Nutrition Management in Renal Disease. Dr. Inge Permadhi MS., SpGK

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1 Nutrition Management in Renal Disease Dr. Inge Permadhi MS., SpGK

2 Kidney functions Excretory of waste products (urea) and drugs Regulation to maintain homeostatic balance from fluids, electrolytes, and organic solutes 1600 L/d blood filtering 180 L ultrafiltrate 1.5 L/d urine excreted Endocrine with diverse metabolic effects : 1,25 (OH) 2 D 3 (25 (OH)D 2 1,25 (OH) 2 D 3 ) Erythropoietin Renin synthesis (angiotensinogen angiotensin I) Metabolism

3 AA and protein metabolism in the human kidney The role of kidney in the homeostasis of protein : Synthesis of NEAA : serine, tyrosine, arginine, threonine, lysine, taurine, and tryptophane Degradation :catabolism of low-molecular weight protein (< Dalton) as insulin, C-peptide, GH, leptin etc) Filtration and reabsorption : 50 70g/d AA filtered 97-98% reabsorbed by the proximal tubules. Urinary excretion of AA : urea

4 Protein turnover 70kg Body protein 12 kg Protein Degradation g/d g/d Free AA pool g Endogenous AA synthesis Protein synthesis Dietary Protein 1g/kgBW/d ~ Amino acid Oxidation 70-90g/d Urea A schematic view of the major system responsible for the maintenance of body protein homeostasis in human

5 ALANINE GLUTAMINE Hepatic Glycogenolysis 50% POSTABSORTIVE GLUCOSE RELEASE 20% Renal Gluconeogenesis Hepatic Gluconeogenesis 30% ENDOGENOUS GLUCOSE RELEASE Participation of liver glycogenolysis, liver gluconeogenesis and renal gluconeogenesis In POSTABSORPTIVE glucose release (Gerich JE et al, Crit Care & Shock 2003 vol 6, no 2)

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8 AA and Protein metabolism in renal failure Protein degradation Increased by: -acidosis/cortisol -Insulin resistance (?) -Micro inflammation (?) Body protein Free AA pool Protein synthesis Decreased by: -Resistance tp GH/IGF-1 -Low nutrient intake -Hemodialysis -Peritoneal dialysis -Altered AA metabolism -Micro inflammation? = cytokine Endogenous AA synthesis by the kidney Dietary protein Reduced by: -anorexia Amino acid oxidation Increased by: -acidosis

9 * BCAA Valine Leucine Isoleucine * * ** Threonine Lysine Serine Essential AA Non-essential AA Special AA oxidation in muscles decrease production Glycine Citruline Cystine Aspartate Methionine Methylhistidine metabolic acidosis ** arginine KIDNEY FAILURE defective phenylalanine hydroxylation reduce protein binding ** Tyrosine Tryptophan **synthesis by renal >> *synthesis by renal < Mitch WE. Handbook of Nutrition and the Kidney, 2003

10 AA and PROTEIN Metabolism during Renal Failure SKELETAL MUSCLE protein breakdown (relative) protein synthesis BCAA oxidation (excess AA) Intracellular glutamine levels Glutamine efflux Glutamine synthesis Alanine synthesis Catabolic hormones: Cortisol Glucagon Cathecolamines ALANINE, GLUTAMINE LIVER Acute phase protein synthesis Albumin synthesis AA oxidation (excess AA) Gluconeogenesis from AAs Glutamine req Glutamine utilization Urea synthesis Urea KIDNEY Glutamine req Glutamine utilization Gluconeogenesis Ammonium excretion

11 Changes in Protein and Amino Acid Metabolism Metabolic acidosis : Acidosis causes the elimination of H + is diminished increase in net protein breakdown increased production of H + Protein catabolism especially from skeletal muscle. Protein synthesis Redistribution amino acids from muscle to the liver. Hepatic gluconeogenesis and ureagenesis Hepatic protein synthesis and secretion of acute phase protein is stimulated.

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13 Potential factors in Uremic Insulin Resistance: Accumulation of uremic toxins Hyperparathyroidism Metabolic acidosis Relative vitamin D deficiency Anemia Insulin resistance Insulin secretion Insulin clearance Plasma insulin Insulin sensitivity Carbohydrate intolerance

14 Carbohydrate Metabolism during Insulin Resistance Liver Gluconeogenesis Glycogenolysis Kidney Gluconeogenesis Renal insufficiency may affect the body s ability to maintain adequate blood sugar levels Insulin resistance Insulin Dependent Tissue Skeletal Muscle Adipose Tissue Glucose Plasma Kidney Non Insulin Dependent Tissue All other tissue such as: brain, kidney, immune tissue, wound tissue, lung Futile Cycle Glucose Uptake Glucose Uptake Glucose Uptake Glucose uptake Glicolysis Glycolysis LACTATE ALANINE, GLYCEROL Lactate Alanine Gluconeogenesis

15 Uremic Hypoglycemia Renal insufficiency may affect the body s ability to maintain adequate blood sugar levels Uremic carbohydrate intolerance Poor caloric intake Impaired hepatic glycogenolysis Certain medication use Prolonged insulin action Impaired conterregulatory response

16 The effect of parathyroid/vitamin D in glucose intolerance Secondary hyperparathyroid is associated with impaired insulin secretion. 1,25-OH 2 D 3 deficiency is contributed to the abnormalities in insulin secretion and glucose intolerant Total serum calcium levels would be expected to rise with advanced hyperparathyroidism. Increasing calcium levels can inhibit insulin secretion in pancreatic High levels of intracellular calcium inhibit phosphorylase phosphatase activity, preventing normal dephosphorylation of glycogen synthase and GLUT 4 in response to insulin Effect of parathyroid hormone or vitamin D changing in calcium balance and cytosolic calcium in insulin target tissue cells cause them resistant to insulin

17 Altered carbohydrate metabolism PERIPHERAL INSULIN RESISTANCE Defects in glucose uptake by dependent insulin tissue HYPOGLYCEMIA

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19 Mechanism of hyperlipidemia in Nephrotic syndrome HDL Diet intestine Bile acid FFA + Glycerol TG x Peripheral Cells VLDL LIVER LDL Cholesterol Chylomicron remnant * HDL /N Chylomicron * VLDL IDL capillaries capillaries Kidney Liver FFA FFA (Lipiduria) LPL * LPL

20 Mechanism of hyperlipidemia in CRF FFA + Glycerol TG Delayed catabolism of TG rich lipoprotein resulting in increased concentrations of apob containing triglyceriderich lipoproteins in VLDL and IDL and reduced levels of HDL VLDL LIVER VLDL IDL LDL capillaries Peripheral Cells Cholesterol FFA * LPL HDL HDL Liver

21 COMMON LIPOPROTEIN ABNORMALITIES IN RENAL DISEASE Renal abnormality Chylomicron remnants VLDL IDL LDL HDL Lp(a) Nephrotic syndrome -- N -- CRF -- Hemodialysis CAPD? Transplantation Atherogenicity Protective ++ CAPD : continuous ambulatory peritoneal dialysis Nutritional Management of Renal Disease, 1997

22 ESPEN GUIDELINES ON ENTERAL NUTRITION: ADULT RENAL FAILURE (

23 Nutritional problems Poor appetite (anorexia) due to renal failure and concurrent illness Hypercatabolism due to underlying illness such as severe infection/sepsis, burns, or postoperative healing Malnutrition, wasting, cachexia.

24 Low nutrient intake Anorexia induced by Inadequate clearance of anorexigens Impaired gastric emptying Increased leptin levels Comorbid illnesses Superimposed illness leading to Altered gastrointestinal motility Altered digestive or absorptive processes Inflammation Nutrient losses during dialysis Metabolic acidemia Comorbidity Endocrine disorders of uremia Resistance to insulin Resistance to IGF-1 and GH Hyperparathyroid Hyperglucagonemia Hypotestosteronemia Blood loss Occult GIT bleeding Venipuncture Sequestrian in hemodialyzer

25 Goal of nutrition therapy To prevent malnutrition at an early stage of renal disease and/or to maintain an optimal nutritional status To manage the metabolic disorders To control the accumulation of waste products To prevent cardio-vascular disease by treating hyperlipidemia To prevent bone disease by treating vitamin D deficiencies and hyperparathyroidism To retard progression of renal dysfunction

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27 Acute renal failure Espen Guidelines, Clinical Nutrition, 2006 Macronutrients Requirements are not so much determined by: Severity of underlying disease The type and intensity of extracorporeal renal replacement therapy Nutritional status Associated complications (the extent of catabolism) Energy : kcal/kg IBW/d Carbohydrate : 3-5 (max 7) g/kgbw/d Fat : (max 1.5) g/kgbw/d Protein (EAA + NEAA) : Conservative therapy : (max 1.0) g/kgbw/d Extracorporeal therapy : g/kgbw/d CCRT, in hypercatabolism: up to maximum 1.7g/kgBW/d CRRT (continuous renal replacement therapies)

28 Micronutrients and Vitamins Recommendation in ARF Espen Guidelines, Clinical Nutrition 2000 Vitamins Water soluble vitamins Riboflavin, thiamine, pyridoxine (5mg/d predialysis or 10 mg dialysis), B 12 vitamin C < 50 mg Fat soluble vitamins Vitamin A, E, K are not recommended Low doses of 1,25(OH) 2 D µg/d or every second day Minerals Phosphorus : 5 10 mg/kg/d (limiting phosphorus food : dairy products, egg yolks, meat) Calcium : <2 2.5 g/d including binder load Iron : supplementation might be necessary in patients on VLPD or patients with long term vegetarian diets Trace elements Routine supplementation with trace elements is not recommended : zinc, selenium, copper, aluminum.

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30 Chronic renal failure Espen Guidelines, Clinical Nutrition, 2006 CONSERVATIVE THERAPY Energy : 35 kcal/kgibw/d Fat : < 30% total calories (saturated fat <10% total cal, cholesterol < 300 mg/d) Carbohydrate : simple sugars < 10% Protein: GFR (ml/min) ESPEN (g/kgbw/d) NKF(g/kgBW/d) * (2/3 HBV) - < (2/3 HBV) or 0.60 or o.75 (intolerance energy intake) EAA + KA * Depending of physical activity, lean body mass, age, gender, degree of malnutrition etc

31 Chronic renal failure Espen Guidelines, Clinical Nutrition, 2006 MINERAL REQUIREMENT Phosphate Potassium Sodium Fluid mg/d mg/d g/d Not limited * Depending of physical activity, lean body mass, age, gender, degree of malnutrition etc

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33 Haemodialysis and CAPD ESPEN NKF Protein (g/kgbw/d) Haemodialysis (>50%HBV) 1.2 (>50%HBV) CAPD (>50%HBV) (>50%HBV) Energy (kcal/kgbw/d) Haemodialysis 35 < 60 yr 35 CAPD < 60 yr 30

34 Haemodialysis and CAPD Phosphate (mg/d) * Potassium (mg/d) * Sodium (g/d) * Fluid (ml) urine volume * Individual requirements may differ in acute condition

35 Haemodialysis and CAPD Folic acid Pyridoxin Vitamin C Vitamin D Zn* Se* 1 mg/d mg/d 3 60 mg/d Should be given according to serum calcium, phosphorus and PTH levels 15 m/d μg/d * In depleted patient

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37 Nutritional Recommendation for Nephrotic Syndrome Espen Guidelines, Clinical Nutrition 2000 Nutrition therapy and pathophysiology 2007 Energy : 35 kcal/kg/day Protein: 0.8 mg/kgbw/day >1.5 mg/kgbw/d proteinuria(soy and flaxseed based proteins may be beneficial in reducing proteinuria) 50 60% HBV Lipid: cholesterol lowering diets 25 30% of total calories Saturated diet : < 7% PUFA : > 10% MUFA : > 20% Cholesterol : 200 mg/day Fiber : 25 30g/day Sodium : 3 g/d Fluids : generally not restricted Vitamin: vitamin D if vitamin D Minerals : Zn and Fe if proven deficient, Calcium (<2 2.5g/d)

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