MNT in chronic renal failure


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MNT in chronic renal failure

  1. 1. Medical Nutrition Therapy in CRF Dr. B. K. Iyer
  2. 2. Terms to know CRD CRI CRF ESRD Chronic renal disease is a patho-physiologic process with multiple causes, resulting in the inevitable decrease of nephron number and function. Chronic renal insufficiency (CRI) is the term for patients with mild-to-moderate renal impairment, those whose GFR falls at 30-70 cc/min. Chronic renal failure Is characterized by progressive destruction of renal mass with irreversible loss of nephrons over a period of at least months to many years. End-stage renal disease is a stage of total or nearly total and permanent kidney failure to render patient permanently dependent upon RRT
  3. 3. Terms to know <ul><li>These different stages of chronic renal impairment form a continuum in time, and the above terms should be used to more readily appreciate the severity of renal disease. </li></ul>GFR RRT Glomerular filtration rate (GFR) progressively decreases with nephron loss. Renal Replacement Therapy (dialysis or transplantation) Uraemia Is the clinical and laboratory syndrome, reflecting dysfunction of all organ systems as a result of untreated or undertreated renal failure
  4. 4. Pathophysiology
  5. 5. Chronic renal disease - causes <ul><li>Glomerulonephritis was the leading cause of CRD in the past, </li></ul><ul><li>Diabetic and hypertensive nephropathy are now much more frequent underlying etiologies. </li></ul>
  6. 6. Chronic renal disease - causes <ul><li>Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: </li></ul>
  7. 7. History of diabetic nephropathy
  8. 8. Chronic renal disease - path <ul><li>Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. </li></ul><ul><li>CRD involves initiating a set of progressive mechanisms that are a common consequence following long- term reduction of renal mass, irrespective of etiology. </li></ul>
  9. 9. Renal compensation <ul><li>With progressive destruction of nephrons, the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons. </li></ul><ul><li>This nephron adaptability allows for continued normal clearance of plasma solutes such that substances such as urea and creatinine start to show significant increases in plasma levels only after total GFR has decreased to 50%, when the renal reserve has been exhausted. </li></ul>
  10. 10. Renal manifestations <ul><li>Patients whose renal adaptation maintains a GFR of 70-100 cc/min and those with CRI (GFR >30 cc/min) generally are entirely asymptomatic and do not experience clinically evident disturbances in water or electrolyte balance or endocrine/metabolic derangements. </li></ul><ul><li>Disturbances generally become clinically manifest through the stages of CRF (GFR <30 cc/min) and ESRD (GFR <10 cc/min). </li></ul>
  11. 11. Renal stages <ul><li>Earliest common stage to all forms of CRD is a loss of renal reserve, (35-50%) even when kidney function appears to be normal. </li></ul><ul><li>GFR can be augmented by 20 to 30% in response to a protein challenge stimulus ( Hyperfiltration ). </li></ul>
  12. 12. Renal stages
  13. 13. GFR upto 50% <ul><li>With reduction in GFR upto 50%, the plasma creatinine value will double. </li></ul><ul><li>A rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL in a patient, although still within the reference range, actually represents a loss of 50% of functioning nephron mass. </li></ul>
  14. 14. GFR upto 30% <ul><li>As GFR declines to levels as low as 30% of normal, patients may stay asymptomatic with only biochemical evidence of GFR decline. </li></ul><ul><li>Early additional clinical and laboratory manifestation of renal insufficiency include – </li></ul><ul><ul><li>nocturia, </li></ul></ul><ul><ul><li>mild anemia and loss of energy, </li></ul></ul><ul><ul><li>decreasing appetite and early disturbances in nutritional status, and </li></ul></ul><ul><ul><li>abnormalities in calcium and phosphorus metabolism (moderate renal insufficiency). </li></ul></ul>
  15. 15. GFR < 30% <ul><li>As GFR falls to below 30% of normal, an increasing number and severity of uremic clinical manifestations and biochemical abnormalities supervene ( severe renal insufficiency ) </li></ul>
  16. 16. GFR < 10% <ul><li>When GFR falls below 5 to 10% of normal ( ESRD ), continued survival without renal replacement therapy becomes impossible. </li></ul>
  17. 17. Uremic syndrome
  18. 18. Background <ul><li>Azotemia: </li></ul><ul><ul><li>Retention of nitrogenous waste products as renal insufficiency develops. </li></ul></ul><ul><li>Uraemia </li></ul><ul><ul><li>more advanced stages of progresive renal insufficiency when the complex, multiorgan system derangements become clinical manifest. </li></ul></ul><ul><ul><ul><li>Uremia involves more than renal excretory failure alone. </li></ul></ul></ul><ul><ul><ul><li>The most likely candidates as toxins in uremia are the by-products of protein and amino acid metabolism </li></ul></ul></ul>
  19. 19. Renal problems <ul><li>A host of metabolic and endocrine functions normally subserved by the kidney are also impaired, resulting in </li></ul><ul><ul><li>Anaemia; </li></ul></ul><ul><ul><li>Malnutrition; </li></ul></ul><ul><ul><li>Impaired metabolism of carbohydrates, fats, and proteins; </li></ul></ul><ul><ul><li>Defective utilization of energy; and </li></ul></ul><ul><ul><li>Metabolic bone disease. </li></ul></ul>
  20. 20. Uraemia <ul><li>Uremic Sx: can be divided into those sets of abnormalities: </li></ul><ul><ul><li>Abnormalities consequent to the accumulation of products of protein metabolism </li></ul></ul><ul><ul><li>Abnormalities consequent to the loss of other renal functions (fluid & electrolyte homeostasis and synthesis of certain hormones). </li></ul></ul><ul><li>Urea may contribute to some clinical signs ( anorexia, malaise, vomiting, and headache ) </li></ul><ul><li>Creatinine contribute to morbidity / mortality. </li></ul>
  21. 21. Clinical abnormalities
  22. 22. Renal problem spillovers <ul><li>As the kidney normally catabolizes a number of circulating plasma proteins and polypeptides, abnormalities associated with their breakdown would be seen. </li></ul><ul><li>Polypeptides hormones affected include: </li></ul><ul><ul><li>Parathyroid hormone, </li></ul></ul><ul><ul><li>Insulin and glucagon, </li></ul></ul><ul><ul><li>LH and prolactin. </li></ul></ul>
  23. 23. Fluid and electrolyte disturbances <ul><li>Fluid </li></ul><ul><li>Vol expansion and contraction </li></ul><ul><li>Hypernatremia and hyponatremia </li></ul><ul><li>Hyperkalemia and hypokalemia </li></ul><ul><li>Hypocalcemia </li></ul><ul><li>Hyperphosphatemia </li></ul><ul><li>Acidosis metabolica </li></ul>Sodium Potassium Calcium Phosphorus pH
  24. 24. Hyperkalaemia <ul><li>Hyperkalemia usually develops when GFR falls to less than 20-25 cc/min </li></ul><ul><ul><li>B ecause of decreased ability of the kidneys to excrete potassium. </li></ul></ul><ul><ul><li>Hyperkalemia in CRF can be aggravated by extracellular shift of potassium, such as occurs in the setting of acidemia or from lack of insulin. </li></ul></ul><ul><ul><li>observed sooner in patients who ingest a potassium-rich diet or if serum aldosterone levels are low, commonly observed with use of (ACE) inhibitors or NSAIDs. </li></ul></ul>
  25. 25. Metabolic acidosis <ul><li>In CRF, the kidneys are unable to produce enough ammonia in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium. </li></ul><ul><li>In very advanced CRF, accumulation of phosphates, sulphates, and other organic anions are the cause of the small anion gap. </li></ul><ul><li>often is mixed, non–anion gap and anion gap. </li></ul>
  26. 26. Volume expansion <ul><li>Extracellular volume expansion and total-body volume overload results from </li></ul><ul><ul><li>failure of sodium and free water excretion. </li></ul></ul><ul><ul><li>generally becomes clinically manifest when GFR falls to less than 10-15 cc/min, when compensatory mechanisms have become exhausted. </li></ul></ul><ul><ul><ul><li>Patients present with peripheral and, not uncommonly, pulmonary edema and hypertension. </li></ul></ul></ul>
  27. 27. Endocrine metabolic disturbance <ul><li>Secondary hyperparathyroidism </li></ul><ul><li>Adynamic osteomalacia </li></ul><ul><li>Carbohydrate intolerance </li></ul><ul><li>Hypertriglyceridemia </li></ul><ul><li>Develops due to: </li></ul><ul><ul><li>hypocalcemia, </li></ul></ul><ul><ul><li>decreased renal synthesis of (1,25-dihydroxyvitamin D, or calcitriol), and </li></ul></ul><ul><ul><li>hyperphosphatemia. </li></ul></ul>
  28. 28. Phosphate retention <ul><li>Begins in early CRF; </li></ul><ul><ul><li>when GFR falls, less phosphate is filtered and excreted but serum levels do not rise initially because of ↑ PTH secretion, which increases renal excretion. </li></ul></ul><ul><ul><li>As GFR falls into the moderate-to-severe stages of CRF, hyperphosphatemia develops from the inability of the kidneys to excrete the excess dietary intake. Hyperphosphatemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D to calcitriol, so serum calcitriol levels are low when the GFR is less than 30 cc/min. </li></ul></ul>
  29. 29. Neuromuscular disturbances <ul><li>Fatigue </li></ul><ul><li>Sleep disorders </li></ul><ul><li>Headache </li></ul><ul><li>Lethargy </li></ul><ul><li>Asterixis </li></ul><ul><li>Muscular irritability </li></ul><ul><li>Peripheral neuropathy </li></ul>
  30. 30. Cardiovascular and pulmonary disturbances <ul><li>Arterial hypertension </li></ul><ul><li>Congestive heart failure </li></ul><ul><li>Pulmonary edema </li></ul><ul><li>Pericarditis </li></ul><ul><li>Uremic Lung </li></ul>
  31. 31. Dermatologic disturbances <ul><li>Hyperpigmentation </li></ul><ul><li>Pruritus </li></ul>
  32. 32. Gastointestinal disturbances <ul><li>Anorexia </li></ul><ul><li>Nausea and vomiting </li></ul><ul><li>Uremic fetor </li></ul><ul><li>Gastroenteritis </li></ul><ul><li>Peptic ulcer </li></ul><ul><li>Peritonitis </li></ul>
  33. 33. Hematologic and inmunologic disturbances <ul><li>Anemia </li></ul><ul><ul><li>Normochromic normocytic anemia </li></ul></ul><ul><ul><li>principally develops from decreased renal synthesis of erythropoietin </li></ul></ul><ul><ul><ul><li>the hormone responsible for bone marrow stimulation for red blood cell (RBC) production </li></ul></ul></ul><ul><ul><li>Gets more severe as GFR progressively decreases. </li></ul></ul><ul><ul><li>No reticulocyte response occurs. </li></ul></ul><ul><ul><li>RBC survival is decreased. </li></ul></ul><ul><li>Lymphocytopenia </li></ul><ul><li>Bleeding diathesis </li></ul><ul><ul><li>Tendency of bleeding is increased from the uremia-induced platelet dysfunction </li></ul></ul><ul><li>Increased susceptibility to infection </li></ul>
  34. 34. Physical Examination
  35. 35. Physical examination <ul><li>Blood pressure </li></ul><ul><li>Fundoscopy </li></ul><ul><li>Precordial examination </li></ul><ul><li>Palpable renal or spleen masses </li></ul><ul><li>Extremity examination for edema </li></ul><ul><li>Asterixis </li></ul><ul><li>Neuropathy </li></ul>
  36. 36. Treatment MNT
  37. 37. Delaying or halting progression of CRF <ul><li>All of the preventive and therapeutic measures aim to prevent or postpone ESRD and renal replacement therapy. </li></ul><ul><li>Aggressive BP control to target value </li></ul><ul><li>Aggressive glycemic control in patients with diabetes </li></ul><ul><li>Treatment of hyperlipidemia </li></ul><ul><li>Avoidance of nephrotoxins - IV radiocontrast, NSAIDs, aminoglycosides </li></ul>
  38. 38. Treating pathologic manifestations of CRF with oral alkali supplementation Metabolic acidosis with loop diuretics or ultrafiltration Fluid overload with calcitriol or vitamin D analogs. Hyper-parathyroidism with calcium supplements +/- calcitriol Hypo- calcemia with dietary phosphate binders and dietary phosphate restriction Hyper-phosphatemia with erythropoietin Anemia
  39. 39. Timely planning for chronic renal replacement therapy <ul><li>Early education regarding natural disease progression, different dialytic modalities, renal transplantation, patient option to refuse or discontinue chronic dialysis </li></ul><ul><ul><li>Timely placement of permanent vascular access (arrange for surgical creation of primary arteriovenous fistula, if possible, and preferably at least 6 months in advance of anticipated date of dialysis) </li></ul></ul><ul><ul><li>Timely elective peritoneal dialysis catheter insertion </li></ul></ul><ul><ul><li>Timely referral for renal transplantation </li></ul></ul>
  40. 40. Renal Replacement Therapies <ul><li>Recommended for patients with pronounced azotemia, electrolyte imbalance, fluid overload, severe acidosis. </li></ul><ul><li>Used in 85% of patients with oliguric ARF and 30% of nonoliguric </li></ul><ul><li>Purpose is to correct imbalances as well as provide sufficient renal support to other organs </li></ul><ul><li>Protein needs are higher in ESRD due to losses that occur during dialysis. </li></ul>
  41. 41. Protein Replacement Therapies <ul><li>If you are in stages 1, 2, or 3 of CKD, your protein intake may be limited to 12-15% of your calorie intake each day. </li></ul><ul><li>If you are in stage 4 of CKD, you may be advised to reduce protein to 10% of calorie intake each day. </li></ul><ul><li>But, Patients who are in stage 5, the last stage of kidney disease, need dialysis to live. This stage is also known as end stage renal disease or ESRD. </li></ul>
  42. 42. Protein Replacement Therapies <ul><li>The kidneys are working at less than 10% capacity. This means that kidneys cannot process the accumulated waste and fluid your body produces on a day-to-day basis. </li></ul><ul><li>Dialysis is required to take over for the failed kidneys and needed indefinitely or until a kidney transplant is possible. </li></ul><ul><li>Dialysis treatments remove protein waste from the blood. </li></ul>
  43. 43. Protein Replacement Therapies <ul><li>A low protein diet is no longer needed to control protein waste buildup since this is accomplished by dialysis. </li></ul><ul><li>Unfortunately, some amino acids are removed during dialysis. A higher protein intake is needed to replace dialysis protein lost and to help keep you well nourished and healthy. </li></ul><ul><li>Protein needs are higher in ESRD due to losses that occur during dialysis. </li></ul><ul><li>. </li></ul>
  44. 44. Maintenance dialysis <ul><li>2 options exist for maintenance dialysis. </li></ul><ul><ul><li>Hemodialysis involves the creation of an arterovenous fistula and dialysis graft, usually in the arm, and treatment at a dialysis center, typically 3 times weekly. </li></ul></ul><ul><ul><li>Continuous peritoneal dialysis involves inserting the dialysate into the patient's abdomen and allowing dialysis to occur continuously or intermittently without requiring the patient to travel regularly to a dialysis center. </li></ul></ul><ul><ul><li>Both methods have advantages and disadvantages, and outcomes are similar. </li></ul></ul>
  45. 45. Haemodialysis <ul><li>Removes concentrated molecules and excess fluid from pts blood through diffusion and ultrafiltration </li></ul><ul><li>3 parts of the system are: </li></ul><ul><ul><li>the dialyzer (artificial kidney), </li></ul></ul><ul><ul><li>the dialysis machine, and </li></ul></ul><ul><ul><li>the dialysate </li></ul></ul><ul><li>Requires vascular access, usually through an AV (arteriovenous) fistula </li></ul>
  46. 46. Haemodialysis <ul><li>Hemodialysis: standard treatment if patient is hemodynamically stable </li></ul><ul><ul><li>However, risk of hypotension and wide swings in body weight in unstable patients </li></ul></ul><ul><li>Continuous haemodialysis (CAVHD, CVVHD) uses an ultrafiltrate fluid similar to plasma </li></ul><ul><ul><li>Clearance occurs through diffusion from high concentration (blood) to low concentration </li></ul></ul>
  47. 47. Haemodialysis
  48. 48. Haemodialysis
  49. 49. Haemodialysis
  50. 50. Haemodialysis
  51. 51. Haemofiltration <ul><li>Continuous haemofiltration (CAVH, CVVH) provides slow, continuous filtration across a membrane </li></ul><ul><ul><li>Driven by arterial pressure (CAVH) or </li></ul></ul><ul><ul><li>Driven by pump (CVVH) </li></ul></ul>
  52. 52. Peritoneal dialysis <ul><li>Blood cleansed by passive movement from capillaries to dialysate (diffusion) </li></ul><ul><li>Ultra-filtration (UF): fluid removed by osmosis due to high osmolality of dextrose in dialysate </li></ul><ul><li>Better control of labs, fluid balance and B.P. </li></ul>
  53. 53. Peritoneal dialysis <ul><li>Advantages: </li></ul><ul><ul><li>for those with heart failure, access problems. Diet liberal, independence. </li></ul></ul><ul><li>Disadvantages: </li></ul><ul><ul><li>anorexia, a.a. losses in dialysate, peritionitis-> catabolism, anorexia, long- term wasting, high B.S., wt. gain, lack of socialization </li></ul></ul>
  54. 54. CAPD – Continuous Ambulatory Peritoneal dialysis <ul><li>Most patients do 4-5 exchanges per day </li></ul><ul><li>A specific volume of dialysate (1500-3000 ml) is infused into the peritoneal cavity via a catheter </li></ul><ul><li>The dialysate dwells for 4 hours as excess fluid and toxins diffuse through peritoneal membrane </li></ul><ul><li>Dialysate and wastes are drained from the body and the process repeated. </li></ul><ul><li>Dialysate is present in the body 24 hours per day </li></ul><ul><li>APD (automated peritoneal dialysis therapy) speeds the process </li></ul>
  55. 55. MNT In ESRD
  56. 56. CKD: Nutritional Management <ul><li>Different principles in different stages </li></ul><ul><li>3 stages </li></ul><ul><ul><li>Pre – dialysis stage or early stages of CKD </li></ul></ul><ul><ul><li>Dialysis stage – ESRD stage </li></ul></ul><ul><ul><li>Post kidney transplant stage </li></ul></ul>
  57. 57. Therapy concerns
  58. 58. MNT concerns Individualized [~1000 mg/day] Individualized [~1000 mg/day] Individualized [based on serum level] Calcium (mg/d) Individualized 500-750 + urine output (1000 if anuric) Unrestricted Fluid (ml/d) Individualized ~ 40 Individualized Potassium (mg/kg IBW) 2000-4000 2000-3000 1000-3000 Sodium (mg/d) <17 indiv <17 indiv 8-12 indiv Phosphorus 30-35 30-35 30-35 Energy (kcal/kg IBW) 1.2-1.5 1.1-1.4 0.6-1.0 Protein [g/kg/day] CAPD or CCPD Haemo dialysis CKD Nutrients
  59. 59. ESRD: Dietary protein & energy requirements <ul><li>By KOPPLE J. D., American journal of kidney diseases, 1998, vol. 32, no. 6, pages 97-104 </li></ul><ul><li>The low dietary energy intakes of MHD and CPD patients are maladaptive. </li></ul><ul><li>Nitrogen balance studies indicate that a safe dietary allowance for protein is approximately 1.2 g/kg/d for MHD patients and 1.2 to 1.3 g/kg/d for CAPD patients. </li></ul><ul><ul><li>Because the nutritional status of patients at the onset of chronic dialysis therapy is a strong predictor of both their nutritional status during the course of chronic dialysis treatment and their subsequent morbidity and mortality, it is important to maintain good nutritional status in patients with chronic renal failure before their development of end-stage renal disease (ESRD) and establishment on chronic dialysis. </li></ul></ul><ul><ul><li>Evidence indicates that there is a reduction in dietary protein and energy intake and a gradual deterioration of nutritional status in patients with chronic renal insufficiency as the glomerular filtration rate (GFR) decreases progressively to less than 50 to 60 mL/min/1.73m2. </li></ul></ul>
  60. 60. ESRD: Nutritional Management <ul><li>Prevent deficiencies </li></ul><ul><li>Control edema and serum electrolytes </li></ul><ul><li>Prevent renal osteodystrophy </li></ul><ul><li>ESRD patients must restrict their fluid intake. </li></ul><ul><ul><li>Without adherence to a specified fluid allowance, patients are more likely to have poorly controlled BP and risk congestive heart failure. </li></ul></ul><ul><ul><li>Hypertension in dialysis patients is largely attributed to +ve sodium balance and volume expansion </li></ul></ul><ul><li>The typical fluid allowance for patients on dialysis is 700 to 1000 mL/day, plus urine output. </li></ul>
  61. 61. ESRD: Nutritional Management <ul><li>A high-potassium diet is normally desirable to control BP and reduce risk for stroke; </li></ul><ul><li>However, ESRD patients on hemodialysis cannot tolerate this because they are unable to excrete K+. </li></ul><ul><li>Evidence indicates that the vast majority of patients comply with potassium restriction. </li></ul><ul><li>Elevated blood phosphorus concentrations are associated with increased mortality in ESRD patients. </li></ul>
  62. 62. Interdialytic Weight Gain <ul><li>Patients on dialysis gain several kg. of fluid between HD treatments </li></ul><ul><li>If pts gain >5%, </li></ul><ul><ul><li>reflect excessive fluid intake, leading to hypertension, edema, ascites, pleural effusion </li></ul></ul><ul><li>Fluid gains of <2% </li></ul><ul><ul><li>reflect minimal fluid and food intake, may be losing body mass </li></ul></ul><ul><li>Measures of Dialysis Adequacy </li></ul><ul><ul><li>Urea Reduction Rate (URR) - Refers to change in urea concentration between pre and post-dialysis blood tests - CMS goal is >65% </li></ul></ul>
  63. 63. Monitor Patient Status <ul><li>BP >140/90 </li></ul><ul><li>Edema </li></ul><ul><li>Weight changes </li></ul><ul><li>Urine output </li></ul><ul><li>Urine analysis: </li></ul><ul><ul><li>Albumin </li></ul></ul><ul><ul><li>Protein </li></ul></ul><ul><li>Kidney function </li></ul><ul><ul><li>Creatinine clearance </li></ul></ul><ul><ul><li>Glomerular filtration rate (GFR) </li></ul></ul>
  64. 64. Monitor Patient Status <ul><li>Blood values </li></ul><ul><ul><li>BUN 10 to 20 mg/dl (<100 mg/dl) </li></ul></ul><ul><ul><li>Creatinine 0.7 to 1.5 mg/dl (10-15 mg/dl) </li></ul></ul><ul><ul><li>Potassium 3.5 to 5.5 mEq/L </li></ul></ul><ul><ul><li>Phosphorus 3.0 to 4.5 mg/dl </li></ul></ul><ul><ul><li>Albumin 3.5-5.5 g/dl </li></ul></ul><ul><ul><li>Calcium 9-11 mg/dl </li></ul></ul>
  65. 65. Treatment In HD MNT
  66. 66. Typical Hemodialysis diet <ul><li>Typical diet order </li></ul><ul><ul><li>2000 calorie, </li></ul></ul><ul><ul><li>80 g protein, </li></ul></ul><ul><ul><li>2 g Na+, </li></ul></ul><ul><ul><li>3 g K+, </li></ul></ul><ul><ul><li>low phosphorus, </li></ul></ul><ul><ul><li>1500 cc fluid restriction </li></ul></ul>
  67. 67. MNT in HD: Protein <ul><li>10-12 g free amino acids lost per treatment during dialysis </li></ul><ul><li>Greater amino acid losses with glucose-free dialysate and high flux dialyzers </li></ul><ul><li>1.2 g protein/kg standard body weight (SBW) with 50% high biological value. </li></ul><ul><li>Most HD patients take in less than 1 g/day </li></ul>NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in Byham-Gray, p. 45-46
  68. 68. MNT in HD: Energy <ul><li>Adults <60 years: 35 kcal/kg SBW </li></ul><ul><li>Adults > 60 or obese: 30-35 kcals/kg body weight </li></ul><ul><li>Actual intakes of HD patients in studies are lower than that (mean 23 kcals/kg in HEMO study) </li></ul>NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in Byham-Gray, p. 46
  69. 69. Treatment In PD MNT
  70. 70. PERITONEAL DIALYSIS <ul><li>Dialysis solutions </li></ul><ul><ul><li>Pt. chooses depending on fluid status </li></ul></ul><ul><ul><ul><li>1.5%, 2.5% or 4.25% glucose </li></ul></ul></ul><ul><li>CAPD </li></ul><ul><ul><li>~4 – 2L. Exchanges/day </li></ul></ul><ul><ul><li>Dwells ~6 hours (dialysis) and drain </li></ul></ul><ul><ul><li>~60% glucose absorbed (3.7 kcal/g) </li></ul></ul><ul><li>CCPD </li></ul><ul><ul><li>~10 L exchanged throughout night </li></ul></ul><ul><ul><li>40% glucose absorbed 2 nd to rapid exchanges </li></ul></ul>
  71. 71. MNT for PD: Energy & proteins <ul><li>Energy: </li></ul><ul><ul><li>35 kcals/kg/day SBW or adjusted body weight for pts<60 years; 30 kcals/kg for those >60 </li></ul></ul><ul><ul><li>Calories provided in the dialysate should be included in total intake (may absorb as much as 1/3 of daily energy needs) </li></ul></ul><ul><li>Proteins </li></ul><ul><ul><li>PD patients lose 5-15 grams of protein a day, primarily as albumin </li></ul></ul><ul><ul><li>Goal 1.2-1.3 g/kg SBW or ABW / day </li></ul></ul>
  72. 72. Peritoneal dialysis <ul><li>Sample glucose absorption </li></ul><ul><ul><li>g glucose per liter x volume = total g of glucose </li></ul></ul><ul><ul><ul><li>Example: one – 2 L. exchange of 1.5% solution = 30 g glucose </li></ul></ul></ul><ul><ul><li>Total g of glucose x absorption rate (~60%) = g glucose absorbed </li></ul></ul><ul><ul><ul><li>Example: 30 g glucose x 60% = 18 g glucose absorbed </li></ul></ul></ul><ul><ul><li>g glucose absorbed x kcal per g glucose (3.7)= calories absorbed </li></ul></ul><ul><ul><ul><li>Example: 18 x 3.7=66.6 calories/2 L. exchange </li></ul></ul></ul><ul><ul><li>Patient does 4 exchanges/d </li></ul></ul><ul><ul><ul><li>67 x 4 = 268 calories/d from diaysate </li></ul></ul></ul>
  73. 73. Background basics MNT
  74. 74. What are AGEs? <ul><li>Advanced glycation end products (AGEs) are a heterogeneous group of molecules that accumulate in plasma and tissues with advancing age, diabetes, and renal failure. </li></ul><ul><li>There is emerging evidence that AGEs are potential uremic toxins and may have a role in the pathogenesis of vascular and renal complications associated with diabetes and aging. </li></ul>
  75. 75. What are AGEs? <ul><li>AGEs accumulate in renal failure as a result of decreased excretion and increased generation resulting from oxidative and carbonyl stress of uremia. </li></ul><ul><li>In vivo and in vitro studies indicate that AGEs have a vital role in the pathogenesis of diabetic nephropathy and the progression of renal failure. </li></ul><ul><li>Available dialytic modalities are not capable of normalizing AGE levels in patients with end-stage renal disease. </li></ul>
  76. 76. What are AGEs? <ul><li>AGEs accumulate in renal failure as a result of decreased excretion and increased generation resulting from oxidative and carbonyl stress of uremia. </li></ul><ul><li>In vivo and in vitro studies indicate that AGEs have a vital role in the pathogenesis of diabetic nephropathy and the progression of renal failure. </li></ul><ul><li>Available dialytic modalities are not capable of normalizing AGE levels in patients with end-stage renal disease. </li></ul>
  77. 77. Measuring proteins in the body <ul><li>There is no direct test to measure and evaluate the protein status in our body. </li></ul><ul><li>So we follow indirect tests and they include </li></ul><ul><ul><li>Anthropometric measurements, </li></ul></ul><ul><ul><li>Hepatic secretory proteins in blood (serum albumin, transferrin, retinol binding protein, prealbumin), </li></ul></ul><ul><ul><li>Plasma amino acids, </li></ul></ul><ul><ul><li>creatinine height index, </li></ul></ul><ul><ul><li>endogenous excretion of creatinine, and </li></ul></ul><ul><ul><li>estimation of cell-mediated immunity. </li></ul></ul>
  78. 78. Osmosis <ul><li>Osmosis is the movement of water from an area of lower solute concentration to an area of higher solute concentration. </li></ul><ul><ul><li>Semipermeable membrane </li></ul></ul><ul><ul><ul><li>Membrane must be more permeable to water </li></ul></ul></ul><ul><ul><ul><li>A greater concentration of solutes on one side of the membrane </li></ul></ul></ul>
  79. 79. Diffusion <ul><li>Diffusion is the movement of a solute molecule from an area of greater concentration to an area of lesser solute concentration. </li></ul>
  80. 80. Colloid Osmotic Pressure <ul><li>The tendency of plasma proteins to hold water in the intravascular spaces. </li></ul><ul><li>Albumin is the plasma protein which exerts the greatest osmotic pressure </li></ul><ul><ul><li>Albumin is formed in the liver </li></ul></ul><ul><ul><li>Most abundant plasma protein </li></ul></ul><ul><ul><li>Binds to hormones and transports them </li></ul></ul><ul><ul><li>Acid-base balance </li></ul></ul>
  81. 81. Colloid Osmotic Pressure <ul><li>The tendency of plasma proteins to hold water in the intravascular spaces. </li></ul><ul><li>Albumin is the plasma protein which exerts the greatest osmotic pressure, although a small role is played by globulin and fibrinogen, too. </li></ul><ul><ul><li>Albumin is formed in the liver </li></ul></ul><ul><ul><li>Most abundant plasma protein </li></ul></ul><ul><ul><li>Binds to hormones and transports them </li></ul></ul><ul><ul><li>Acid-base balance </li></ul></ul>
  82. 82. Osmolality <ul><li>Osmolality is the preferred measure of osmotic activity in clinical assessment & is a measure of the concentration of molecules per kilogram of water. Tonicity describes the effective osmolality of a solution. </li></ul><ul><li>Normal osmolality: 285-295 mOsm/kg </li></ul><ul><li>Formula: 2(Na)+K+ BUN + Glucose </li></ul><ul><ul><ul><ul><ul><li>3 18 </li></ul></ul></ul></ul></ul><ul><li>Osmolarity is a measure of the concentration of of molecules per liter of solution. </li></ul>
  83. 83. Isotonic <ul><li>An isotonic solution has the same osmolality as the extracellular fluid. </li></ul><ul><li>Examples </li></ul><ul><ul><li>D5W </li></ul></ul><ul><ul><ul><li>evenly distributed in the body compartments </li></ul></ul></ul><ul><ul><ul><li>used to replace deficits of total body water </li></ul></ul></ul><ul><ul><li>Normal Saline </li></ul></ul><ul><ul><ul><li>Each liter adds 1/4 liter to ECF </li></ul></ul></ul><ul><ul><ul><li>Each liter adds 3/4 to interstitial fluid </li></ul></ul></ul>
  84. 84. Hypertonic <ul><li>Hypertonic solutions have a higher concentration of solute and are more concentrated than extracellular fluids. </li></ul><ul><li>Examples </li></ul><ul><ul><li>3% saline </li></ul></ul><ul><ul><li>5% saline </li></ul></ul><ul><li>Net movement </li></ul><ul><ul><li>intracellular to extracellular </li></ul></ul>
  85. 85. Hypotonic <ul><li>Hypotonic solutions have a lower concentration of solutes and is more dilute than extracellular fluid </li></ul><ul><li>Examples </li></ul><ul><ul><li>1/2 Normal Saline </li></ul></ul><ul><ul><li>1/3 Normal Saline </li></ul></ul><ul><li>Net movement </li></ul><ul><ul><li>extracellular to intracellular </li></ul></ul>
  86. 86. Isotonic Fluid Imbalance <ul><li>Sodium and water Increase or decrease in the same proportion </li></ul><ul><li>Hypovolemia </li></ul><ul><ul><li>Fluid Volume Deficit </li></ul></ul><ul><li>Hypervolemia </li></ul><ul><ul><li>Fluid Volume Excess </li></ul></ul>
  87. 87. Concepts Related to Fluid Volume Deficit <ul><li>Low urine output </li></ul><ul><li>Urine specific gravity high </li></ul><ul><li>Poor skin turgor </li></ul><ul><li>Poor tongue turgor </li></ul><ul><li>Dry mucous membranes </li></ul><ul><li>Decreased or absent of tearing </li></ul><ul><li>Decreased or absent salivation </li></ul>