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REVIEW ARTICLE


Diet in Nephrotic Syndrome

Sanjeev Gulati

Director, Deptt of Nephrology,

Fortis Institute of Renal Sciences and Transplantation Hospitals, Vasant Kunj, New Delhi



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ephrotic syndrome is constellation of heavy proteinuria associated with hypoalbuminaemia, oedema and hyperlipidaemia.1 In adults the nephrotic range proteinuria is defined as urinary protein level of, more than 3.5 g per 1.73m2 of body-surface area per day.While in children it is defined as proteinuria more than 40 mg/m2/h. However as sometimes 24 hour urine collection may be difficult a urine protein/creatinine value of more than 2-3 mg/mg indicates nephrotic range proteinuria and correlates with results from 24-hour urine collection. This amount of proteinuria, irrespective of its origin, is usually associated with sodium retention, low albumin, oedema, hyperlipidaemia, and associated complications. Although overall diabetic nephropathy is the most common cause of nephrotic range proteinuria, several primary glomerular diseases are also responsible for the great majority of cases of the nephrotic

syndrome.

It is essential to emphasize the pathophysiology underlying the nephrotic syndrome to understand the key role diet plays in the management of nephrotic syndrome. A well-planned diet can replace lost protein and ensure efficient utilization of ingested proteins through provision of adequate calories. Dietary changes can also help control hypertension, edema, and hyperlipidemia, and slow the progression of renal disease.

Classically oedema is explained by two hypothesis, the "underfill" and the "overfill" theory..2 Generalized edema implies that there is increased total sodium content of the body.Primarily edema can be ameliorated only if a negative sodium balance is achieved. 3 During the initial phase of


mmol per day.4 however dietary sodium intake cannot be reduced to these levels. Additional use of diuretics along with a reduced sodium intake can facilitate a negative sodium. Because of the avidity of the kidney for sodium in patients with the nephrotic syndrome, potent loop diuretics, such as furosemide, are required. This can reasonably achieve 50 mmol of urinary sodium (approximately 3 g of sodium chloride) excretion per day. Distal nephron, where sodium reabsorption is increased in patients with the nephrotic syndrome may reduce the net sodium excretion. This can be reduced by combining loop diuretics with thiazides 5 and potassium-sparing diuretics.

The majority of children with nephrotic syndrome have a steroid sensitive condition that is associated with minimal histological changes in the glomeruli (MCNS). The initial management involves the control of oedema and prevention of infection while awaiting the response to corticosteroids. This can be achieved with fluid and salt restriction and combination of diuretics as discussed earlier.

A dietician, preferably a renal dietician should be involved in the initial management both to review the dietary history as well as advising on the practical issues dietary management. Some practical tips in he management of these patients are as follows


I. Fluid Restriction

Any food that is liquid at room temperature counts as a fluid (Table 1).


Table 1 :Foods included as Fluids

edema formation, sodium excretion may be as low as 10

Address for correspondence:

Sector B, Pocket 1,Aruna Asaf Ali Marg New Delhi - 110070

Ph: 91-11-42776222 Ext. 5015, 5006

Fax: 91-11-42776221 Mobile:9871600885

Milk, water, juice, soda, and other beverages

Email: sgulati2002@gmail.com

Managing Fluid Restriction: Management of fluid is important to keep edema and hypertension under control. Strategies for restricting fluid intake are given in Table 2.


Table 2 :Strategies For Restricting Fluid Intake


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Try using small glasses. Small amounts of fluid in a big glass looks less than same amount in a smaller glass.

Identify the amount of fluid the glass or cup holds, so that fluid need not be measured every time.

Keep track of how much fluid is drunk each day; keep record amounts at any convenient place.

Avoid salty foods, as they increase thirst. Iced tea or lemonade quenches thirst better.

The following recommendations may help to decrease salt in diet:

Do not use salt in cooking or at the table. Cook with herbs and spices

Use salt substitutes- LoNa or TATAt Lite (however these are high in potassium).

Eating home-prepared meals, using fresh ingredients, instead of canned, frozen, or packaged meals. When eating out, request to hold the salt in food preparation.

Low-sodium seasonings which do not require restriction are given in Table 4


Table 4 :Seasonings Which Do Not Require Restriction

Frozen pieces of fruit (i.e., melon, berries, and grapes)

can help quench thirst.

Chewing gum can help to quench thirst.

Rinsing the mouth with cold water, without swallowing.

Sucking on a lemon wedge.

Staying out of the sun can help from beoming thirsty on a hot day.


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  1. Sodium Restriction in Diet

    A low-sodium diet or salt restriction helps prevent or reduce fluid retention in the body. With most sodium-restricted diets, high-sodium foods are limited and salt is not allowed in food preparation or at the table. The following foods are high in sodium and should be avoided if your child has been prescribed a low-sodium diet: Table 3.


    Table 3 :Foods -To Be Avoided And Foods Permitted

    . All spices . paprika

    . garlic (fresh) . lemon juice

    . onion (fresh) . pepper basil . cinnamon

    . ginger cloves

    . oregano . dry mustard

    . chilli powder . nutmeg

    vinegar


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    The salt and fluid restriction is usually required only until the patient achieves a remission. Thereafter the fluid intake can be liberalised and salt intake should be restricted only if there is concomitant hypertension.

    If the child does respond to prednisolone with infrequent relapses, then there are few long term dietary problems. 6 However, children who frequently relapse and are steroid

    dependent and adults requiring long term treatment will

    Foods to be Avoided

    Canned foods (vegetables, meats, meals)

    Processed foods (meats such as salami, hot dogs, sausage)

    Cheese Pasta mixes

    Soups (canned and dried)

    Snack foods (chips, popcorn, salted nuts etc.), dips, sauces, and salad dressings


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    Foods Permitted (low in sodium)

    Plain breads, cereals, rice, and pasta Vegetables and fruits take)

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    Foods which can be used in limited amounts (high in sodium)

    All sauces (Limit to I tablespoon per meal)

    low-calorie salad dressing (Limit to I tablespoon per meal)

    require long term dietary advice to maintain nutritional status and prevent obesity. Especially in children, growth and endocrine function become important issues in the long term management. 7 Initial assessment should include growth parameters that should always be recorded. Dry weight should be estimated, since this is also needed to calculate the prednisolone dosage.

    The basic advice is a'healthy eating' diet for all the family. It should provide adequate energy based on the estimated average requirement for children of the same chronological age.8


  2. Calorie Intake:

    Energy requirement should meet at least Recommended Daily Allowance (RDA) for normal children of same height age. Calorie intake in the diet should be enough to enhance the efficiency of protein (protein sparing effect) and prevent the patient from lapsing into a catabolic state. When use of chronological age does not account for the growth, height

    age should be the basis for energy estimation (Table 5)

    Tabel 5 :Energy and Protein Requirements According To Age

    Malnutrition is the most potent predictor of death in end-stage renal failure. Therefore, for fear of the risks of

    low-protein diets in the nephrotic syndrome, recommend


    Infants

    Age (Years)

    0 - 0.5

    KCals/Kg/d)

    108

    Protein(g/Kg/d)

    2.9-3.0

    0.5-1.0

    98

    2.3-2.4

    Children

    1-3

    102

    1.9-2.0

    4-6

    90

    1.9-2.0

    7-10

    70

    1.7-1.8

    Males

    11-14

    55

    1.7-1.8

    15-18

    44

    1.4-1.5*

    18-21

    40*

    1.3*

    Females

    11-14

    47

    1.7-1.8

    15-18

    40

    1.4-1.5*

    18-21

    38*

    1.3*


    Infants

    Age (Years)

    0 - 0.5

    KCals/Kg/d)

    108

    Protein(g/Kg/d)

    2.9-3.0

    0.5-1.0

    98

    2.3-2.4

    Children

    1-3

    102

    1.9-2.0

    4-6

    90

    1.9-2.0

    7-10

    70

    1.7-1.8

    Males

    11-14

    55

    1.7-1.8

    15-18

    44

    1.4-1.5*

    18-21

    40*

    1.3*

    Females

    11-14

    47

    1.7-1.8

    15-18

    40

    1.4-1.5*

    18-21

    38*

    1.3*

    normal protein intake.

    The diet should have 1.1-1.2 g/kg/day protein plus gram­ for-gram replacement of urinary protein losses with 60- 70% protein from high biological value origin (so that the child can have all EAA (Essential Amino Acid in adequate amount). However this is much higher in growing children. Protein is required to maintain positive nitrogen balance for growth and maintain body protein turn over. Follow up dietetic review in the clinic at regular intervals will help reinforce previous advice and help ensure that the diet is practical and not unnecessarily restrictive.

    5. Dietary Fats

    Patients with nephrotic syndrome (NS) have one of the most pronounced secondary changes in lipoprotein metabolism

    *Based on RDA and increased energy level.


  3. Protein Intake

It is difficult to define the appropriate level of protein restriction in patients with nephrotic range proteinuria. In the past, high protein intakes and even amino acid supplements were recommended. Diets contammg increased intakes of protein (3-4 g/kg/body weight/day) were prescribed in the belief that they would help to restore serum protein pools. IO More recently, however, it was shown that high protein intake may fail to increase serum albumin levels.11,12 It may even increase the rate of protein catabolism and urinary excretion of protein (12). The latter, apparently paradoxical, finding can presumably be explained by the known increase in the glomerular filtration rate caused by dietary protein. 13 Animal studies, however, have shown that although dietary protein augmentation increased albumin synthesis it had no significant effect upon serum albumin concentrations or muscle protein as all of the additional ingested protein was catabolised to urea and excreted in the urine rather than used to promote growth. 12 Alternatively there have been concerns that high protein diets may accelerate the progression of human and experimental glomerulonephritis14 and therefore the use of low protein diets have also been recommended. However, isocaloric low- protein diets containing 0.6 to 0.8 g of protein per kilogram of body weight per day have not been shown consistently to reduce proteinuria, Although these diets have been shown to decrease proteinuria, there is the possible risk of malnutrition as suggested by animal studies. 15 Such diets are also impractical to follow.

Nevertheless, a remarkable benefit with respect to urinary protein excretion and serum lipid changes has been observed with a low-fat soy-protein diet providing 0.7 g of protein per kilogram per day.16 Protein restricted diets, especially in children may cause malnutrition and hence are no longer recommended.( Table 5).

known, and the magnitude of the changes correlates with the severity of the disease. These changes are of a quantitative as well as a qualitative nature. All apolipoprotein B (apo B)-containing lipoproteins, such as very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and lipoprotein(a) [Lp(a)], are elevated in nephrotic syndrome. High-density lipoproteins (HDL) are reported to be unchanged or reduced. In addition to these quantitative changes, the lipoprotein composition is markedly changed, with a higher ratio of cholesterol to triglycerides in the apo B-containing lipoproteins and an increase in the proportion of cholesterol, cholesterol ester, and phospholipids compared with proteins. Also apolipoproteins show major changes, with an increase in apolipoprotein A-I, A-IV, B, C, and E.

The management of hyperlipidaemia is controversial and could be of some importance if the nephrotic state is prolonged and the patient sis steroid resistant. 17 The manipulation of dietary fat intake has a limited effect in reducing serum lipids and current interest is focused on the use of lipid lowering agents such as simvastatin. 1 8 In view of the effect of dyslipidemia on cardiovascular risk and possibly on the progression of renal disease,19 treatment seems sensible, although evidence from controlled studies is not available. There is some role for nonpharmacologic intervention. A soy-protein diet caused a significant decrease in cholesterol, LDL, and apolipoprotein B, whereas serum triglyceride levels did not change.16 Treatment with fish oil decreased triglycerides and VLDL but increased LDL cholesterol.20 A meta-analysis showed that dietary therapy reduced cholesterol levels, but the pooled effect of diet on LDL did not reach statistical significance.21 The use of monounsaturated or polyunsaturated margarines and oils are also advocated as part of the general healthy eating advice with a reduction of a saturated fat intake. Attempts at dietary manipulation of lipids in the diet may be more relevant in the children with prolonged nephrotic states.

6. Supplements:

Patients with nephrotic syndrome are often low in B vitamins and zinc, and can benefit from supplements. In addition, since a significant portion of serum calcium is protein­ bound, it tends to be low when serum proteins are reduced. We have demonstrated that children with low calcium and Vitamin D intake may be at risk of low bone mass (22). Hence it is recommended that these children should be supplemented with calcium and Vitamin D as long as they are on steroid therapy. No modification is routinely needed for potassium, but potassium losses due to diuretics may require supplementation.

A leaflet/booklet on healthy eating should be available to the family.


Weight control:

Prednisolone treatment undoubtedly stimulates the child's appetite and dietary advice about the prevention of excessive weight gain is important. Many children and their parents become upset with changes in body image, and this is particularly true with adolescents. In between meal snacks, such as biscuits, chips, fries and soft drinks should be avoided with low energy alternatives promoted.

Healthy eating advice should again be repeatedly reinforced.

progressive renal failure, and eventual death.25 If such patients are to survive they require intensive dietetic support because of the anorexia that is complicated by fluid restriction. A protein intake of 2-4 kglbody weight/day with maximum energy intake within the fluid allowance may be indicated. Nutritional supplements will be essential to achieve nutritional requirements and administration by the nasogastric or preferably gastrostomy route will be indicated should the child fail to meet their nutritional requirements orally.2 6 The losses of protein can be reduced by unilaterial or bilateral nephrectomy combined with early dialysis and transplantation.


Summary

The aim of nutritional management of Nephrotic syndrome is:

Replace the protein loss by having an adequate intake of proteins.

Sodium intake in diet should be restricted to minimise edema and hypertension ..

Fat intake should be low.

Fluid intake should be restricted.


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References:

1.

Food Allergy:

As the aetiology of MCNS is unknown, there are some parents who become concerned that dietary factors may 2. be responsible especially as MCNS is commoner in atopic families. There are reports suggesting food hypersensitivity, 3. particularly to milk and dairy products, may be aetiological

factors in the glomerular damage in both young and adult 4.

patients. If a trial of a few foods diet is contemplated it

should be under close dietetic supervision.

One should be aware that some families may seek advice 5.

from alternative medicine sources, especially if they have

concerns about the use of corticosteroids.

Steroid resistant nephrotic syndrome: This group of 6.

patients is usually very heterogenous with an underlying

renal pathology that does not respond to at least four weeks 7.

of daily prednisolone treatment. Prolonged initial steroid

dosage combined with oedema, 'anorexia', and catabolic state 8.

may require a period of nutritional support either with oral

or nasogastric tube fed supplements(23).

Watson AR. Nephrotic syndrome. In: Campbell AGM, McIntosh N, eds. Forfar and Arneils textbook of paediatrics. 4th Ed. Edinburgh: Churchill Livingstone, 1992: 1057-61.

Stephan R. Orth and Eberhard Ritz. The Nephrotic Syndrome. N Engl J Med 1998; 338: 1202-1211

Wilcox CS, Mitch WE, Kelly RA, et al. Response of the kidney to furosemide. I. Effects of salt intake and renal compensation. J Lab Clin Med 1983;102:450-8.

Vande Walle JG, Donckerwolcke RAMG, van Isselt JW, Derkx FHMJoles JA, Koomans HA. Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms. Lancet 1995;346:148-52.

Fliser D, Schroter M, Neubeck M, Ritz E. Coadministration of thiazides increases the efficacy ofloop diuretics even in patients with advanced renal failure. Kidney Int 1994;46:482-8.

Haycock GB. Renal disease. In: McLaren DS, Burman D, Belton NR, Williams AF, eds. Textbook of paediatric nutrition. 3rd Ed. Edinburgh: Churchill Livingstone, 1991: 238-40.

Rees L, Greene SA, Adlard P, et al. Growth and endocrine function in steroid sensitive nephrotic syndrome. Arch Dis Child 1988; 63: 484-90.

Committee on Medical Aspects of Food Policy, Department of Health. Dietary reference values for food energy and nutrients for the United Kingdom. London: HMSO, 1991.

Vitamin supplementation and iron treatment may also be indicated. 24 Many such adults and children are often hospitalised for long periods and the clinical course may be complicated by diarrhoea and other nosocomial infections from the ward. During these time their nutritional states require reassessment and diet needs to be appropriately modified.

Congenital nephrotic syndrome: This is a rare condition that in the past was associated with failure to thrive,

  1. Shapiro AC, BandiniLG and Kurtin PS. Estimating energy requirements for children with renal disease. A comparison of methods. Journal of the American Dietetic Association, 1992; 92 (5): 571-573.

  2. Blainey JD. High protein diets in the treatment of the nephrotic syndrome. Clin Sci 1954; 13: 567-81.

  3. Kaysen GA, Gambertoglio J, Jimenez I, Jones H, Hutchison FN. Effect of dietary protein intake on albumin homeostasis in nephrotic patients.Kidney Int 1986;29:572-7

  4. Al-Bander H, Kaysen GA. Ineffectiveness of dietary protein augmentation in the management of the nephrotic syndrome. Pediatr Nephrol 1991;5:482-6

  5. Don BR, Kaysen GA, Hutchison FN, Schambelan M. The effect of angiotensin-converting enzyme inhibition and dietary protein restriction in the treatment of proteinuria. Am J Kidney Dis 1991;17:10-7

  6. Brenner BM, Mayer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease. NEngl J Med 1982; 302: 652-9.

  7. Feehally J, Baker F, Walls J. Dietary manipulation in experimental nephritic syndrome. Nephron 1988; 50: 247-52.

  8. D'Amico G, Gentile MG, Manna G, et al. Effect of vegetarian soy diet on hyperlipidaemia in nephrotic syndrome. Lancet 1992;339:1131-4.

18. Grundy SM,Vega GL. Rationale and management of hyperlipidaemia of the nephrotic syndrome.Am J Med 1989; 87: 3-11.

19.. Rabelink AJ, Hene RJ, Erkelens DW. Effects of simvastatin and cholestyramine on lipoprotein profile in hyperlipidaemia of nephrotic syndrome.Lancet 1988; ii:1335-8.

  1. Wheeler DC. Lipids -what is the evidence for their role in progressive renal disease? Nephrol Dial Transplant 1995;10:14-6.

  2. Massy ZA, Ma JZ, Louis TA, Kasiske BL. Lipid-lowering therapy in patients with renal disease. Kidney Int 1995;48:188-98

  3. Gulati S, Godbole M, rk Sharma, Singh U, Gulati K, Srivastava A Are children with idiopathic nephrotic syndrome at risk for metabolic bone disease? Am J Kidney Dis. 2003 Jun;41(6):1163-

  4. Consensus statement on management of steroid sensitive nephrotic syndrome Indian Pediatrics - Indian Pediatrics 2001, 38 (9) : 975-86.

  1. Strauss J, Zillerueb G, Freundlich M, Abitol C. Less commonly recognised features of childhood nephrotic syndrome. In: Gruskin AB, ed. Pediatr Clin North Am 1987; 34: 591-607.

  2. Rapola J, Huttenen NP,Hallman N. Congenital and infantile nephrotic syndrome. In: Edelman CM, eds. Pediatric kidney disease. 2nd Ed. Boston: Little Brown, 1992: 1291 -305.

  3. Coleman JE, Watson AR. Gastrostomy buttons: the optimal route for nutritional support in children with chronic renal failure. J Renal Nutrition 1992; 2 (suppl 1): 21-6.