malnutrition and role of nutrition in bmd:ckdthe objectives for the management of metabolic bone...

$: Malnutrition and Role of Nutrition in BMD:CKDThe objectives for the management of metabolic bone disease in patients with CKD are to maintain the blood levels of calcium a\൮d phosphorus$
Fayza KhanMSC (Foods and Nutrition) R.D

President ,PNDS

Malnutrition and Role of Nutrition in BMD:CKD

PNDS Continuing Nutrition Education Seminar Saturday, 30th November 2013

Outline

Objective Malnutrition in CKD population Bone Mineral Disorder in CKD Goals of Nutrition Therapy CKD-BMD Nutritional Management guidelines (Cal , phos, Vit

D, PTH) Dietary Management of PEM and BMD-CKD

Pakistan Nutrition & Dietetic Society- CNE 2013

Objective To recognize the importance of early nutrition intervention

in the management of Malnutrition and Bone Mineral Disorder.


Inflammation Uremic Toxins

Poor Dietary Intake &

Increased Metabolic Stress

Decreased Protein Synthesis

DECLINE IN NUTRITIONAL STATUS

Malnutrition

Presenter

Presentation Notes

Inflammation, uremic toxins can contribute to poor dietary intake and Increased in metabolic stress. Collectively this leads to a reduction in body protein synthesis, hence a decline in nutritional status, termed as MALNUTRITION Recent evidence indicates weight loss and reduction in appetite are key precipitating factors for malnutrition and independent predictors of poor outcome in CKD ‘

Malnutrition in CKD National Institute of Clinical Excellence defines malnutrition as

BMI scores of 18.5 or less. Muscle wasting and/or loss of subcutaneous fat on exam

Unintentional weight loss of 10% or more in previous 3-6 months.

BMI < 20 and unintentional weight loss >5% in 3-6 months

(National Collaborating Centre for Acute Care 2006)


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Presentation Notes

The above simple audit measures have been linked to increased mortality and other adverse outcomes.

Prevalence of Malnutrition

42-77% Malnutrition (mean s.alb 2.39 g/dl) is prevalent in ESRD population of developing countries

With Malnutrition mortality increases by 18–70%

Advances in Renal Replacement therapy ,Vol. 10,No.3 (July),2003:pp213-221)

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Presentation Notes

’Malnutrition in Chronic kidney disease (CKD) is common but is often undiagnosed or lately diagnosed.

Goals of Nutrition Therapy Maintain optimal Nutritional Status:

Prevent or correct nutritional deficits

To slow progression: Control hypertension by reducing sodium intake Reduce protein intake IF EXCESSIVE Manage DM

Treat Complications:Malnutrition, Metabolic Acidosis, Hypercalcemia ,Mineral Imbalance and Bone Disorder, Anemia ,CVD & dyslipidemias


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Presentation Notes

Plays a central role in the management of individuals with renal disease. It is believed that high mortality seen in CKD is a result of several abnormalities conspiring to induce or aggravate a heightened degree of cardiovascular morbidity and predisposition to wasting syndrome. In CKD ,several dietary elements require consideration. These should be individualized to the particular needs of the patient, bearing in mind their clinical condition, blood biochemistry ,etiology of disease and treatment.

Screening for malnutrition

CKD Stage 1-4

Actual Body Weight (< 85% of IBW)

Reduction in body weight (of 5% or more in 3 months or 10% or more in 6 months)

BMI (kg/m2) < 20 Subjective Global Assessment

(SGA)


Dialysis

Serum Albumin & Dry Wt (Monthly)

SGA (3-6 months) In case of consistent decrease of

0.3g/dl S.alb over 2-3 months then

Dietary interviews , anthropometry, Dual energy X-ray absorptiometry and C-reactive Protein

The Renal Association ,Clinical Practice Guidelines Reviewed in 2013

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Presentation Notes

Evaluation of nutritional status is fundamental to identify malnutrition. A clinically useful assessment should identify malnutrition, the related risk and evaluate the response from nutrition intervention. There have been a no. of assessment tools available to evaluate nutritional status in CKD population including Must screening , SGA, Patient MUST Screening Tool SGA (Subjective Global Assessment) PG-SGA (Patient Generated Subjective Global Assessment) NIS (Nutrition Impact Symptom) modified for CKD All patients with stage 4-5 CKD should have the following parameters measured as a minimum in order to identify under nutrition .

Nutritional Status Evaluation and Management

Moderate UndernutritionSpontaneous intakes≤ 30 kcal/kg/day≤ 1.1 g protein /kg/day

Severe UndernutritionBMI < 20Body wt loss > 10% within 6 moAlbumin < 35 g/l

Spontaneous intakes > 20kcal/kg/d

Spontaneous intakes < 20kcal/kg/d orStress conditions

Enteral Nutritionif EN is not possible:Central venous PN

Dietary counseling Oral

supplements

Lack of compliance

IDPN

N O I M P R O V E M E N T

ESPEN Guidelines

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Presentation Notes

Nutrition strategies involve two aspects at their initiation The decision :Assessment of patients nutritional status as determined by diet history , lab values,SGA, Anthropometric and the most important clinical judgment is important in the decision making . The patients ability to meet his nutritional requirements by eating, those with GI disorders and critically ill may require artificial nutritional support. The time to initiate nutritional support should be determined by the patient's nutritional status and magnitude of his catabolism. The more severe the degree of malnutrition and the more pronounced the magnitude of catabolism, the earlier nutrition support should be initiated. To diminish protein and energy depletion Appropriate amount of dietary energy and protein intake Continuous dietary counseling by RD. For CKD stage (1-5) 1-3 months and dialysis patients every month. More frequently if there is inadequate food intake or presence of an illness that can worsen nutritional status Nutritional support in patients who are unable to meet their dietary needs Oral supplements Tube Feedings IDPN OR PN

Chronic Kidney Disease Mineral and Bone disorder (CKD-BMD)

CKD

Abnormal levels and bioactivity of: Calcium, Phosphorus, PTH, 25(OH)D,

1,25(OH)2 D

Bone Abnormalities Vascular and Valvular Disease (Calcification)

Fractures , pain , decrease in mobility strength or growth

Cardiovascular Disease Events

Disability ,Low Quality of Life,Hospitalizations & Death

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Presentation Notes

Due to abnomal levels and bioactivity of calcium ,phos , PTH and vit D. either bone abnormalities (Disturbances in bone modeling and remodeling) are seen like fractures, pain , decrease in mobility and strength or Extra skeletal calcification in soft tissues and arteries may occur leading toward poor quality of life and disabilities.

Phos and Calcium metabolism in CKD As GFR falls due to fall in the activity of Vit D (conversion

impaired , Vit D dependent Calcium absorption from intestine is impaired ) Blood concentration of calcium falls.

Phos excretion decreased due to decrease tubular function stimulate fibroblast growth factor and Vit D become limited(D2 conversion is limited , skin conversion is limited, protein malnutrition promote Vit D deficiency.

Continued..

Reduced Vit D activity stimulate increased PTH secretions to release calcium from bones ,Phos also releases and cause hyperphosphatemia .Hyperphosphatemia also cause to increase PTH. Active Vit D is given to suppress PTH production.

As a result of these metabolic changes progressive and persistent increase in PTH occur.

Extreme high levels of PTH has been associated with worsened survival of patients with ESRD.

Renal Bone Disease Osteodystrophy

Depending upon the type of renal bone disease, Cal, Phos, PTH may be normal ,decreased or elevated.

Osteomalacia OR Bone Demineralization

Mixed Bone Disease Have features of both

Osteitis Fibrosa CysticaHigh Bone turn over DiseaseHyperparathyroidism (HPTH)

Adynamic Bone DiseaseLow Bone Turn Over due to over suppression of PTH

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Presentation Notes

As kidney function decline, complex interactions occur that affect calcium, Phos , Parathyroid gland. Hyperparathyroidism may be seen, resulting in Bone and mineral disorders Secondary HPTH is the major form of renal bone disease characteretised by high bone turnover and elevated levels of PTH

CKD-BMD Management

Given the risk of BMD associated with hyperparathyroidism attempts to normalize levels of ca , P, and regulate the levels of PTH have been central to the management of CKD.

CKD Stage 3

CKD Stage 4

CKD Stage 5(on dialysis)

P (mg/dL) 2.7 - 4.6 2.7 - 4.6 3.5 - 5.5*

Ca (mg/dL) “Normal” “Normal”8.4 - 9.5;

Hypercalcemia = >10.2

Intact PTH (pg/mL) 35 - 70 70 - 110 150 - 300*


Presenter

Presentation Notes

The objectives for the management of metabolic bone disease in patients with CKD are to maintain the blood levels of calcium and phosphorus as close to normal as possible and to undertake measures to prevent the development or to begin the treatment of established hyperparathyroidism and to prevent the development of parathyroid hyperplasia. to prevent extraskeletal calcifications and to avoid oversuppression of bone turnover to the extent that adynamic bone might be induced. It also is necessary to avoid the accumulation of substances that may be toxic to bone, such as aluminum

Intervention for bone disease in CKD

Phosphorus restriction Adequate , not excessive protein Phosphorus binding medications Usually calcium based salts Vitamin D and analogs

Early intervention may help prevent vascular calcification and secondary hyperparathyroidism


Calcium

Control of calcium levels helps control PTH

Average dietary intake 500-800 mg /day

Total elemental Calcium provided by Calcium based phosphate binders is 1500mg/day.

Total intake of elemental calcium including dietary calcium should keep between 1500-2000mg/day.

continued..


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Presentation Notes

Total body contains 1300 mg of calcium, 0.6% in soft tissues,90% in skeleton,0.1% extracellular fluid Protein bound 40%, free ( Ionized calcium)48% , calcium with phosphate,citrate,bicarb 12%

•Hypercalcemia is one of frequent complication by the use of Ca containing binder and use of active Vit D sterol.

•Calcium acetate-Calcium carbonate•Calcium citrate----------increase aluminum absorption

•Hypercalcemia occurs specially in those with low bone turnover disease.

•Hypocalcaemia cause development of hyperparathyroidism and increase risk of mortality. Active Vit D and analogs are effective in lowering PTH and increase calcium

•Calcimemertics or calcium imitating drugs are useful in suppressing PTH but close monitoring is essential (Slatopolsky et al,2000)


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Presentation Notes

Calcium-based phosphate-binding medications can increase total daily intake and elevate calcium. Calcium acetate and calcium carbonate Calcium citrate is not recommended in CKD patients because it may increase aluminum absorption. Other binders, used more often in RRT are typically composed of resins (sevelamer carbonate) and earth metals (lantha-num carbonate).

Phosphorus Serum phosphorus levels may be “normal” until CKD is advanced

Dietary Phosphorous levels should be restricted to 800-1000mg/day when serum levels go beyond 4.6mg/dl

Phosphorus restriction in early RF may help in the prevention of high PTH levels and development of renal bone disease

Dose and timings of phosphate binders should be individually adjusted to the phosphate content of meals and snacks to achieve desired levels.

GI upset is one of the side effect with most binders therefore interfere compliance (Toma sello et al,2004)

Continued…..


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Presentation Notes

17 mg /kg bw / day dietary phos intake is recommended To combat severe constipation, high fiber foods, exercise contribute to patient’s compliance. Bulking agents, DOSS and Miralax are acceptable as they doesnot require extrafluid.

During counseling patients ,absolute amount of dietary P ,Its type , source and ratio to dietary protein should also be considered.

A Mixed combination of dietary animal and plant food rich in phytic acid should be encouraged.

Dietary phosphate control should not compromise protein intake. Dietary education improves phosphate control.

Dietary protein restriction decreases phosphorus intake. If further restriction is needed, counsel patients to reduce intake of foods with added phosphorus


(Uribarri, 2007)

Presenter

Presentation Notes

Counsel patients to read ingredient lists for “phos” to identify foods with phosphate addi-tives, as these additives may be absorbed more efficiently than food sources.• Limiting whole grains may help if further reduction is needed.• Phosphorus binders may be prescribed to lower phosphorus levels. Counsel patients to take binders with meals to help limit absorption of phosphorus from food and beverages.

Calcium Phosphorus Product

If calcium phos product is greater than 70 , metastatic calcification is imminent. Clinical management aims to keep it below 55

(S. Cal mg/100 ml)* (S.Phos mg/100 ml)(9.0 mg / 100ml)* (6.5 mg/100ml ) = 58.5

Observational studies in dialysis patients have linked hyperphosphatemia ,cal phos. product and HPTH with higher cardiovascular mortality.


Phosphorus absorption varies by source

Organic Phos 40-60% Absorbed

Dairy products Meat ,fish, poultry Seeds and nuts Soy Dried beans and peas Whole grains(Pytate based P less

bioavailable)

Inorganic Phos >90% readily absorbed

Food additives Dietary supplements Calcium fortification


Inorganic P P is the main component of many preservatives and additive salts in processed foods

Not protein bound More easily disassociate and absorbed

in intestinal track

P burden from P containing food additives is disproportionately higher relative to organic P found in animal and plant foods sources of protein

Soft Drinks, convenience foods, fast food , colas, soft drinks

Clear colored soft drinks and teas are low in P

Quantity of P in a 50 gm portion of Cheese varies from <100 mg in Brie cheese to almost 500 mg in processed soft cheese.


Presenter

Presentation Notes

To extend shelf life,to improve color,enhance flavour and retain moisture.

Dietary P and Protein intake in CKD

Protein intake ----- P intake ----Hyperphosphatemia

A recent 3 yr epidemiological study of 30,075 prevalent MHD patient showed a decline in Pre dialysis serum P & Dietary P restriction ----

Protein intake----Protein Wasting and Poor Survival / Increased risk of death

Protein intake and a concurrent phos intake with serum P declined over time seems to be associated with lowest mortality in patients withCKD

Shinaberger CS, Green land S, Kopple Jd et al Am J Clin Nutr 88:1511,2008


P to Protein Ratio Food group Phos (mg) Protein

( gms)P to Protein Ratio (mg/gm)

Whole grainRefined

8533

Beans and Peas ½ C 119 7.6 15.8

Egg White 5 3.6 1.4

Egg Yolk 65 2.6 22.8

Lentils ½ C 178 8.9 20.0

Milk low fat 1 Cup 230 8.1 28.3

Red Meat (Ground Beef) 3 oz 165 21.9 7.5

Cheese Cheddar 1 oz 145 7.1 20.4

Chicken Drumstick 81 12.5 6.5

Chicken Liver 1 79 4.8 16.5

Sunflower Seeds 3 Tb Sp 370 6.2 59.7


Presenter

Presentation Notes

P to Protein Ratio which is recommended by k/doqi guidelines has saveral advantages. Independent of the size of food portion or serving It focuses simultaneous attention on both dietary P and Protein , which both are important in the nutritional treatment of patients with CKD The ratio is higher for foods, tat have usaully higher for the food that have unusually higher amount of p additives but similar amount of Protei It calls on attention to foods containing higher amount of P and no or little amount of protein It results in heightened awareness of food sources of excessive P are often low nutritive dietary value Only limitation of P content and P to protein ratio is that they donot provide information about the bioavailability or intestinal absorption of P in different foods.

PTH (Parathyroid hormone)PTH regulates serum calcium levels. Low levels of 1,25(OH)2D,

hypocalcemia, and hyperphosphatemia stimulate PTH secretion.

Secondary Hyperparathyroidism is associated with the most common cause of bone disease in CKD

• Normal PTH < 65 pg/mL Measured as iPTH PTH varies by level of kidney function and type of bone disease

Dietary phosphorus restriction and use of active vitamin D or its analogs may help control PTH levels in CKD. Calcium supplementation may help as well.


Presenter

Presentation Notes

Also called as Prothrmone.Metabolic actions include mobilizing calcium and phosphorus from bone, increasing intestinal absorption and renal tubular reabsorption of calcium, and decreasing renal tubular reabsorption of phosphorus. PTH enhances conversion of 25(OH)D to 1,25(OH)2D.

Vitamin D

The kidneys activate 25(OH)D (Calcidiol) to 1,25(OH)2D (Calcitriol or active vitamin D).

Reduction of kidney function results in decreased production and conversion of calcidiol to calcitriol.

Vitamin D ≥ 20 ng/mL Measured as 25(OH)DMaintain within normal range (IOM, 2011).


Supplementation may be indicated. Specific requirements in CKD have yet to be determined.

Ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) may be used in early CKD to replete vitamin D

Active vitamin D(calcitriol) or its analogs (doxercalciferol, paricalcitol, or alfacalcidol) may be used as eGFR declines (ibid).

Monitor for hypercalcemia and hyperphosphatemia when using supplements.

Active vitamin D increases calcium and phosphorus absorption.



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Presentation Notes

As management of PEM is aimed to replenish protein and energy depletion and to provide sufficient calories and protein to maintain positive nitrogen balance and good nutritional status. Composition of diet I.e source of energy and protein needs to be considered.

1 Slice BREAD OR ½ C Cooked CEREALS OR RICE OR ½ Med CHAPATI = 60-80 kcals

I Tbsp Fat = 100-120 Kcals


Sources of Energy (CHO & Fats)RB

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Presentation Notes

Encourage intake of Carbs and fats=== main sources of energy.

2 Oz of Cooked Lean MEAT,CHICKEN,FISH, ½ CUP LENTILS or 1 EGG = 7-8 gms Protein


Sources of Protein

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Presentation Notes

Protein sources ……contains phos as well

1 Cup YOUGURT OR MILK = 300-350 mg Calcium 1 Slice Cheese = mg Calcium

Sources of Calcium

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Presentation Notes

Milk and milk products contibutes only 50% of the dietary calcium intake if taken as recommended


Nutrients Breakfast Lunch Dinner Snack 2Energy (Kcal) 430 612 430 330Protein (gms) 12 34 38 3Calcium (mg) 87 154 313 8Phos (mg) 150 320 320 10

Sample meals with nutrient content

Kcal 475+200Protein 22+8Cal 170+200Phos 166+200

Kcal 330Protein 3 Cal 8Phos 10

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Presentation Notes

Sample breakfast, lunch and snack options with caloric , protein calcium , phos content of the meals for ckd patients

Food Exchanges with Nutrients Food groups Energy

(kcals)Protein(Gms)

Calcium(mg)

Phos (mg)

Chicken or fish or lentils 100gms cooked

220 32 25.5 306

Vegetables 2 Servings 50 4 36 74

Fruit 2 Servings 120 2 9 8.7

Chapatti / cereals / bread 8-10 Servings

640 18 216 188

Oil 6 Tb Sp 600 - - -

Milk or its product 1 cup 150 8 291 227

Approx. Total 1780 64 577 803


ADA-CKD Evidence based clinical practice guidelines

Nutrition therapy provided by a RD is recommended for individuals with CKD.

Should be initiated at the diagnosis of CKD

Studies regarding effectiveness of diet therapy report significant improvements in anthropometric and biochemical measures sustained for at-least one year.

ConclusionMalnutrition Morbidity Mortality

Focus on

Nutritional assessment

Monitoring & Follow up Periodic assessment

Co-ordination between Physician & Dietitian

Identification of risk factors

Anticipatory guidance

Assure compliance

Economical

Easy to use

Combination of anthropometric biochemical & dietary

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Presentation Notes

malnutrition and role of nutrition in bmd:ckdthe objectives for the management of metabolic bone...

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