Sodium homeostasis in term and preterm neonatesArchives ofDisease in Childhood, 1983, 58, 335-342 Sodiumhomeostasis in term andpreterm neonates I Renal aspects J AL-DAHHAN, GB HAYCOCK,

Archives of Disease in Childhood, 1983, 58, 335-342

Sodium homeostasis in term and preterm neonates

I Renal aspects

J AL-DAHHAN, G B HAYCOCK, C CHANTLER, AND L STIMMLER

Evelina Department ofPaediatrics, Guy's Hospital, London

SUMMARY Eighty five 24 hour sodium balance studies and creatinine clearance measurements wereperformed in 70 infants of gestational age 27-40 weeks and postnatal age 3-68 days. The kidney'scapacity to regulate sodium excretion was a function of conceptional age (the sum of gestationalage and postnatal age) and an independent effect of postnatal age was also observed-extrauterineexistence increased the maturation of this function. The sodium balance was negative in ICO% ofinfants of <30 weeks' gestation, in 70% at 30-32 weeks, in 46% at 33-35 weeks, and in 0% of>36 weeks, and the incidence of hyponatraemia closely paralleled that of negative sodiumbalance. Despite a low glomerular filtration rate (GFR) urinary sodium losses were highest inthe most immature babies but fractional sodium excretion (FENa) was exponentially related togestational age. An independent effect of postnatal age could be identified on FENa but not inGFR. These findings indicate that in infants of >33 weeks' gestation sodium conservation ispossible because of a favourable balance between the GFR and tubular sodium reabsorption, butthat below this age GFR exceeds the limited tubular sodium reabsorption capacity. The rapidincrease in sodium reabsorption in the first few postnatal days seems to be due to maturation ofdistal tubular function, probably mediated by aldosterone. We suggest that the glomerulotubularimbalance for sodium is a consequence of the immaturity of the tubuloglomerular feedbackmechanism, and we estimate that the minimum sodium requirement during the first 2 weeksof extrauterine life is 5 mmol (mEq)/kg/day for infants of <30 weeks' gestation and 4 mmol(mEq)/kg/day for those born between 30 and 35 weeks.

The improved survival rate of very low birthweight(VLBW) infants achieved in recent years has led tothe recognition that the requirements for care ofsuch babies differ from those appropriate forterm infants. It has been reported'-3 that VLBWinfants frequently become hyponatraemic when fedon human milk or conventional 'humanised' infantformulae, while mature newborns have no difficultymaintaining normal electrolyte values on the samediet. The importance of 'late hyponatraemia" inrelation to somatic and central nervous systemgrowth and development is unknown but it isunlikely to be beneficial and its cause and con-sequences are therefore important subjects forfurther investigation. We undertook the presentstudy to clarify the physiological mechanismsunderlying sodium homeostasis in the immaturehuman newborn, and to relate these to other aspectsof neonatal renal physiology; and to determine theoptimum dietary sodium requirement for pre-

mature babies in relation to gestational and post-natal age.

Patients

Seventy healthy newborn infants were studied in thenurseries and special care baby unit of this hospital.Their gestational ages ranged from 27 to 42 weeks,and birthweights from 800 to 4200 g. Gestationalage was estimated from the mother's menstrualhistory and on physical assessment of the infantusing the criteria of Dubowitz et al.4 All the infantswere in good condition at the time of the study andnone required mechanical ventilation or other majorprocedures. Preterm infants, kept in their incubatorsthroughout, were fed by nasogastric tube, and termbabies were breast or bottle fed by their mothers onthe obstetric wards and in the nurseries. Water andelectrolyte administration followed the unit's routinefeeding policy (Table).

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336 Al-Dahhan, Haycock, Chantler, and Stimmler

Table Routine fluid regimen given to babies duringthe studyDay Preterm Term Small for dates

1 65 65 1002 80 80 1103 90 90 1204 100 105 1405 120 120 1506 140 130 1607 175 145 1708 200 150 200

The investigation was approved by the ethicalcommittee of the hospital and informed consent wasobtained from parents. A total of 100 studies wasperformed on or after the third postnatal day.

Methods

Balance studies. Each study lasted for 24 hours. Thevolume of all feeds was recorded and a sample ofmilk from the same batch was stored for subsequentanalysis. The sodium and potassium content of anydrugs or intravenous fluids given during the studywas included. Twenty four hour urine collectionswere made by spontaneous voiding into Abbott urinebags, using the irethod of Tarlow.5 A plastic tubewas attached to the bag and continuous gentlesuction was applied using a Robert's pump. Stoolswere collected on plastic sheets on which the babiesrested and which were replaced immediately aftereach stool was passed: stools were frozen andstored for analysis. A heparinised blood sample(0-8 ml) was collected by heelprick at the middle ofthe 24 hour period.

Laboratory methods. Creatinine was estimated inurine and plasma by a kinetic modification of thealkaline picrate method6 using a modified LKBautomatic analyser. Sodium and potassium con-centrations in plasma and urine were measured onan IL flame photometer. Stools were pooled foreach 24 hour study period and transferred to aweighed dry container in which they were homo-genised using a Volter mixer. 1 g of homogenatewas placed in a glass tube to which 1 ml concentratednitric acid was added. After thorough mixing thetubes were heated at 100'C and stirred inter-mittently until the solution was completely clear.The samples were then diluted and flame photometryperformed. Duplicate 1 ml milk samples werecleared in the same way before flame photometry.

Statistical methods. Data were analysed usingStudent's t test and linear and exponential cor-relation and regression.

Results

The term conceptional age is used throughout tomean the sum of gestational age and postnatal ageat the time of each study. Twenty-four hourcreatinine clearance increased exponentially withconceptional age, expressed both in absolute termsand after correction for body surface area (Fig. 1).The relation between conceptional age and fractionalsodium excretion (FENa) is shown plotted semi-logarithmically in Fig. 2.We tried to distinguish between the effecis of

conceptional age and postnatal age on the matura-tion of glomerular filtration rate and tubular sodiumreabsorption by dividing the observations into 5groups according to postnatal age: the conceptionalages did not differ appreciably between any 2 of thegroups (Fig. 3). The relation between GFR andconceptional age in babies aged 5-6 days and26-28 days is shown in more detail in Fig. 4. Thematuration of GFR and sodium reabsorption werecompared directly by plotting them on linear axesagainst conceptional age (Fig. 5).

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Fig. 1 Creatinine clearance, corrected (closed circles)and uncorrected (open circles) for body surface area,plotted against conceptional age. In this and subsequentfigures the regression statistics were calculatedfrom x(conceptional age) expressed in days, although the axis ismarked in iveeks for convenience.

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Sodium homeostasis in term and preterm neonates 337

-0 0354x(days)y=2582 86en=100r =-0 80P<0 001

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n fn128 30 32 34 36 38 40 40ConceptionaL age ( weeks )

Fig. 2 Fractional sodium excretion, expressed aspercentage offiltered load, against conceptional age.

The solid line is the calculated regression line;broken lines connect studies performed on the sameinfants on different days.

The results of the sodium and potassium balancestudies, in which net balance is plotted againstpostnatal age for 4 groups born at different gesta-tional ages, are presented in Figs. 6 and 7. Plasmasodium concentrations below 130 mmol (mEq)/lwere recorded on at least 1 occasion in 43 % ofbabies born at 27-29 weeks, 13% of those born at30-32 weeks, but in no infant born after 32 weeks:the lowest recorded value was 107 mmol (mEq)/l onthe twelfth postnatal day in an infant born at 29weeks. The urinary potassium :sodium (K+ :Na+)ratio is shown plotted against conceptional age in Fig.8. As in Fig. 2 the broken lines connect sequentialstudies performed on the same infants.

Discussion

The studies were performed after the first 3 days ofextrauterine life, since during the first 1 or 2 daysafter the birth the GFR may reflect a transitionalstate of circulatory adaptation rather than thefunctional state of the kidney once this adaptationhas taken place.7 The data were not analysedaccording to birthweight because the functionalmaturation of the kidney has been shown to be agedependent rather than weight dependent.8 Endo-genous creatinine clearance was chosen over other

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2-4 5-6 7-12 13-25 26-68

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rate (GFR) (creatinineclearance), corrected and

1 uncorrectedfor surface area,andfractional sodium

05 excretion grouped bypostnatal age at the time ofstudy. The bars indicate + 1

01 logarithmic standardoo05 deviation. No 2 groups

differed significantly withrespect to conceptual age.

0D01 Glomerular filtration rate is0 005 essentially identical in all

groups; fractional sodiumexcretion (FENa) is

0.001 significantly lower in infantsof >25 days than in those of2-12 days (P< 0-001).

Conceptionat agedays (1 SD)

230-1 245 2 238 5 241 8 246 7(±183) (±23 3) (±28-8) (±24-8) (±185)

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Fig. 4 7he relation between conceptional age andglomerular filtration rate in infants of 5-6 days'(open circles) and 26-68 days' (closed circles) postnatalage, corrected (top half) and uncorrected (bottom half)for body surface area. The regression lines do notdiffer significantly either in slope (P >0-4) or in verticalseparation (P >0-2). Similar analyses performed on

the other postnatal age groups (see Fig 3) showed thatnone of the groups differs from any other or from theoverall regression line for the whole study group (Fig 1).

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Fig. 5 Fractional sodium excretion and glomerularfiltration rate (mean ± I SEM) against conceptional age.Note the differcnt relation between the 2 variablesbefore and after 33 weeks' conceptional age.

theoretically more accurate measures of GFRbecause ofconvenience and because it is a sufficientlyreliable method in this age group.9-'1 The GFR,both absolute and corrected for surface area, rosewith conceptional age and the relation was ex-ponential rather than linear,9 which indicatesincreasingly rapid glomerular functional maturationwith age.8 12-14 The failure of Guignard et aL.'5 toshow such a relation was probably due to lack ofdata from babies of <35 weeks' gestation. Ourfinding that GFR is the same in babies of similarconceptional ages but different postnatal ages(Figs. 3 and 4) agrees with the results of Fawer etal.'6 and indicates that after the first few dayspostnatal age per se has little or no influence onGFR, which increases in a 'programmed' fashionaccording to absolute developmental age. Aperia etal.9 showed that GFR increased between 1 and 5weeks of age at approximately the same rate in termand preterm infants, but that during the first weekit rose more rapidly in term babies. Svenningsen14reported similar findings, although the effect ofpostnatal age was not examined in detail beyond thefirst week. It seems likely that these very earlydifferences between preterm and term infantsreflect differences in the rapidity with which thecirculatory alterations are made at delivery. Afterthis period each infant finds its own predetermined'track'-a function of conceptional age, alongwhich subsequent development proceeds. Thisimplies further that intrauterine and extrauterinematuration of glomerular function proceeds at thesame pace.'7The non-linearity of the increase in GFR supports

the impression that several mechanisms contributeto the developmental changes in GFR. Althoughglomerulogenesis continues until 34 weeks' gesta-tion,'8 the number of glomeruli is unlikely tobe a limiting factor since most are not functioningat birth even in term infants. The major factoris probably increasing renal blood flow andglomerular perfusion9 20 secondary to rising renalarterial pressure and falling renal vascular resis-tance, but changes in glomerular permeability towater2' and glomerular surface area22 may alsocontribute.Our finding of high urinary sodium excretion rates

in preterm infants agrees with reports from manycentres.3 8 23-28 Since GFR is lower in preterm thanin term infants the higher sodium excretion ratesseen in the former must be attributed to lowertubular reabsorption of the ion.28 IfGFR and FENa,representing glomerular and tubular functionrespectively, are plotted against conceptional age onthe same time axis (Fig. 4) it is apparent that above33 weeks salt reabsorption is efficient despite the

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Sodium homeostasis in term and preterm neonates 339

Group 2 (30-32 weeks)

pi.flE IISodium:- -1

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day )

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igiiI I11 12 13 - 2 34Postnatal age ( days)

Utl UU.

5 6 7 8 9 10 11 12 13

Fig. 6 The relation between postnatal age and sodium balance in infants born at 27-29 weeks', 30-32 weeks',33-35 weeks', and 36-40 weeks' gestation.

rapidly increasing GFR. Before this age salt wastingoccurs, implying that in the more mature infantsthere is effective coupling between glomerular andtubular function. The fact that proximal tubularreabsorptive capacity in very premature infants lagsbehind filtration rate8 suggests that the mechanismthat will later ensure glomerulotubular balance is notyet functionally mature. We agree with Aperia et al.9that this is likely to be due to failure of tubulo-glomerular feedback at the macula densa.Our findings give no insight into the specific site

of inadequate sodium reabsorption in immaturebabies. Sulyok et al.29 suggested that distal tubularfunction increases rapidly in this respect during thefirst 2 postnatal weeks, but since these results werenot obtained during maximal water diuresis there isdoubt about the reliability of this conclusion. Wehave shown an accelerating effect of extrauterineexistence (postnatal age) on sodium reabsorptionbut not on GFR (Fig. 3). This conclusion is furthersupported by examination of Fig. 2, in which theaverage slope of the broken lines connectingsequential studies on the same infants is clearlysteeper than that of the overall relation. It istempting to suggest that this is related to the

increase in activity of the renin-angiotensin-aldosterone system that has been shown to occurshortly after birth and correlates well with urinarysodium excretion in 1 week old infants.30We did not estimate plasma aldosterone concen-

trations, but plasma and urinary aldosterone valuesare high in both premature and term babies.2428 31The action of aldosterone on the mature distaltubule causes an increase in sodium reabsorp-tion and potassium secretion and thus the urinarypotassium:sodium ratio is an index of aldosteronedependent distal tubular activity.32 This ratio waslow in the most immature infants, rising steadilywith increasing conceptional age (Fig. 8). Thisconfirms the results of Aperia et al.,28 who alsofound that the ratio showed no correlation withaldosterone excretion rate in very immature babies.The most likely explanation of these findings is thatthe responsiveness of the tubule to aldosterone, atfirst very low, rises progressively with maturation,and that this maturation is accelerated after birth.The positive balance for potassium (Fig. 5) seeneven in the most immature infants with markedsodium wasting is further evidence of resistance tothe action of the hormone.

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340 A/-Dahhan, Haycock, Chantler, and Stimmler

3- Group 1 (27-29 weeks)

2-

1 dPotassium -1_

Inatake L

Output

Ontake 3 1 2 3 4 5Balance

(mmol(mEq) /kglday)

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6 7 8 9 10 11 12 13

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1 2 3 4 5 6 7 8 9 10 11 12 13Postnatal age (days)

Fig. 7 The relation between postnatal age and potassium balance; groups as in Fig 6.

Unresponsiveness to aldosterone might be ex-plained in several ways. The immature tubule maylack receptors for the hormone, an antagonist to itsaction may be present, or the transporting enzymesystem (Na+-K+ ATPase) may be deficient. Thefirst 2 explanations are conjectural, but there may beevidence to support the third. Schmidt and Horster33showed activity of the enzyme to be low in allsegments of the newborn rabbit tubule. In ratsthere is increased enzyme activity throughout fetallife, although an appreciable postnatal rise has alsobeen shown.34 3Sodium balance was most strongly negative in the

least mature infants but with increasing maturitychanged to positive as a result of declining output(input changed little). These results are qualitativelyand quantitatively similar to those reported bySulyok,30 but the larger negative sodium balancedescribed by Engelke et al.27 probably reflects theinclusion of some very sick babies in their study.Positive balance was achieved in the least matureinfants (27-29 weeks' gestation) by the end of the

second postnatal week, in those of 33-35 weeks bythe middle of the first postnatal week, and in thoseof 36 weeks and over before the third day of age(when our study began). Thus although the mostprematurely born babies achieve positive balance ata lower conceptual age than the more mature ones,they require a longer postnatal period to adjust.Here again our results are in general agreement withthose of Sulyok23 and Honour et al.24

Preterm infants fed on conventional artificialformulas or pooled human milk receive insufficientsodium to compensate for high urinary losses,leading to a high incidence of hyponatraemia.Indeed the sodium intake provided (1-2 mmol(mEq)/kg/day) is even less than the calculatedintrauterine sodium accretion rate required forniormal fetal growth.36 A sufficient intake to preventhyponatraemia should be provided and this maybe achieved by giving a salt supplement orspecial high sodium formulas in the early postnatalperiod. An estimate of the minimum dietaryrequirement for sodium may be calculated by

u FM l9 X X- l


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Sodium homeostasis in term andpreterm neonates 341

20 - y= 00578e 0207xr = 0 527

10 _ n=99P<0.001

5 0 ,1_~~~~~~~~~~v

O // 0

02_~~~~~~~~~

01_

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Fig. 8 The relation between urinary sodium.:potassium(Na+:K+) ratio and conceptional age. The solid line isthe calculated regression line: broken lines connectstudies performed on the same infants on different days.

adding measured urinary and faecal losses to theintrauterine sodium accretion rate. Thus we suggestthat infants born before 30 weeks' gestation shouldreceive at least 5 mmol (mEq)/kg/day, and those of30-35 weeks 4 mmol (mEq)/kg/day, during the first2 postnatal weeks. Since all the infants studiedachieved positive external sodium balance by theend of the second postnatal week on human milkor SMA, there appears to be no need to extendsupplements beyond this.

We thank Sister Barbara Nichol and the nursingstaff of the special care baby unit, Guy's Hospital,for invaluable assistance and support; Miss AnnChapman for typing the manuscript.

References

Roy R N, Chance G W, Radde I C, Hill D E, Willis D M,Sheepers J. Late hyponatremia in very low birth weightinfants ( < 1 - 3 kilograms). Pediatr Res 1976; 10: 526-3 1.

2Day G M, Radde I C, Balfe J W, Chance G W. Electrolyteabnormalities in very low birthweight infants. Pediatr Res1976; 10: 522-6.

3Thodenius K. Renal control of sodium homeostasis ininfancy. Acta Paediatr Scand [Suppl] 1974; 253: 1-28.

4Dubowitz L M S, Dubowitz V, Goldberg C. Clinicalassessment of gestational age in the newborn infant.JPediatr 1970; 77: 1-10.

5 Tarlow M J. Urine and stool collection for metabolicstudies in the newborn. Arch Dis Child 1974; 49: 490-2.

6 Cook J G H. Creatinine assay in the presence of protein.Clin Chi,n Acta 1971; 32:485-6.

7Leake R D, Trygstad C W. Glomerular filtration rateduring the period of adaptation to extrauterine life.Pediatr Res 1977; 11: 959-62.

8 Siegel S R, Oh W. Renal function as a marker of humanfetal maturation. Acta Paediatr Scand 1976; 65: 481-5.

9 Aperia A, Broberger 0, Elinder G, Herin P, Zetter-strom R. Postnatal development of renal function inpreterm and full term infants. Acta Paediatr Scand 1981;70: 183-7.

10 Stonestreet B S, Bell E F, Oh W. Validity of endogenouscreatinine clearance in low birthweight infants. PediatrRes 1979; 13: 1012-4.Sertel H, Scopes J. Rates of creatinine clearance in babiesless than one week of age. Arch Dis Child 1973; 48:717-20.

12 Leake R D, Trygstad C W, Oh W. Inulin clearance inthe newborn infant: relationship to gestational and post-natal age. Pediatr Res 1976; 10: 759-62.

13 Leake R D, Oh W. Effect of gestational age and postnatalage on glomerular filtration rate and tubular maxima ofglucose in human infants (abstract). Pediatr Res 1974; 8:475/183.

14 Svenningsen N W. Single injection polyfructosan clear-ance in normal and asphyxiated noenates. Acta PaediatrScand 1975; 64: 87-95.

15 Guignard J P, Torrado A, DaCunha 0, Gautier E.Glomerular filtration rate in the first three weeks of life.JPediatr 1975; 87: 268-72.

16 Fawer C L, Torrado A, Guignard J P. Maturation ofrenal function in full term and premature neonates.Helv Paediatr Acta 1979; 34: 11-21.

17 Arant B S, Jr. Developmental patterns of renal functionalmaturation compared in the human neonate. J Pediatr1978;92: 705-12.

18 Potter E L, Thierstein S T. Glomerular development inthe kidney as an index of fetal maturity. J Pediatr 1943;22:695-706.

9 Robillard J E, Weissman D N, Herin P. Ontogeny ofsingle glomerular perfusion rate in fetal and newbornlambs. Pediatr Res 1981; 15: 1248-55.

20 Aperia A, Broberger 0, Herin P. Maturational changesin glomerular perfusion rate and glomerular filtrationrate in lambs. Pediatr Res 1974; 8: 758-65.

21 Larsson L, Maunsbach A B. The ultrastructural develop-ment of the glomerular filtration barrier in the ratkidney: a morphometric analysis. J Ultrastruct Res 1980;72:392-406.

22 John E, Goldsmith D 1, Spitzer A. Developmentalchanges in glomerular vasculature: physiologic im-plications (abstract). Clin Res 1980; 28: 450.

23 Sulyok E. The relationship between electrolyte and acid-base balance in the premature infant during earlypostnatal life. Biol Neonate 1971; 17: 227-37.

24 Honour J W, Valman H B, Shackleton C H L. Aldo-sterone and sodium homeostasis in preterm infants.ActaPaediatr Scand 1977; 66: 103-9.

25 Ross B, Cowett R M, Oh W. Renal functions of lowbirthweight infants during the first two months of life.Pediatr Res 1977; 11: 1162-4.

26 Sulyok E, Varga F, Gyory E, Jobst K, Csaba I F. On themechanisms of renal sodium handling in newborninfants. Biol Neonate 1980; 37: 75-9.

27 Engelke S C, Shah B L, Vasan U, Raye J R. Sodiumbalance in very low-birthweight infants. J Pediatr 1978;93: 837-41.


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28 Aperia A, Broberger 0, Herin P, Zetterstrom R. Sodiumexcretion in relation to sodium intake and aldosteroneexcretion in newborn preterm and full term infants. ActaPaediatr Scand 1979; 68: 813-7.

29 Sulyok E, Varga F, Gyory E, Jobst K, Csaba I F.Postnatal development of renal sodium handling inpremature infants. JPediatr 1979; 95: 787-92.

30 Sulyok E, Nemeth M, Tenyi I, et al. Relationship betweenmaturity, electrolyte balance, and the function of therenin-angiotensin-aldosterone system in newborn infants.Biol Neonate 1979; 35: 60-5.

31 Dillon M J, Gillin M E A, Ryness J M, de Swiet M.Plasma renin activity and aldosterone concentration inthe human newborn. Arch Dis Child 1976; 51: 537-40.

32 Ganong W F, Mulrow P J. Rate of change in sodium andpotassium excretion after injection of aldosterone intothe aorta and renal artery of the dog. Am J Physiol 1958;195:337-42.

33 Schmidt U, Horster M. Na-K-activating ATP-ase:

activity maturation in rabbit nephron segments dissectedin vitro. Am JPhysiol 1977; 233: F55-F60.

34 Potter D, Jarrah A, Sakai T, Harrah J, Holliday M A.Character of function and size in kidney during normalgrowth of rats. Pediatr Res 1969; 3: 51-9.

35 Aperia A, Herin P. Development of glomerular perfusionrate and nephron filtration rate in rats 17-60 days old.Am JPhysiol 1975; 228: 1319-25.

36 Shaw J C L. Parenteral nutrition in the management ofsick low birthweight infants. Pediatr Clin North Am 1973;20: 333-58.

Correspondence to Dr G B Haycock, EvelinaDepartment of Paediatrics, Guy's Hospital, StThomas Street, London SEI 9RT.

Received 2 February 1983

Fifty years ago

Ketogenic diet in the treatment ofpyuriain childhoodJ BASIL RENNIE (Glasgow)

In October 1931, Helmholz published the results ofthe treatment of pyuria in children by means of theketogenic diet. This form of treatment was sug-gested by the observation that the urine of a patientbeing treated for epilepsy by ketogenic diet remainedfree of bacterial cloudiness after being kept for aweek.

Summary: (1) Six cases of chronic pyogenic infectionof the urinary tract were treated with ketogenic diet.(2) At the end of treatment the urine was sterile in4 cases and growth on culture scanty in a 5th, but3 relapsed in three weeks. The 6th case showed no

change in the condition. (3) In the 2 cases who werepermanently cured the duration of the disease wasshort and no abnormality of the urinary tract wasobserved. In each of the 4 cases in which treatmentfailed abnormality of the urinary tract was demon-strated by pyelography. (4) It would appear thatketogenic diet is of little value as a curative agentin pyuria associated with abnormality of theurinary tract.Archives of Disease in Childhood 1933; 8: 47-50.

(Brilliantly simple observation and action byHelmholz, overtaken 5 years later by the advent ofsulphanilamide. Rennie continued his interest inrenal disorders and was one of the first to differ-entiate idiopathic nephrotic syndrome of childhoodfrom other more serious variants: he became aphysician in Glasgow. PRE).


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Sodium homeostasis in term and preterm neonatesArchives ofDisease in Childhood, 1983, 58, 335-342 Sodiumhomeostasis in term andpreterm neonates I Renal aspects J AL-DAHHAN, GB HAYCOCK,