M.K. Mani

Diet In Renal Diseases

There are only a few renal dis­eases in which it is possible to influ­ence tile changes in the kidney bydietary means. These include manyof the inborn tubular disorders whichare rare. The main aspects of renaldiseases that are being consideredhere are the dietary management of(a) renal failure, and (b) renal stones.

DIET IN RENAL FAILURE

Carbohydrates and fats can begiven freely to the patient with renalfailure, but proteins should be prohib­ited, and minerals and water greatlyrestricted. Thiswas the basis of Bull'sInfamous regime, a nauseating con­coction of olive oil and glucose, whichwas administered orally or via an intra­gastric route, and, if it induced vomit­ing, the vomitus was strained andgiven again. More palatable versionsof this were devised in our country,with cream and sugar mixed and fro­zen to make a reasonably palatableice cream. Fortunately. the advent ofdialysis has made this diet obsolete.

In the 1960s, Giordano' andGiovanetti2 showed that restriction ofdietary protein improved the symp­toms of the patient with chronic renalfailure, lowered blood urea and madethe patient feel better. This thereforebecame standard practice, both forchronic and for acute renal failure.Incidentally, protein-rich foods are alsoabundant in minerals, and restrictionof their intake helps the patient inmore ways than one.

We continue to practise restric­tion of protein in the diet, allowing alimited amount of protein of high bio­logical value to provide essential aminoacids. The amount of protein shouldnot be reduced below 0.6 gm/kg/day,and this should be of high biologicalvalue. as otherwise the patient will beunable to maintain a satisfactory ni­trogen balance. This came to be knownas the Giordano-Giovanetti diet, andmany modifications of this are in useall over the world, and in India. Thehabitual diets of many healthy Indiansdo not provide even this amount ofprotein, and subsisting on this level ofprotein intake should pose no problem.

A modification of this diet was toreduce the protein intake even belowthis level and add essential aminoacids or their keto analogues3. Thehigh cost of these supplements pre­cludes their use in our country. It isessential that adequate energy beprovided so that endogenous proteinis protected, and 35 kcal/kg/day is theaccepted figure.

Progression of chronic renalfailure: While our original intention inreducing dietary protein was to pro­duce symptomatic improvement in ourpatients, it soon became obvious thatthe rate. of loss of residual renal func­tion was faster in patients who did notrestrict their protein intake than in.those who did. The restriction of pro­tein intake could protect the kidneysand keep them going for a much longertime. This has been amply proved inanimal studies, and over a short termin humans, but is still doubtful in thelong run in humans, which is whatmatters to us. It appears from thework of Rosman et a/4 that protectionwas only noted in patients who had faradvanced disease, and was not veryeffective in the earlier stages. Fur­ther, women were not as much benefittedas men, and only patients with chronicglomerulonephritis had significantchange in the rate of decline in renalfunction.

The mechanism of such protec­tion seems clear on animal studies.Amino acids release glucagon fromthe kidneys, and this releases a stillhypothetical substance known as glo­merulopressin from the liver. This in­creases renal blood flow and glomerularfiltration in remnant nephrons, andthis has been shown to promote focalglomerular sclerosis in the glomeruli,thus accelerating the decline in renalfunction. All amino acids, and there­fore all proteins, do not have this ef­fect. It seems safe to allow vegetableproteins in greater measure.

There is also evidence to sug­gest that high phosphorus intake isdetrimental to the kidneys, and meatand milk contain an abundance ofphosphorus in highly absorbable form.Further, meat is a very rich source of

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potassium, and the restriction on itsintake can be virtually life saving topatients with chronic renal failure.

Keto analogues of essential aminoacids, given with a very low proteindiet, have been used to slow progres­sion of renal failure, and are effectivein patients who are compliant6. How­ever, compliance is a serious problemand the cost of these keto-acids ishigh. These measures are successfulonly in moderate renal failure, and notwhen the disease is far advanced.

I remain sceptical about the abil­ity of protein restriction to reduce therate of decline of renal function inchronic renal failure, as so many ofour patients consume far less amountsof protein than the figures recommended,and yet the decline continues at moreor less the same rate as that de­scribed in more affluent societies. Thereis, however, the need to maintain somedegree of restriction, especially onanimal protein, because symptomsare less in patients on protein re­stricted diets, and also because thesediets have less phosphorus and acidradicals.

Lipids contribute to continuingglomerular injury? Macrophages in­gest lipoproteins and are stimulatedto produce growth factors which pro­mote collagen synthesis and prolif­eration of mesangial cells. Lipids serveas a substrate for the production ofeicosanoids, which are vasoactive andincrease proteinuria, with its harmfuleffects on the glomerulus, and alsoattract inflammatory cells. Loweringof lipid levels slows the deteriorationin renal function in glomerular dis­eases associated with the nephroticsyndrome. The use of fish oil shiftseicosanoid synthesis to less vasoac­tive and chemotac.tic metabolites, de­creases proteinuria, and reduces glo­merular scarring. The need to lowercholesterol levels in nephrotic patients,with or without renal failure, is thusestablished. However, hyperlipidaemiais very uncommon in chronic renalfailure in Indian patients.

Potassium: Hyperkalaemia canlead to sudden death in chronic renal

failure, and should be guarded against.The capacity of the kidney and of thecolon to excrete potassium increasesin chronic renal failure as there is

increased activity of the renin-angio­tensin-aldosterone system. When re­nin production is defective as in dia-

Calcium oxalate stones:Calcillillis one of the ingredients of the StOlil1It seems obvious that the more tlllIcalcium in the diet, the more will llllexcreted in the urine, and thereforll

the greater will be the tendency IIIstone formation. However, this is sin!

plistic reasoning. Intestinal absorption of calcium is tightly regulated,and depends to a great extent on thilcalcium content of the body. If tllilbody is replete with calcium, absorption is low, and correspondingly urinary excretion is low too. Some ston(formers have specific defects of tubular excretion or intestinal absorptiollof calCIUm. Calcium restriction in tholatter could lead to deficiency in thebody, and to secondary hyperparathyroidism. The only clear indication for dietary restriction of calciumwould be intestinal hypercalciuriaPatients consuming large amounts ofmilk or milk prOducts may be advisedto restrict themselves to a cup of milkand one of curds each day.

RENAL STONES

Again, the dietary mrlll:III'QlllJ1of the nephrotic syndrome III ,'1111,11'"

poses problems. A high plOlliltl Iincreases proteinuria, and 1l1:.Idlmore difficult to control the 110111111'1

state. However, one cannot lil~11 !proteins in a child, because Olin II

to provide enough for growlll 111111

nately, most cases of the Il('phllillsyndrome in children are due' III 11111Imal lesion nephropathy which will I !spond to steroids in a short tllllO, LIlli

do not require modification III iii 1For others, it has been suggeslotl IIIwe give 3 to 4 gm of protein/kq 11I1t!

weight/24 hours. My usual P' dell! .however, is to give a normal dl I, 'I"adjust only the salt intake as called 1111

einuria, and is therefore SI'II t1ttit:

ing in nephrotics. I would ""II',,allow the patient to contilllJ(' tIll Il~ .her normal protein intake 111'''1' 'I"

need to be regulated.

The most common renal ~tOlltl

are those containing calcium, usu:dlin the form of oxalates. Calcium plll)~phate stones are usually associ;1111(jwith renal tubular acidosis, and strtlVilstones with infection, so there is Ilotmuch role for dietary managelllnl!1Uric acid stones are to some exlllilldependent on the diet. I will therefolrJconsider dietary management of c,iIcium oxalate and uric acid stones.

• Avoid high potassium sources likecoconut water, dried fruits and nuts,and soft drinks. 'Only one fresh fruit

per day is advisable (in the case of alarge fruit like papaya, one slice), .Ifsalad is consumed, it is best to aVOidfruit on that day.

• No restriction on cooked vegetables,rice, wheat, oils, sugar, Suitable re­striction must be added for the rarepatient with hyperlipidaemia.

If the patient is oedematous, therewould be no salt in the food and noneshould be added at the table, and the

liquid intake should be restricted to300 ml. This is in addition to the milkwhich has been permitted as indi­cated earlier. It is importa.nt to place alimitation on all liquids and not only 01")

water as otherwise considerab.leamou~ts of water rri'ayenter the diet inthe form of gravies, the Indian dietbeing extremely sloppy in consistency.It should not be forgotten that me­tabolism of solids will add approxi­mately 1 litre of water to the bodydaily. Once the patient is free fromoedema, salt and liquid intake may begradually increased till the limits oftolerance are reached.

The patient with predominantinterstitial changes and also in a saltlosing state may, however, requiresalt supplements and large quantitiesof water.

Special problems in children:It is difficult to find the suitable diet forchildren with chronic renal failure, andthere is no unanimity of opinion onwhat should be done. Children areless likely to accept diet restrictions,and if they do not get what they want,they are likely to stop eating and getundernourished. All calculations re­garding the protein and calorie re­quirements mentioned for adults arecomplicated in children by the factthat we must make allowance for the

proteins needed for growth. It is fairlywell accepted now to give the childthe recommended dietary allowancefor his or her size and age. One couldgive 15 kilo calories per cm height,and 1.5 to 2 gm protein per 100 kcal.What I usually do is to let the childtake a normal diet except to avoiddangerous doses of potassium.

The nephrotic syndrome: Theold idea of forcing a high protein dieton nephrotic patients has now beenabandoned, A high protein intake leadsto hyperfiltration and increased prot-

betics, the risk of developing hyper­kalaemia is far greater.

The Indian diet and mode of cookingoffer advantages for the patient withchronic renal failure. The major sourceof potassium is meat, and even non­

vegetarians in India do not consumemeat in large quantities as In the West.Further, our common mode of cookingmeat and vegetables, chopping them

into pieces and boiling them in water,leaches out the potassium. My expert­ence has been that only a small minor­ity of Indian patients have dangerouslevels of serum potassium. These pa­tients-should be watched and appropri­ate precautions taken~ For the rest, itshould suffice to caution against takingtoo much potassium.

Acidosis: Severe acidosis 'cancause tachypnoea by stimulating the.respiratory centre. It also causes ve­nous contraction which increases ve­nous return to the heart, and reducescardiac contractility, and the two to­gether produce pulmonary oedema. Itis thus a life-threatening situation. Fur­thermore, some of the acid is bufferedwithin cells in exchange for potas­sium and therefore acidosis causeshyperkalaemia with its attendant dan­gers. Chronic acidosis is buffered inbone, with the loss of calcium, andosteodystrophy results. It Is thereforewise to keep serum bicarbonate lev­els above 18 mEq/1. As amino acidscarry acid radicals, the restriction ofprotein intake helps to prevent severeacidosis. Severe acidosis in Indianpatients is a rarity.

Salt and water: The capacity ofthe diseased kidney to excrete saltand water varies from patient to pa­tient, and therefore the intake of thesetwo items must be individualised.Whereas in other oedematous statesit is enough to fe.strict salt intakes, inrenal failure the capacity of the kidneyto excrete free water is also impaired,and therefore a limit must be placedon water intake too.

Recommendations for diet inch~onic. renal failure: The averageIndian diet IS especially suitable forthe management of chronic renal fail­ure, and not much modification isneeded. To most patients, I prescribea very simple menu which is as follows:

• One egg or 50 gm (uncooked weight)of meat or fish, and 100 ml of milk orcurds. The vegetarian may take 300ml of mi,lk or curds and avoid eggs,meat and fish.

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The possible harm from a lowIcium intake is that calcium forms arnplex with oxalate in the bowel

hlch is not readily absorbed, andUIUS the dietary oxalate is kept in thef')wel and passed in the faeces. In1\ absence of calcium, oxalate isI 'Ore readily absorbed, and second­ry hyperoxaluria may result.

Oxalate is the end product of then\etabolism of a number of substances.About 40 per cent comes from ascor­

Ie acid, and 50 per cent from glycolate,Iycine, and hydroxyproline. These

Me components of proteins, and highprotein intake would therefore increasetheir excretion in the urine. Only about10 per cent of urinary oxalate is di­actly derived from dietary oxalateontaining foods, and therefore thecope for reducing urinary oxalatexcretion by dietary restriction of ox­late-rich substances is small. It would

be wise to avoid excessive intake ofthe following items especially rich inoxalate, namely leaves including thenumerous varieties of edible greensand tea, nuts, chocolate, and beetroot.It is not necessary to ban these itemsentirely.

As we have already seen, diet isresponsible for only 10 per cent ofoxalate in the urine. An excessive

intake of ascorbic acid is similarlyinadvisable, and so very large amountsof citrus fruits and juices should beavoided. Again, a total embargo is notcalled for as the pathway of the con­version of ascorbic acid to oxalate isreadily saturated. It is to be noted thattomato does not figure anywhere onthis list. Every stone former in thecountry, and many people with otherrenal diseases, are being deprived ofthe use of this tasty component of ourdiet, for no valid reason. It is neithervery high in oxalate content nor inascorbic acid.

There is a close relationship be­tween renal tubular reabsorption ofsodium and calcium. When the bodyIS replete with sodium, tubular reabsorp­tion of water from the proximal convo­luted tubule is diminished, along withall the solutes in it. There will there­I re be more calcium in the urine.Conversely, in a sodium depleted pa­tl'3nt, sodium along with calcium willb J reabsorbed more from the proxi-'rral tubule. In the distal tubule reabs­orption of calcium is largely ~harge­related. If more sodium is availablelor reabsorption, the contents of the

tubular lumen will be relatively nega­tive, and this will tend to retain the posi­tively charged calcium ion in the lumen.

While there is no evidence tolink a high sodium intake with thedevelopment of calcium containing renalstones, it is certainly helpful to restrictsodium intake moderately when at­tempting to treat patients, as this low­ers the amount of calcium in the urine.

A very high protein intake is as­sociated with renal stone formation.Protein increases glomerular filtration,and therefore calciuria would increase.There is increased acid productionwith increased protein intake, and thisreduces citrate excretion in the urine.More citrate is absorbed from the proxi­mal tubule when acid excretion is high,and more is utilised for gluconeogen­esis in the cell. Urin~ry citrate che­lates calcium and forms a readily solubleproduct which takes calcium away fromstone formation ..

Protein also increases urinaryuric acid excretion, and uric acid is apromoter of calcium oxalate precipi­tation in the urine. For all these rea­sons, it is advisable to restrict animalprotein intake in stone formers.

The single most important di­etary manipulation of benefit in stoneformers is the consumption of largevolumes of water. Water dilutes allthe salts in the urine, and takes themout of the stage of unstable super­saturation in which stones are likelyto form. The larger the liquid intake,especially at night, the less the chanceof stone formation. It should be notedthat the patient should actively forceliquid intake during the night. My ad­vice is to drink a glass of water everyhour, two on retring to sleep, and twomore when he wakes up to pass urine.

There is a theoretical objectionto drinking large amounts of water.There are inhibitors of stone forma­tion in the urine, and they may bediluted by the water and thus be lesseffective. However, clinical evidenceindicates that people are much more!ikely to form stones in hot dry regionsIn. the absence of enough water todnnk, and less likely if they drink wa­ter copiously.

Uric.aCid. stones: The tendencyto form unc aCId stones is not relatedas well to the actual amount of uricacid as it is to the pH of the urine. Uricacid itself is relatively insoluble whilesodium urate is far more solubl'e. So-

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dium urate forms in an alkaline urineand the relative amount of uric acid isdirectly proportional to the acidity ofthe urine. Vegetables give rise to al­kali in the body, and protein of animalorigin to acid, as already discussed.Meat intake is harmful to the uric acidstone former, both because it contrib­utes a large amount of uric acid frompurine metabolism and because it ren­ders the urine acidic, as already dis­cussed. The best treatment for a uricacid stone former is to become a veg­etarian! Among meats, offal (internalorgans like liver, brain and pancreas)and red meats are especially harmful,white meat relatively less so.

As with calcium stones, a largeliquid intake is also beneficial.

The author is the Chief Nephrologist. Apollo

Hospital. Madras.

References

1. Giordano, C.: Use ot exogenous and endo­genous urea for protein synthesis in normal anduraemic subjects. J Lab Clin Med. 62: 231-246,1963.

2. Giovanetti, S., Maggiore, Q.: A low-nitrogendiet with proteins of high biological value for severechronic uraemia. Lancet, I: 1000-1003, 1964.

3. Alvestrand, A., Ahlberg, M., Furst, P., Bergstrom,J.: Clinical results of long-term treatment with a lowprotein diet and a new amino acid preparation inpatients with chronic uraemia. Clin Nephrol, 19: 67­73, 1983.

4. Rosman, J.B., Langer, K., Brandl, M., Piers­Becht, T.P.M., van der Hem, G.K., ter Wee, P.M.,Donker, J.A.M.: Protein-restricted diets in chronicrenal failure: A four-year follow-up show~ limitedindications. Kidney In I, 36: S96-S102, 1989.

5. Kontessis, P., Jones, S., Dodds, R., Trevisan,R., Nosadini, R., Fioretto, P., Borsato, M., Saurdod,D., Viberti, G.C.: Re:lal, metabolic and hormonal

responses to ingestion of animal and vegetableproteins. Kidney Int, 38: 136-144, 1990.

6. Walser, M., La France, N.D., Wa~d, L., Van­Duyn, M.A.: Progression of chronic renal failure inpatients given keto-acids following amino acids.Kidney Int,"32: 123-128, 1987.

7. Moorhead, J.F.: Lipids and progressive renaldisease. Kidney Int, 39.Suppl 31: 835-S40, 1991.

NEW PUBLICATION

Recent Trends in Nutrition:Proceedings of the First Inter­national Symposium of the Nutri­tion Foundation of India in Dece­mber 1990. Contains 17 papersby leading scientists, edited byDr C. Gopalan, 220 pp, priceRs 395 and published by OxfordUniversity Press, Delhi. .