Medical Nutrition Therapy for Renal Disorders PDF

Medical Nutrition Therapy for Renal Disorders Socorro Milagros C. Alcancia, RND, PhD Renal Disorders Each kidney consist of 1million functioning nephrons, consisting of a glomerulus connected to a series of tubules. Tubules are composed of different segments: Proximal convoluted tubule Loop of Henl...

Medical Nutrition Therapy for Renal Disorders Socorro Milagros C. Alcancia, RND, PhD Renal Disorders Each kidney consist of 1million functioning nephrons, consisting of a glomerulus connected to a series of tubules. Tubules are composed of different segments: Proximal convoluted tubule Loop of Henle Distal tubule Collecting duct Glomerulus A spherical mass of capillaries surrounded by a membrane. Bowman’s capsule- it produces the ultrafiltrate. Tubules Reabsorb the majority of components composing the ultra fibrate: Proximal convulated tubule: major nutrient reabsorption Loop of Henle: water and sodium balance Distal Tubule: acid-base balance Collecting Tubule: water reabsorption Hormones Vasopressin Renin Angiotensin II Aldosterone Erythropoietin Activation of vitamin D3 Vasopressin Anti diuretic hormone or ADH From the pituitary glands Exerts pressor effect;elevates blood pressure Acts on the distal and collecting tubules to reabsorb water Renin Enzyme secreted by the renal cortex Secreted in response to: 1.Decreased Na intake 2. Sodium loss 3. Hypovolemia or decreased fluid volume Acts on angiotensin (protein substrate from the liver) to form angiotensin I &II. Angiotensin II Active pressor substance Increase heart beat Retention and reabsorption of Na Excretion of K Aldosterone Retention and Acts on the reabsorption Excretion of K distal tubule of Na Erythropoietin (EPO) Stimulates erythropoiesis in the bone marrow A hormone secreted by the kidney which acts on stem cells of the bone marrow. Stimulates RBC production Activation of Vit D3 Ergocalciferol Th active metabolite, 1,25 Under the influence of dihydroxycholecalciferol parathyroid hormone or 1,25 (OH)2O3 or 1,25 (PTH) dihydroxyl D3. Absorption of Ca and P for bone mineralization Renal Functions Filtration- RBC and protein remain in the blood Reabsorption- 100% glucose and amino acids;80—85% water, Na, K, Cl Secretion- additional ions to maintain acid-base balance, hormones that control blood pressure, blood components. Excretion- wastes, urea, excess ketones, excess water Roles of Kidneys from Blood Filtration Regulation of blood pressure by the secretion of the enzyme renin Renin catalyzes the formation of angiotensin I from the plasma protein angiotensinogen In the lungs, angiotensin I is converted to angiotensin II, a vasoconstrictor that narrows the diameters of the arterioles thus raising blood pressure. Angiotensin II stimulates the release of aldosterone that stimulates the kidney to increase Na and water reabsorption thus increases plasma volume and raised blood pressure. Kidneys produce hormone erythropoietin which stimutales the production of RBCs in the bone marrow. Kidneys convert vitamin D to its active form (1,25 dihydroxyvitamin D3 , thus helping to regulate calcium balance and bone formation. Renal Solute Load Solute excreted in 1 Liter urine mainly, measures urea (nitrogen) and electrolytes (Na) Laboratory Tests in Renal Diseases Decreased glomerular filtration rate(GFR), creatinine clearance Elevated serum creatinine, BUN MANIFESTTAION OF RENAL DISEASE Acute Kidney Injury (AKI) Chronic Kidney Disease End-Stage Renal Disease Kidney Stones Acute Kidney Injury Acute Renal failure(ARF) Characterized by a sudden reduction in glomerular filtration rate(GFR), the amount of filtrate per unit in the nephrons, and altered ability of the kidney to excrete the daily production metabolic waste. This can occur in association with oliguria or normal urine flow, but occurs in previously healthy kidneys. Causes of AKI Prerenal Factors (6-70% of cases) Intrarenal Factors (25-40% cases) Postrenal Factors (5=10% cases) Low blood volume or pressure: Vascular disorders: sickle-cell Obstructions(ureter or hemorrhage, burns, sepsis, shocks, disease, diabetes mellitus, bladder);strictures, tumors, stones, anaphylactic reactions, nephrotic transfusion reaction. trauma syndrome, GIT losses, diuretics, Obstructions (within kidney): Prostate disorders: cancer or anti hypertensive medications. inflammation, tumors, stones, scar hyperplasia Renal artery disorders: blood clots tissue Renal vein thrombosis or emboli, stenosis, aneurysm, Renal injury: infections, Bladder disorders: neurological trauma environmental contaminants, conditions, bladder rupture Heart disorders: heart failure, heart drugs, medications, E. Coli food Pregnancy attack, arrythmias poisoning  Consequences of AKI Decline in renal filtration alters the composition of blood and urine since the kidneys are not able to regulate the levels of electrolytes, acid and nitrogenous wastes in the blood. Urine may ne diminished in quantity (oliguria) or absent( anuria) leading to fluid retention. Fluid and electrolyte imbalances: Reduced excretion of fluids and electrolytes results in Na retention and elevated levels of K, PO4, Mg in the blood. Hyperkalemia can alter heart rhythm and lead to heart failure. Hyperphosphatemia promotes excessive parathyroid hormones secretion which leads to losses of bone calcium. Edema results due to Na retention and reduced urine production. Uremia due to impaired kidney function, nitrogen- containing compounds and other waste products accumulate in the blood (uremia). Complications include hormonal imbalances, electrolyte and acid-base imbalances, disturbed heart and GIT functioning, neuromuscular disturbances and depressed immunity.. Treatment of AKI Involves a combination of drug therapy, dialysis and nutrition therapy 1. Restore fluid and electrolyte balances 2. Minimize blood concentrations of toxic waste products Both medical care and dietary measures are highly individualized to suit each patient’s needs. For oliguric patients: recovery from kidney injury begins with a period of diuresis where large amounts of fluid (up to 3 liter daily) are excreted. Drug Treatment Medications prescribed would depend on the cause of illness and the complications that develop immunosuppressants for inflammatory conditions. Diuretics: edema Patients with hyperkalemia: potassium-exchange resins are given, they bind K in the GIT and reduce its absorption. Rapid correction of hyperkalemia requires the use of insulin, which drives extracellular K into cells; glucose is co administered to prevent hypoglycemia for reduction of serum phosphorus levels: phosphate binders are provided with meals to prevent phosphorus absorption Presence of acidosis: bicarbonate administered orally or intravenously. Nutrition Therapy Amo Nutrient unit Protein 0.8-1 g/KIBW increasing as GFR returns to normal: 60% should be HBV proteins 10-40 Kcal/kg BW Energy 30-50 mEq/day in oliguric phase(depending on urinary output, edema, dialysis and serum K Potassium level) replace losses in diuretic phase Sodium 20-40mEq/day in oliguric phase depending on urinary output, edema, dialysis and serum Na levels) replace losses in diuretic phase Fluid Replace output from the previous day(vomiting, diarrhea, urine) plus 500 ml Phosphorus Limit as necessary Chronic Kidney Disease Characterized by gradual, irreversible deterioration of the kidneys; since the kidneys have a large functional reserve(kidneys’ ability to function despite loss of nephrons), the disease progresses over many years without causing symptoms. Etiology Primary glomerular disease Autoimmune disease Metabolic disease Chronic exposure to toxic substances/drugs damaging to kidneys Infections Renal vascular disease Renal tubular disease Chronic kidney infections(pyelonephritis) Hydronephrosis Characterized by extensive scarring of renal tissue Nutritional Goals Minimize uremia Minimize the severity of symptoms Prevent worsening of complications Control blood pressure and water retention Delay necessity of dialysis Retard the progression of renal failure  Dietary Management Protein controlled depending on creatinine clearance, GFR and dialysis needs. Energy should be sufficient to prevent catabolism. Control of the following: Potassium- depends on laboratory results, use of drugs, vomiting and dialysis exchanges Sodium- depends on blood pressure and hydration status Fluid-depends on blood pressure, hydration status and output Phosphorus- depends on lab values of P and Ca or high fiber Low K to control K level. Supplementation of the following: Zinc to improve taste Fe to compensate for losses and for erythropoietin therapy Vitamin B complex since this is deficient in low-protein diets Calcium supplements because Ca bind P and to prevent osteodystrophy. Stage of Description GFR (mL/min Disease pe1.73 m2 1 Kidney damage with >90 Evaluation of CKD normal or increased GFR 2 Kidney damage with 60-89 mildly decreased GFR 3 Moderately decreased 30-59 GFR 4 Severely decreased GFR 15-29 5 Kidney failure < 15 (undergoing dialysis) To calculate GFR GFR (M)= weight (kg) x 140-age 72 X serum creatinine (mg/dL) GFR(F)=weight (kg) x 140-age x 0.85 72 x serum creatinine (mg/dL)  Treatment of CKD Aim : to slow disease progression to prevent or alleviate symptoms 1. Drug therapy: Antihypertensive drugs- to slow disease progression and reduce CVD risks Ace inhibitors can reduce proteinuria to help prevent additional kidney damage. Injection or IV administration of erythropoietin (epoetin) to treat anemia Phosphate binders (taken with food) to reduce serum P levels Sodium bicarbonate to reverse acidosis Cholesterol-lowering medications Supplementation with. Active Vit D( calcitriol) to raise serum calcium and reduce parathyroid hormone levels. 2. Dialysis 3.Nutrition Therapy  Glomerular Diseases The glomerulus is responsible for the production of an ultrafiltrate and responsible in preventing certain substances from entering the ultrafiltrate. Nephrotic Syndrome Glomerulonephritis Nephrosclerosis Pyelonephritis Nephrolitiasis ARF Chronic Renal Insufficiency Dialysis Kidney Transplant Nephrotic Syndrome Cluster of symptoms characterized by increased glomerular permeability, marked proteinuria, oliguria, hyperlipidemia and low metabolic rate. Nephrosis Syndrome causes by significant urinary protein losses that result from severe glomerular damage. The condition results due to the damage to the glomeruli increases their permeability to plasma proteins, allowing proteins to escape into the urine. The loss of plasma protein (3.5 g/day) results in serious consequences such as edema, blood lipid abnormalities, blood coagulation in disorders and infections NS can progressive to renal failure Causes of NS Glomerular disorders, diabetic nephropathy, immunological and hereditary diseases, infection or illicit drugs and cancers. Consequences of NS The liver attempts to compensate for the losses by increasing the synthesis of various plasma proteins with some being produced in excessive amounts. This results in a number of complications. Edema: the hypoalbuminemia characteristic of NS results in a fluid shift from blood plasma to the interstitial spaces, leading to edema. To impaired sodium excretion contributes to edema. Blood Lipid and Blood Clotting Abnormalities: people with NS frequently have elevated levels of LDL, VLDL, the atherogenic LDL variant, lipoproteins. Other effects: protein lost in the urine include immunoglobulins (Antibodies) and vitamin D- binding protein. Immunoglobulin depletion increases susceptibility to infection. Loss of Vita D- binding protein results in lower vitamin D and calcium levels, increasing the risk of rickets in children. PEM and muscle wasting develop due to continued proteinuria. Treatment of Medical: Drug prescribed: diuretics, ACE Nephrotic inhibitors(reduced protein loses), lipid- lowering drugs, anti-inflammatory drugs( usually corticosteroids such as prednisone) Syndrome and immunosuppressant (cyecloporine) Nutrition Goal 01 02 03 04 Replace Prevent Control Prevent losses cataboli water progress sm/ retentio ion of malnutri n, blood renal tion pressure disease. Dietary Management Kcal, sufficient to meet the TER and DBW; prevent hyperlipidemia and hypertension Protein should be 0.8-1.0 g/KDBW + losses. Half of the protein should come from high quality sources such as milk products, meat, fish, poultry, eggs and soy products. Energy:35 kilocalories /KDBW daily will sustain weight and spare protein. Dditional energy is needed if there is weight loss or infection. Sodium and fluid controlled- depending on the output; to control edema and hypertension and hyperlipidemia Lipids low because of proteinuria Monitor vitamin and mineral nutriture because of losses of binding proteins. Seatwork Compute the stage of the following patient 1. Male 60 y/o, 47kg with serum creatinine 1.4 mg/dL 2. Male 40 y/o, 60kg with serum creatinine 1.1 mg/dL 3. Female, 63 y/o 50 kg with serum creatinine 1.3mg/dL 4. Female, 70 y/o 45 kg with serum creatinine 0.9 mg/dL