic and physiological shifts of fluid, electrolytes, and minerals (eg, phosphorus, magnesium, and potassium) that occur as a result of aggressive nutrition support. The delivery of calories, particularly in the form of carbohydrate, may induce refeeding syndrome in a malnourished patient. Carbohydrate delivery stimulates insulin secretion, which causes an intracellular shift of these electrolytes and minerals with the potential for severe hypophosphatemia, hypomagnesemia, and hypokalemia. For patients who are at risk for refeeding, calories should be initiated and advanced slowly.
Cyclic infusion- refers to the infusion of a PN formulation over less than a 24-hour period, allowing a period of time off PN. Continuous PN infusion can result in hyperinsulinemia and fat deposition in the liver and, thereby, potentially increase risk of liver complications. Cyclic PN infusion has been shown to reduce serum liver enzymes and conjugated bilirubin concentrations when compared to continuous PN infusion.
Enteral Nutrition- should be optimized because even small amounts of enteral intake may be beneficial in promoting enterohepatic circulation of bile acids. A trial of jejunal feeding at a slow rate during a portion of the day or night may be beneficial for the patient with chronic intestinal pseudo-obstruction who is receiving gastric decompression. Patients with short bowel syndrome should be encouraged to maximize oral intake because at least some of their intake will be absorbed.
Monitoring Parenteral Nutrition
As with any invasive therapy TPN must be monitored closely. The dietitian should carefully observe those items that are relevant to nutrition. Baseline data, preferably obtained before TPN is begun, usually includes: Complete Blood Count, Blood Glucose, Serum Creatinine, Blood Urea Nitrogen, Serum Electrolytes, Albumin, Transaminoases (Serum Glutamic Oxaloactic Transaminase (SGOT), Serum Glutamic Pyruvate Transaminase (SGPT)), Calcium, Phosphorus, Magnesium.
During TPN, blood glucose, electrolytes, and urea nitrogen should be used to monitor hydration, renal function, and electrolyte balance. Calcium, phosphorus, and magnesium are monitored until serum levels stabilize. Urine should be checked daily for glucose and acetone to indicate carbohydrate tolerance. Hepatic function may be monitored by serum bilirubin and the liver enzymes, SGOT or SGPT, lactic dehydrogenase (LDH), and alkaline phosphatase. Plasma triglycerides are used to assess the capacity to clear plasma lipids. Body weight is obtained daily to check fluid overload.
NUTRITIONAL THERAPY IN RENAL DISEASE
REVIEW OF ANATOMY & PHYSIOLOGY
The major function of the renal system is to help maintain homeostasis in the body by controlling the composition and volume of blood. This is accomplished by removing and restoring secreted amounts of water and solutes.
The two kidneys are located in the back abdominal cavity, one on each side of the spinal cord. They are embedded in fatty tissue for protection and surrounded by a sheath of fibrous tissue which helps to hold them in place. Each kidney is approximately 4.5 in. long, 1 inch thick, 2-3 inches wide and weighs 4-6 ounces. The average urinary output is 1.2 – 1.5 liters/day; however, the total volume depends on many variables such as water intake, nature of the diet, activity, environmental and body temperature and age.
The ureters deliver urine from the kidneys where it is made and to the bladder where urine is stored. The average storage capacity of the bladder is 0.5 liters. The urethra takes the urine from the bladder to the outside of the body.
The outer portion of the kidney is called the cortex, the inner portion the medulla. Urine is formed by the kidneys, collected in the renal pelvis, and from here flows through the ureters into the bladder.
Blood is delivered to the kidneys from the abdominal aorta via the renal artery. It is sent back to the heart via the renal veins to the vena cava.
The functional unit of the kidney is the nephron. There are greater than one million nephrons in each kidney, each capable of forming urine.
There are two types of nephrons: cortical and juxtamedullary. Cortical nephrons have glomeruli lying close to the surface of the kidney and a short loop of Henle which penetrates varying distances into the outer medulla. The juxtamedullary nephrons have glomeruli which lie very close to the renal medulla and have a very long loop of Henle which dips deep into the medulla.
The efferent arteriole of the cortical nephron goes on to form the peritubular capillaries which surround the tubules in the cortex. These short cortical nephrons have poor concentrating ability and poor sodium-retaining capacity.
The efferent arteriole of the juxtamedullary nephrons continue not only as peritubular capillaries but as a series of vascular loops called the vasa recta. The deep medullary loops of Henle form the counter current mechanism, which works to concentrate the urine and conserve sodium. Any renal disease where there is a loss of concentrating ability indicates damage to the juxtamedullary nephrons.
Approximately 1 liter of blood, or 25% of the entire cardiac output at rest, flows through the kidneys each minute. Thus, in 4-5 minutes a volume of blood equal to the body’s total volume passes through the renal circulation.
Blood enters the nephron through the afferent arteriole, which divides into a tuft-like network of approximately 50 capillaries. This is called the glomerulus. Pressure from the blood causes fluid and dissolved substances to pass through the capillary walls into the Bowman’s capsule. This fluid is called the glomerular filtrate and is approximately the same composition as blood plasma, with the exception of protein and blood cells, which are too large to pass through healthy capillary walls. Approximately 180 liters of filtrate is formed daily, yet only 1-2 liters of this becomes urine. Most of what is filtered is reabsorbed into the blood by a series of steps that conserve the nutritious substances such as glucose and amino acids. It also allows the waste products such as urea and creatinine to leave the body in the filtrate, which is later called urine.
Some products enter the glomerular filtrate by a process known as secretion. These products enter the tubular lumen from the peritubular blood by active and passive transport. Examples of these secreted substances are: potassium, hydrogen, ammonia, and certain medications. Some of these secretions are partially formed as a result of three processes: filtration, selective reabsorption, and secretion.
Important blood constituents are entirely or almost entirely reabsorbed and are excreted in the urine, only when blood concentrations are above normal. Examples of these highly reabsorbed substances include water, glucose, chlorides of sodium, calcium, and magnesium. Normally 99% of water filtered is reabsorbed.
The end-products of metabolism such as urea, uric acid and creatinine are seen in high concentrations in the urine because they are reabsorbed in limited quantities or not at
The process of reabsorption takes place in a series of renal tubules which are surrounded by peritubular capillaries. These capillaries take the reabsorbed products back into the general circulation for use by the body.
The glomerular filtrate flows through the proximal tubule, the loop of Henle, the distal tubule, and the collecting tubule into the renal pelvis of the kidney.
Approximately 60-80% of the glomerular filtrate is reabsorbed by the proximal tubule. The active reabsorption of water and chloride occurs in the peritubular capillaries.
Loop of Henle
In the descending limb of the loop of Henle approximately 75% of the remaining water is reabsorbed. The tubule wall is impermeable to NaCl so the filtrate becomes very concentrated (hypertonic). In the ascending limb, the epithelial tissue is impermeable to water, but freely permeable to NaCl. Thus, the volume of the filtrate does not change, but NaCl is reabsorbed and the filtrate becomes hypotonic.
The distal nephron consists of the distal convoluted tubule, cortical collecting tubule and the medullary collecting duct. Each of these segments is sensitive to antidiuretic hormone (ADH), a hormone secreted by the pituitary gland. When body fluids become too concentrated ADH is secreted, which then causes massive amounts of water to be reabsorbed thereby decreasing the loss of water in the urine. In the absence of ADH, dilute urine is excreted.
The final product of filtration, secretion, and reabsorption is urine. The collecting ducts collect the urine from several nephrons and then pass it into larger collecting ducts (papillary ducts) and into the renal pelvis. From here urine is conveyed through the ureters into the bladder.
Hormonal Regulation of Reabsorption
As previously mentioned ADH can increase the distal tubule’s permeability to water, leading to reabsorption and urine concentration. Aldosterone also acts on distal tubule cells to stimulate the reabsorption of sodium. The tubular cells excrete either potassium or hydrogen ions in exchange for sodium reabsorbed. Aldosterone helps maintain normal blood potassium and/or pH. Aldosterone secretion is largely controlled by the renin-angiotensin system.
Role of Kidneys in Blood Pressure
The juxtaglomerular apparatus is a structure consisting of cells surrounding the afferent arterioles leading to the glomerulus. These cells secrete renin. Renin is an enzyme important in the regulation of blood pressure. Although the exact mechanism for renin release is not definitely established, juxtaglomerular cells are thought to be sensitive to pressure changes (baroreceptors) within the afferent arterioles. Decreased arteriole pressure from decreased renal blood flow, decreased sodium concentration in the distal tubule and probably activation of the sympathetic nervous system may cause release of renin. Renin converts angiotensinogen, a liver protein, to angiotensin I. In the plasma angiotensin I is converted to angiotensin II, which stimulates the adrenal cortex to produce aldosterone. Elevated aldosterone levels cause sodium reabsorption and therefore water reabsorption in the distal tubules and collecting ducts. This increased plasma volume contributes to blood pressure elevation. Angiotensin II also causes peripheral vasoconstriction.
Other Kidney Functions
In addition to maintaining fluid and electrolyte balance, controlling blood pressure and excreting waste products, the kidney performs other functions;
Stimulation of Red Blood Cell Production – The kidneys secrete an enzyme that splits erythropoietin from a plasma protein. This active erythropoietin then stimulates the bone marrow to produce red blood cells.
Regulation of Calcium/Phosphorous Balance and Vitamin D For Bone Health – Vitamin D is converted to its active form, (1,25 dihydroxycholecalciferol), in a two stage process starting in the liver and ending in the kidney. Active Vitamin D promotes calcium absorption from the intestine. Normally, low calcium levels along with elevated phosphorus levels would stimulate the parathyroid hormone (PTH) and active vitamin D. The active vitamin D and PTH work together to reabsorb calcium from the bone to raise serum levels and maintain a proper serum calcium and phosphorous ratio.
Maintenance of Acid Base Balance – The kidneys play an important role in the maintenance of the proper blood pH which is between 7.37 and 7.42. This acid- base regulation is accomplished by:
– the excretion of hydrogen ions,
– the controlled reabsorption of bicarbonate and,
– the secretion of ammonia, which crosses from the cells into the tubules and there combines with a hydrogen ion form unabsorbable ammonium ions which are then excreted.
TESTS/PROCEDURES & LAB USED TO ASSESS RENAL FUNCTION
Creatinine Clearance Test
Creatinine is an end-product of muscle metabolism which is released from the muscles at a constant rate. Under normal conditions it does not build up in the blood because it is excreted in the urine at approximately the same rate at which it is liberated from the muscles. The serum creatinine level usually ranges from 0.7 to 1.5 mg/100 mg (varies with lab). Creatinine is excreted in the urine by filtration at the glomerulus, but it is not reabsorbed by the tubules. Thus, creatinine clearance is a good indicator of glomerular filtration rate (GFR). GFR is normally 120-125 ml/min. In chronic renal failure the GFR falls below this value. A GFR at or below 25 ml/min. signifies the need for nutrition intervention in the form of a protein restriction. Creatinine clearance is calculated by the following equation:
Ccr = (Ucr) (V)
Ccr = clearance of creatinine (ml/minute) Ucr = Urinary creatinine (mg/dl)
Pcr = Plasma creatinine (mg/dl) V = volume of urine (ml/min.)
A small amount of creatinine is secreted by the tubule which causes a slight overestimation in GFR. However an error inherent in plasma creatinine concentration determination cancels this effect and creatinine clearance therefore approximates GFR.
Intravenous Pyelogram (IVP)
An IVP is an x-ray taken of the abdomen at intervals of 1-5 minutes after a contrast medium has been injected intravenously. The contrast medium circulates in the bloodstream and then to the kidneys where it is excreted. The cortex, pelvis, size, and shape of the kidneys can be evaluated. Any cyst, lesion or obstruction will cause a distortion of various areas of the kidneys. If the GFR is severely depressed the dye will not be excreted and kidneys will be difficult to visualize.
This test may be used when the results of the IVP are not clear or further investigation of a nonfunctioning kidney is necessary. The procedure involves passing a catheter up the ureter and delivering a contrast medium directly into the kidney. It is avoided when possible because it involves anesthesia and a possibility of infection.
Casts are a mucoprotein matrix in which red blood cells, white blood cells and other proteins are embedded. This mucoprotein matrix is secreted by the distal tubule cells and can be seen by microscopic evaluation of urine. Normally there is not enough protein in the renal tubules to form more than an occasional cast. However, in renal disease increased proteinuria and/or renal excretion of cells may cause an excessive excretion of casts in the urine. Casts are classified according to shape and content and are of great diagnostic value.
Broad grandular casts – typical of end-stage kidney disease
Oval fat bodies and fatty casts – common in nephrotic syndrome
White cell casts – seen in pyelonephritis
Red cell casts – seen in active glomerulonephritis
The specific gravity of urine depends on the weight and number of any particles in the urine. Specific gravity may vary from 1.001 when an individual is given large amounts of water to 1.040 when an individual is deprived of water. This represents the kidney’s ability to concentrate or dilute urine. In chronic renal failure, the kidney loses its ability to concentrate or dilute urine. When 80% of the nephron mass is destroyed, the specific gravity of urine becomes fixed near 1.010 which is the specific gravity of plasma.
In this process a biopsy needle is used to obtain a specimen of renal tissue which can be examined under a microscope. A renal biopsy is done to help diagnose and follow the progress of diffuse renal disease. The patient lies on his stomach with sandbags
positioned under his abdomen to fix the kidney against the back. The site is located by x-ray reference. Complications include intrarenal and perirenal bleeding as well as further kidney damage. The procedure is not used with uncooperative patients or those with a coagulative disorder.
An ultrasound is a safe non-invasive technique that a patient does not have to be prepared for. It can be used repeatedly and therefore is useful in monitoring the progress of events (i.e. as with renal transplants) since it can detect obstructions, change in kidney size, and perinephric collections of urine, lymph, blood, or pus. This test is often used to compliment other tests since false negatives can occur.
A plain film (x-ray) of the abdomen is not as revealing as an IVP, however, it is advantageous in that it can be performed at short notice and causes no discomfort. It is often possible to detect the outline of the kidneys so that their size, shape, and position can be determined. Any shadows on the x-ray film may indicate the presence of calculi (stones) or renal calcification.
DISEASES OR CONDITIONS THAT AFFECT RENAL FUNCTION
A variety of disease conditions and foreign agents may interfere with the normal function of the kidney.
Mild and occasional bladder infections may progress to more involved chronic, recurrent infection that could eventually affect kidney function. In pyelonephritis there is an inflammation of the kidney body and pelvis. The etiology of this inflammation is due to bacteria that have ascended from the bladder. With recurrent urinary tract infection there is also a greater chance of bacteria eventually entering the kidney and causing infection.
Infections and stone formations in the urinary tract could cause an obstruction which may block the flow of urine.
Collagen and Immunologic Diseases
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease of connective tissue, of unknown etiology, that affects the joints, skin, kidneys, nervous system, and mucus membranes. Severe cases can lead to extensive kidney damage. Scleroderma is a chronic disease of unknown etiology that causes sclerosis (hardening) of the skin and certain organs including the gastrointestinal tract, heart, lungs, and kidneys.
Inflammatory and Degenerative Diseases
Inflammation of the membranes and blood vessels of the nephrons may be short term (i.e. as in acute glomerulonephritis) or this inflammation may progress to involve a variety of nephrons, disrupting normal function (i.e. chronic glomerulonephritis). With the development of nephrotic lesions, chronic renal failure may occur.
Damage From Other Diseases
Diabetes is the number one cause of chronic kidney disease (nephropathy). According to the Davita dialysis website, about 44% of their dialysis patients have diabetes.
Circulatory diseases (i.e. prolonged hypertension), closely associated with the renin-angiotensin-aldosterone mechanism, are capable of causing arteries of the kidney to degenerate and hinder efficient function. Nephrosclerosis and glomerulosclerosis occur in patients with severe hypertension. In both of these disorders there is a hardening of arterioles that decreases perfusion to kidney tissue.
Polycystic kidney disease is an inherited disorder of the kidneys. This disease may be caused by a defect in the renal tubular system that produces cysts that invade the kidneys. As the cysts increase in number, they eventually squeeze out the normal tissue, interfering with kidney function.
Damage from Other Agents
Toxic nephropathy leads to kidney damage resulting from exposure to environmental agents such as solvents, insecticides, similar agents that are poisonous to the body, and certain drugs.
Glomerulonephritis is a type of nephritis (inflammation of the kidney) affecting the glomerulus. It may be acute or chronic and commonly follows infections especially streptococcal infection. In most cases it has a sudden onset and is often completely resolved in a year. The chronic form of glomerulonephritis involves an extensive amount of renal tissue damage and eventually results in the need for dialysis. Symptoms of glomerulonephritis may include proteinuria, hematuria, and varying degrees of edema, hypertension, and azotemia. If the disease progresses to renal insufficiency, oliguria (excretion of less that 400 ml of urine in a 24 hr. period) or anuria results.
Nephrotic Syndrome (Nephrosis)
Nephrotic syndrome is defined by a group of symptoms resulting from impaired nephron function and kidney tissue damage. Massive proteinuria and edema are the most evident symptoms of this syndrome. A variety of causes and diseases may result in nephrotic syndrome, including acute glomerulonephritis, diabetes, and collagen disease (i.e. SLE). Massive proteinuria and edema occur as a result of increased capillary permeability in the
glomerulus and possibly throughout the body. Low serum albumin levels cause third spacing of fluid from the blood volume. Increased reabsorption of sodium occurs in response to the depressed blood volume.
Acute Renal Failure
In acute renal failure (ARF) the loss of nephron function occurs rapidly with a sudden shutdown of renal function following metabolic insult or traumatic injury to normal kidneys. Depending on the extent of damage, a complete recovery frequently occurs.
Characteristics of acute renal failure (ARF) include a sudden reduction in glomerular filtration rate and an alteration in the kidney’s ability to excrete waste products and preserve the internal environment. ARF is often associated with oliguria. The causes of ARF are classified into three categories;
– Pre-renal – inadequate renal perfusion (i.e. cases of severe dehydration);
– Intrinsic disease – occurs within the renal parenchyma (may be caused by trauma, surgery, etc.).
– Post-renal – due to an obstruction (i.e. cancer of the bladder)
The two distinct phases of ARF include the oliguric phase and the diuretic phase. Extensive catabolism and tissue destruction occur during the oliguric phase. Hemodialysis may be necessary in order to reduce the metabolic acidosis, correct the uremia, and lower the rapidly increasing hyperkalemia.
The diuretic phase is considered the oliguric post-recovery period. During this phase, renal function and ability to excrete collections of excess water and electrolytes have improved. Patients at this stage may still have elevated lab values (i.e. BUN, creatinine). The major concern at this phase is excessive sodium, fluid, and potassium losses from diuresis.
Chronic Renal Failure
Chronic renal failure (CRF) is associated with an irreversible loss of kidney function. CRF can occur over several months to years. It occurs due to a variety of problems associated with the kidney’s inability to excrete waste products, reabsorb nutrients, maintain fluid and electrolyte balance, produce hormones, and perform other metabolic functions. As the failure becomes more severe and a greater number of nephrons are damaged, the kidney is no longer able to compensate. The progression of CRF occurs in three stages that are not sharply separated. These three phrases are:
– Decreased renal reserve
– Renal insufficiency
– Renal failure (90 % of nephrons are damaged)
Chronic renal failure may progress toward end-stage renal disease (ESRD). The form of treatment at this stage would be either a kidney transplant or dialysis.
NUTRITIONAL CONSIDERATION IN RENAL DISEASE
Because the kidneys play a major role in maintaining homeostasis in the body, loss of nephron function affects almost all other organ systems. In addition, renal disease is progressive and requires various therapies in response to the loss of renal function. The goals of Medical Nutrition Therapy of patients with renal failure include:
– minimizing the characteristic uremic symptoms if possible
– achieving and maintaining optimal nutritional status
– slowing the progression of kidney failure
– controlling edema and electrolyte imbalances
– preventing renal osteodystrophy
Impaired kidney function results in altered filtration, absorption, and excretion of metabolites, as well as diminished urinary output. Modifications in the diet depend on the cause of renal impairment as well as the individual’s nutritional status. Lab values such as serum sodium, potassium, BUN, creatinine, albumin, calcium, phosphorus; the GFR; changes in urinary output; and the presence of acidosis must be closely monitored in tailoring the diet to meet an individual’s nutritional needs.
Serum levels of nitrogenous metabolites such as urea and creatinine become elevated as the loss of nephron function progresses. It is essential to control dietary protein intake to limit nitrogenous waste from accumulating in the blood. An elevated urea load is partly a result of dietary protein metabolism. Elevated creatinine levels result from increased catabolism of muscle.
Uremia is a toxic condition caused by the retention of urinary constituents in the body (i.e. urea, creatinine, uric acid metabolism). Urea is present in the greatest amount. Uremia occurs as a result of the severe loss of renal function that may include weakness, anorexia, nausea, vomiting, pruitis (itching), neuropathy, mental disturbances, and coma in advanced cases.
Hyperglycemia and hypoglycemia are frequently secondary to glucose intolerance and frequently observed in patients with uremia. This results from erratic and delayed insulin action due to resistance to insulin by tissues.
There is a high incidence of hyperlipidemia manifested by increased serum triglycerides and VLDL cholesterol levels in CRF. A decrease in extrahepatic lipoprotein lipase and possibly an increase in triglyceride synthesis are believed to be responsible for this complication.
With renal insufficiency the number of functioning nephrons decrease and the remaining nephrons become enlarged to compensate for the loss. For a limited amount of time these hypertrophied nephrons are able to maintain sodium balance. With an increase number of damaged nephrons, obligatory losses of sodium increases. A patient may become sodium depleted at this stage. With further reduction in the number of functioning nephrons, the kidney’s ability to excrete sodium decreases and adaptive mechanisms are lost. As a result, sodium retention occurs along with a subsequent retention of fluid. Patients with CRF are poised precariously between sodium depletion and sodium overload. The amount of sodium included in the diet must be continually individualized.
In renal failure, hyperkalemia (potassium greater than5.5 mEq/l) usually does not occur as long as at least 1 liter of urine is produced daily. But as urine output decreases and acidosis increases, hyperkalemia results. Potassium is essential to heart muscle function, too much can stop the heart. Control of potassium in the diet is essential at this stage.
Nutritional Therapy in Acute Renal Failure
Nutrition therapy in ARF is focused on dealing with the patient’s uremic symptoms, metabolic acidosis, and fluid and electrolyte imbalances. The increased energy and protein needs resulting from physiological stress (i.e. trauma, surgery, etc.) also need to be considered. Difficulties arise in providing protein and energy to meet nutritional needs in the presence of acidosis, decreased urine output, and excessive nitrogenous waste.
– Protein: 0.6-0.75 gm/kg(dry weight)/day with total loss of kidney function; as kidney function improves, protein intake can increase. Dry weight is weight without excess fluid (edema/ascites).
0.8-1.2 g/kg of body weight noncatabolic, without dialysis
1.2-1.5 g/kg of body weight catabolic and/or initiation of
– Energy: ~35-50 kcal/kg dry weight. ~25-35 kcal/kg of body weight depends on stress/status of nutrition and include kcal from continuous renal replacement therapy.
– Sodium: Anuric/oliguric phases: 500mg-2 gm/day
Diuretic phase: losses are replaced depending on urinary and serum sodium
levels, edema, and frequency of dialysis
– Potassium: Anuric/oliguric phases- 1-2 gm/day (depending on serum potassium levels) Diuretic phases- 1-3 gm/day; replace losses as needed.
-Phosphorus: 8-15 mg/kg
-Calcium: maintain serum value within normal limits
– Fluids: A range of 500 cc/day to ad lib. Anuric phase: 300-500 cc + output.
Polyuric phase: input = output, fluid status needs to be monitored during both phases of ARF.
Nutritional Therapy in Chronic Renal Failure
The goals in chronic renal failure include the following:
– Maintaining nutritional status through adequate protein, calorie, vitamin and mineral intake.
– Minimizing uremic symptoms while still maintaining a positive nitrogen balance.
– Controlling edema and electrolyte imbalance by monitoring sodium, potassium, and fluid intake.
– Preventing the development of renal osteodystrophy by monitoring calcium, phosphorous, and vitamin D intake.
– Designing a diet for a patient that is palatable, attractive, and fits into his/her lifestyle.
Nutritional Therapy in Pre-ESRD (without dialysis)
– Protein: Individualized according to GRF; 70-80% should be of high biological value (HBV)
GFR (ml/min) Recommended gm protein/kg/day
-Protein: GFR <50 mL/min 1.73m2 kg of body weight x 0.60 g/kg – 0.80 g protein/kg of body weight
If diabetic nephropathy is present: kg of body weight x 0.80-0.90 g pro/kg
– Energy:30-35 kcal/kg/day; calories in pre-ESRD are often high to prevent tissue
catabolism, especially with lower protein diets.
Adults with CKD, not on dialysis: 23-25 kcal/kg
Overweight adults with CKD and diabetes, not on dialysis: 1,780-1823 kcal
– Sodium: Individualized; usually less than 2.4 g/d
– Potassium: A restriction is usually not necessary unless serum potassium is elevated and/or urine output is less than 1 l/day.
Less than 2.4 g/d (Stages 3-4 CKD)
– Fluids: Often not restricted unless symptoms of fluid overload develop. Balance allowance with urine output to avoid edema. Collaborate with physician to determine fluid needs.
– Phosphorus: Should be limited to 800 to 1,000 mg/d 10-12 mg /gm/protein prescribed when serum phosphorus > 4.6 mg/dL or intact parathyroid hormone is elevated (Stages 3-4)
Calcium: total elemental intake (including dietary calcium, calcium supplementation, and calcium-based binders) should not exceed 2 g/d (Stages 4-4)
Nutritional Therapy in Hemodialysis
Hemodialysis is a process that employs the use of an artificial kidney machine to remove toxins from the bloodstream. This machine contains two chambers, separated by a thin membrane. Blood is drained (often from a patient’s arm) and flows into one chamber. The second chamber contains dialysate (a solution similar to normal plasma). The waste molecules in the blood are able to pass through the small membrane holes and into the dialysate, where they are then able to be removed. Since blood cells are too large to pass through the pores of the membrane, the majority of blood cells are returned to the
Inpatients receive dialysis in a hospital (usually there is a separate area for dialysis). When discharged, outpatients go to a dialysis center to receive treatment. Patients can dialyze during daytime hours (3-4 hours for 3 days/week), or dialysis may be done overnight in a center( usually 8 hours three times a week). Some patients do daily dialysis at home as well.
Nutritional Needs for HD patients
– Protein:≥1.2 gm/kg (dry weight) /day (approximately 10 gm of amino acids are
lost per treatment). ≥ 50% high biological value
– Energy: Individualized; 30-35 kcal/kg(dry weight)/day.
<60 yrs of age: kg of body weight x 35 kcal; >60 yrs of age: kg of body weight x 30 kcal/kg to 35 kcal/kg
– Sodium: Individualized; usually less than 2.4 g/day
– Potassium: Individualized; less than 2.4 g/day
– Phosphorous: 800-1000 mg day; or 10-12 mg phosphorus per gram of protein when serum phosphorus > 5.5 mg/dL or intact PTH is elevated. Phosphate binders are taken with meals. Almost every food contains phosphorus, binders absorb or trap phosphorus in food, making it unable to be digested and it is eliminated through the stool. Approximately 600 mg of phosphorus is removed in eat dialysis treatment (only half of phosphorus intake recommendation. Binders can be calcium based (Tums or Phoslo) and are given to patients with low serum calcium levels. Many patients have normal serum calcium levels and are given calcium free binders (Renvela: tablet or powder, Fosrenol: chewable).
– Fluid: Individualized; 1000 ml + output or as indicated.
-Calcium: Individualized; total elemental intake (including dietary calcium, calcium supplementation and calcium-based inders should not exceed 2 g/day
Nutritional Therapy in Peritoneal Dialysis
Peritoneal Dialysis uses the semi-permeable membrane of the patient’s peritoneum (a membrane lining the abdominal cavity). Therefore blood does not need to circulate out of the body. A catheter or tube is surgically implanted in the abdomen and into the peritoneal cavity. Dialysate consisting of a high dextrose concentration is instilled into the peritoneum. This solution remains in the cavity for several hours. The concentration of sugar in the dialysate creates an osmotic pressure. Excess waste molecules and water from the blood are pulled across the peritoneum into the abdominal cavity. The fluid in the abdomen is drained off when the process is complete. There are three types of peritoneal dialysis:
Continuous Cyclic Peritoneal Dialysis (CCPD): this form of peritoneal dialysis is designed to be used at home while a patient sleeps; this is an 8 hour process.
Intermittent Peritoneal Dialysis (IPD): dialysis treatments are done several times a week for 8-10 hours each time.
Continuous Ambulatory Peritoneal Dialysis (CAPD): this form of peritoneal dialysis does not require a kidney machine or other automated equipment. Dialysate is drained into and out of the abdominal cavity by gravity several times
a day (continually).
Nutritional Needs for PD Patients
o Protein: ≥1.2-1.3 gm/kgdry weight/day. There may be higher requirement needs (1.5-1.8 gms/kg/d) for PD patients who are ill or unstable. More protein is lost with PD than HD. ≥ 50% high biological value
o Energy: 35 kcal/kg dry weight/day for < 60 yrs; 30 kcal/kg to 35 kcal/kg of body weight for > 60 yrs, including dialysate calories; calorie level is usually individualized; approximately 80% of carbohydrate (dextrose 3.4 kcals/gm) can be absorbed from the dialysate. These additional calories/d may have to be considered a part of the patient’s total intake, especially if the patient is glucose intolerant.
o Sodium: Individualized; usually =2 g/day; monitor fluid balance
o Potassium: Individualized; usually 3 gm/day; adjust to serum levels. Usually not restricted like HD patients.
o Fluid: Individualized; urine output plus 1,000 mL
o Phosphorus 800 mg/da to 1,000 mg/day when serum phosphorus > 5.5 mg/dL or PTH elevated
o Calcium: ≤ 2 g/day; include binder load
o Phosphorus: 800-1000mg/day when serum phosphorus > 5.5 mg/dL or PTH elevated (10-12 mg/gram protein prescribed).
Nutritional Therapy in Renal Transplantation
Renal Transplant involves surgically implanting a kidney from a live donor or cadaver into an eligible recipient. Rejection of the foreign tissue by the candidate is one of the major complications of renal transplants. Corticosteroids and other immunosuppressive therapy are used to decrease the immune response. These medications can cause protein wasting, weight gain (increased appetite), hyperglycemia and hyperlipidemia. Post transplant patients are at risk for developing CAD or diabetes.
o Protein: 1.2-2.0gm/kg/day (controversial); patients taking large doses of steroids require higher protein intakes to offset the catabolic actions of these drugs. Protein requirements often decrease as the patient advances from the acute to the post transplant phase.
o Energy: 30-35kcal/kg/day during the acute post-transplant period. During the chronic post transplant period caloric intake should be adjusted to achieve and/or maintain the patient’s desirable body weight and optimal glucose and lipid tolerance.
o Sodium: 2-4 gm/day; recommended due to hypertension that often persists after a renal transplant.
o Potassium: Usually ad lib, however, patients receiving cyclosporine may require a potassium restriction (2-3 gm/day). Adjust as needed.
o Fluid: Not restricted unless symptoms of fluid overload develop. If urine output reduced, fluid should be reduced to: urine output + approximately 500 mL per day
Nutritional Therapy in Nephrotic Syndrome
The major goal in nutrition care in nephrotic syndrome is to help control the edema and the malnutrition resulting from the massive protein losses that are present. Avoid aggressive repletion of protein losses, it could result in more protein lost in urine.
o Protein: 0.8 -1gm/kg; soy protein has been shown to decrease urinary protein excretion and blood lipid levels
o Energy: 35 kcal/kg/day, unless patient is obese; high in complex carbohydrate
o Fat: ,30% of total energy:
-polyunsaturated fatty acid 10%
-fish oil may be useful for IgA nephropathy (12 g/day)
o Cholesterol: 200 mg/d
o Sodium: 1-2 gm/day.
o Fluids: May be restricted according to degree of edema.
o Potassium: not restricted
o Fats: Dietary fat modification does not seem to have an impact on hyperlipidemia associated with nephrotic syndrome.(should be <30% of
o Phosphorus: <12 mg/kg/day
o Calcium: 1,000 mg/day to 1,500 mg/day, not to exceed 2.000 mg with calcium supplementation and/or calcium-containing phosphate binders
As nephron function becomes impaired there is reduced filtration and excretion of phosphate, sulfate, and organic acids from the metabolism of food. These anions accumulate in body fluids and subsequently displace bicarbonate. Depressed bicarbonate levels contribute to the development of metabolic acidosis. Decompensated metabolic acidosis may also occur as a result of the inability of the kidney to form ammonia, which leads to a reduction in secreting hydrogen ions. Acidosis will ensue as levels of H+ increase with a subsequent reduction in bicarbonate.
Calcium and Phosphate Balance
Activation of vitamin D and normal action of the parathyroid hormone (PTH) in maintaining a proper calcium and phosphorous ratio are impaired with progressive renal insufficiency. Renal osteodystrophy (calcium is lost from the bones and there is poor bone formation) occurs as a result of impaired vitamin D metabolism, hyperphosphatemia, hypocalcemia, and hyperparathyroidism. When calcium and phosphorous product is > 70, hardening of the blood vessels and tissues occur. If this occurs, patients are started on calcium and phosphorous binders.
Since the kidneys participate in the production of red blood cells through renal erythropoietin factor, abnormalities will occur as renal insufficiency progresses. Production of a depressed number of red blood cells (RBC) results. Those red blood cells that are produced survive a shorter time than normal. Anemia results from the low red blood cell levels.
SUMMARY OF PATHOPHYSIOLOGY EFFECTS OF RENAL FAILURE
COMMONLY CALLED THE UREMIC SYNDROME
Sleep Disturbances Anxiety
Muscular Irritability Psychosis
Anorexia Red Eye Syndrome
Nausea Band Keratopathy
Vomiting Hypertensive Retinopathy
PERIPHERAL NEUROPATHY CARDIOVASCULAR
Restless Leg Syndrome Hypertension
Motor Weakness ASHD
Hyperparathyroidism Carbohydrate Intolerance
Thyroid Abnormalities Hyperlipidemia
SUMMARY LIST OF CAUSES OF CHRONIC RENAL FAILURE
PRIMARILY GLOMERULAR DISEASE
Acute poststreptococcal glomerulonephritis
Berger’s (IgA/IgG) mesangial nephropathy
Focal proliferative glomerulonephritis
Chronic membranous glomerulopathy
Non-Goodpasture’s antiglomerular basement membrane disease
Rapidly progressive glomerulonephritis
CONGENITAL ANOMALIES OF KIDNEYS
Medullary cystic disease
METABOLIC RENAL DISEASE
Gout with hyperuricemic nephropathy
PRIMARILY TUBULAR DISEASE
Chronic potassium depletion
Fanconi’s syndrome and variants
Heavy metal poisoning (lead, cadmium, etc.)
Malignant hypertension (necrotizing arteriolitis)
Bilateral renal artery stenosis
Bilateral fribromuscular hyperplasia
Bilateral renal vein thrombosis
URINARY TRACT DISEASE
Upper tract obstruction
Lower tract obstruction
Congenital anomalies of bladder, neck and/or urethra
COLLAGEN AND IMMUNOLOGIC DISEASE
Diffuse systemic sclerosis (scleroderma)
Systemic lupus erythematosus
Light chain nephropathy
IgG/IgM mixed cryoglobulinemia