pediatrics 1979 vardi 782 7

782 PEDIATRICS Vol. 63 No. 5 May 1979

The Heart in Acute Glomerulonephritis: AnEchocardiographic Study

Pnina Vardi, M.D., Walter Markiewicz, M.D., Joseph Levy, M.D., Olga Adler, M.D.,

Egon Riss, M.D., and Abraham Benderley, M.D.

Front the’ !)epartment.s- of Pediatrics, Cardiology, and Diagnostic Radiology, Ra7nbanl .�Iedieal Center, Aba

Kbiousbiy School of .%h’dicine, Haifa, Israel

ABSTRACT. Patients with acute glomerulonephritis often

are seen with signs suggesting heart failure. Whether thesesigns are due to fluid overload secondary to kidney damageonly, or whether there is associated inyocardial damage hasnot been elucidated. Fourteen children with acute glomeru-

lonephritis were studied by echocardiography during the

edematous phase of the disease and five months later toevaluate cardiac function in this disease. Left ventricular sizeand function remained normal in all children throughout thestudy. The most consistent finding was enlargement of theleft atrium during the edematous phase with a return towardnormal values five nionths later. There was no correlation

between blood pressure and the echocardiographic findings.This study suggests that signs of heart failure in acuteglomentlonephritis are not due to myocardial damage but

probably reflect fluid overload. Pediatrics 63:782-787, 1979,echocardiography, acute glornerulonephritis, heart failure,

left atrial enlargement.

In many patients with acute glomenilonephri-tis (AGN), signs and symptoms suggesting conges-

tive heart failure develop. Despite numerous

investigations, it is not clear whether myocardial

function is depressed in this disease, or whether

the signs suggesting heart failure are due to fluid

overload, or to other factors such as hyperten-sion.i In this study, we evaluated a group of

children with AGN by echocardiography to gain

further insight into the cardiac status of these

patients.

PATIENTS AND METHODS

Fourteen children were studied during an

epidemic of poststreptococcal AGN. All had the

classic signs of AGN including hematuria,

proteinuria, edema, elevated sedimentation rate,

and antistreptolysin 0 titer and depressed concen-

tration of the third component of the complement

(G3). None had a previous history of kidney

disease, and all had previously been healthy,except for one child who had chronic hemolyticanemia due to thalassemia (subject no. 4). On

admission to the hospital, all children underwent

a full clinical examination including a 12-lead

electrocardiogram and roentgenogram of thechest. Echocardiographic studies were performedwithin two days of admission in all subjects, on

discharge from the hospital in eight subjects, andfive months thereafter in all 14 subjects.

The ultrasonic studies were performed on anultrasonoscope, using a 2.25 MHz transducer

focused at 7.5 cm, and a recorder. All the childrenwere examined in the semi-left lateral decubitus

position with the head elevated by a wedge.Routine techniques were used for evaluation of

the aorta, left atrium, left ventricle, interventricu-lar septum, right ventricle, and pericardiuni.�

Left ventricular contractile state was evaluated

by calculating the ejection fractiont and the

percentage of fractional shortening’ from the left‘ventricular dimensions (Fig 1). Left atrial and

aortic dimensions were obtained at the level ofthe aortic leaflets. Left atrial dimension was

measured at end systole from the anterior border

of the posterior aortic wall to the strong anterior

edge of the posterior atrial wall echo (Fig 2).

Aortic dimension was measured at end diastole.

The upper limit for normal values of left atrium,aorta, and left ventricle used in the study are

those reported by Feigenbaunr and varied de-

pending on the l)ody surface area. The upper

Received April 7; revision accepted for publication August 8,

1978.ADDRESS FOR REPRINTS: (P.V.) Department of Pediat-rics “A,” Rambam Medical Center, Haifa, Israel.

at Indonesia:AAP Sponsored on January 16, 2015pediatrics.aappublications.orgDownloaded from

http://pediatrics.aappublications.org/

ARTICLES 783

#{149}cg i

� - �T*� � � � �

1� � � � � � I � � � � � � II �

Fig 1. Representative (subject 6) echocardiographic examination of the ventricles taken on

admission (left) and five months later (right). Left ventricular end diastolic dimension remainsunchanged. (ACW = anterior chest wall; RV right ventricle; IVS interventrictilar

se1)ttllll; LV = left ventricle; En = endocardium; P pericardium.)

limit for a noinial left atrial-aorta ratio in our

laboratory is 1.26, whereas the lower limit for

normal ejection fraction and percent of fractional

shortening in children is 55% and 25%, respective-

ly.

For the pllI’pose of this studs’, hypertension was

diagnosed when blood pressure was higher than

1:30/90 flilli Hg. Left ventricular hvpertrophy

was diagnosed by EGG using criteria suggested by

Liebm an . ‘ Chest roentgenograms were reviewed

by an exl)erienced radiologist for evidence of

cardiotnegalv and heart failure. Statistical analy-

sis was performed using two-tailed paired Student

t-tests for analysis of changes in cardiac dimen-

sions, and using the Fisher exact test for the

correlation l)etWeen the presence of hypertension

and increased size or thickness of heart cham-

bers.

RESULTS

There were eight boys and six girls with an age

of 6.7 ± 0.9 years (mean ± SEM) (range 3 to 12

years). Mean body surface area was 0.8 1 ± 0.06

sq m with a range of 0.5 to 1.2 sq m. The clinical

findings on admission and at discharge are given

in Table I. All children were treated by bed rest,low-potassium diet, and penicillin. Patients with

hypertension were treated with water restriction

and intramuscular injections of reserpine. Nonehad evidence of residual kidney damage, andnone was receiving any treatment at the time the

third echocardiogram was performed. All chil-dren had normal sodium, potassium, chloride,bicarbonate, and calcium values throughout thestudy. Mean body weight was 22.4 ± 2.3 kg on

admission and 21.0 ± 2.3 kg on discharge

(P < .01). Mean heart rate increased from

80.6 ± 5.1 to 92.3 ± 3.9 beats per minute duringthe same period (P < .05).

The echocardiographic findings are given in

Table II, and the correlation of selected echocar-

diographic data with roentgenographic and clini-cal findings is given in Table III. Eleven childrenhad an enlarged left atrium on admission. Left



784 HEART IN GLOMERULONEPHRITIS

Fig 2. Representative echocardiographic study of the aorta and left atrium of the same patient,showing reduction of left atrial size from 3.4 cm on admission (left) to 2.8 cm five months later(right). (RVOT = right ventricular outflow tract; AAo = anterior aortic wall; PAO = posterior

aortic wall; Ao = aorta; LA left atrium.)

TABLE I

CLINICAL FINDINGs IN 14 CHILDREN WITH ACUTE

CLOMERULONEPHHITIS

Clinical bindings’ Number of Patients

On On

Adm iss’ion is5

Hypertension 7 0

Clinical edema 14 0

Proteinuria, cylindruria 14 0

BUN <20 rng/dl 10 0

LVH on ECGt 0 0

Cardiolnegaly on roentgeno- 7 ...

grainl

Congestive heart failure on 7 ...

roentgenogram�

#{176}Nlean of two weeks later.

tLVH = Left ventricular hypertrophy.:1:(;ht’st roentgenograln was not available for review in one

patient.

atrial size returned to normal values in all but onesubject when measured five nionths later. Mean

left atrial size was 3. 1 1 ± 0. 14 cm on admissionvs 2.52 ± 0.10 cm five months later (P < .01).The mean left atriumaorta ratio was similarly

significantly reduced from 1.61 ± 0.07 to

1.33 ± 0.05 (P < .01) during the same period.Seven of eight children already demonstrated areduction in the left atrial size when studied at

the end of hospitalization, a mean of 14 days afterthe first study had been done. Five of these seven

children demonstrated a further reduction in leftatrial size when studied five months later. Leftventricular internal dimension, percentage offractional shortening, and ejection fraction werenormal in all children throughout the study.There was a small but significant decrease in thethickness of the interventricular septum (P < .05)and of the left ventricular posterior wall (P < .05)



TABLE II

ARTICLES 785

ECHOCARDIOGRAPHIC FINDINGS

hnthng Mean ± SEM P N#{176}

On Admission 5 Months Later

Left atrium (cm) (ES)t 3.11 ± 0.14 2.52 ± 0.10 <.01 14Left atrium/aorta 1.61 ± 0.07 1.33 ± 0.05 <.01 14Aorta (cm) (ED)� 1.96 ± 0.10 1.91 ± 0.07 NS 14Left ventricular internal dimension (cm) 3.65 ± 0.15 3.68 ± 0.13 NS 12

(ED)Interventricular septum (cm) (ED) 0.61 ± 0.05 0.50 ± 0.04 <.05 12Left ventricular posterior wall (cm) (ED) 0.58 ± 0.06 0.48 ± 0.04 < .05 12Right ventricle (cm) (ED) 1.16 ± 0.15 0.85 ± 0.08 NS 12Ejection fraction (%) 79 ± 1.7 78 ± 2.5 NS 12Percentage of fractional shortening 41 ± 1.7 41 ± 2.3 NS 12

5N = Number of patients with adequate echocardiographic measurements.

tES = End systole.

IED = End diastole.

during the study period, whereas no significant

change was observed in the size of the aorta and

right ventricle. No significant relationship was

noted between the presence of hypertension, left

atrial enlargement, and increased thickness of the

left ventricular posterior wall or interventricular

septuni.

DISCUSSION

In many patients with acute glomerulonephri-tis, signs and symptoms suggesting congestive

heart failure . � Various etiologic factors

have been put forth to explain the appearance of

heart failure. In recent years, the attention hasfocused on three possible causative factors:

TABLE III

ConsE�TIoN BETWEEN SELECTED ECHOCARDIOGRAPHIC AND CLINICAL FINDINGs

Subject

No.

Echocardio graphic Findings0 X -Ray an d Clinical Findingst

-�

LA (cm)

-5----,

LVED (cm)

-.-.----‘

%FS

.-‘

Heart

Siz4

CHFI BP

(mm Hg)

BSA

(sq m)

-

Age

(Years)

I III I 111 1 lii

1 2.9(E) 2.4 3.2 2.9 41 45 CDM + 180/120 0.6 32 3.1(E) 1.8 3.4 3.3 35 45 CDM + 120/ 70 0.6 4

3 2.9(E) 1.9 2.9 2.8 34 35 N 0 130/100 0.6 3

4 4.0(E) 3.2(E) 3.8 4.2 39 33 CDM + 150/100 0.7 55 2.9(E) 2.5 4.2 3.8 45 47 N 0 120/ 80 0.8 7

6 3.4(E) 2.8 4.1 4.1 34 44 N + 150/110 0.9 87 3.3(E) 2.8 4.3 4.0 35 35 CDM + 180/120 1.1 10

8 2.6 2.8 3.8 3.5 47 25 N 0 120/ 80 0.9 7

9 3.1(E) 2.8 4.0 3.8 42 53 CDM + 140/100 1.1 1110 2.3 2.2 2.9 3.7 48 41 CDM 0 120/ 80 0.6 3

11 2.8(E) 2.3 NA 3.0 NA 46 N 0 120/ 80 0.5 4

12 2.8 2.7 NA 3.2 NA 37 NA NA 130/ 80 0.7 5

13 4.2(E) 2.6 3.2 4.0 50 40 CDM + 130/ 90 1.0 12

14 3.3(E) 2.5 4.0 4.0 45 50 N 0 170/120 1.2 12

#{176}LA= left atrium; LVED left ventricular dimension at end diastole; %FS percentage of

fractional shortening; I and III refer to echocardiographic measurements on admission and fivemonths later, respectively; E = enlarged; NA not available or inadequate.

tCHF = Congestive heart failure; BP blood press’ure; BSA = body surface area;CDM = cardiomegaly; NA = not available or inadequate.:1:Found on chest roentgenogram.



786 HEART IN GLOMERULONEPHRITIS

myocardial damage, hypertension, and hyper-

volemia secondary to the renal disease.

Gore and Saphir’ found myocarditis at post-mortem examination in 16 of 160 patients who

died of acute and subacute glomerulonephritis.

The histologic findings consisted of interstitial

edema with few inflaiiiiiiatory cells and little or

no myocardial cell destruction. The role of such

serious myocarditis in causing heart failure has

been questioned. Thus Davies found a normal

cardiac output in five patients with AGN. De

Fazio and associates’ studied seven patients withAGN by cardiac catheterization and found an

increased cardiac output and stroke volume, an

elevation of the pulnionarv capillary wedge and

pulmonary artery pressure, and normal peripher-al and pulmonary arteriolar vascular resistance.

De Fazio et at interpreted these findings asindicating normal nivocardial function and

suggested that the hemodynamic changes ob-

served might be due to hypervolemia.

The suggestion that overload of the vascular

tree may play a critical role in the causation of

circulatory congestion has been advanced by

others.�� Thus Eisenberg,’2 in studying the

blood volunie of ten patients with AGN, found

that the plasma volume was significantly

increased during the edematous phase, without

alteration in circulatory red cell mass. Some

investigators’ have suggested that hypertension is

a causative factor in the development of heart

failure. However, other authors noted that there

was a poor correlation between the presence and

severity of hypertension and the development of

congestion.

In this study, we present data on the heart sizeand function in a group of children examined

during and after an episode of AGN. The percent-

age of fractional shortening and the ejection

fraction remained normal throughout the study.

These measurements are useful indices of myocar-

dial contractilityli although they may be

faulted by variations in other hemodynamic van-

ables. Thus, consideration must be given to the

possibility that the myocardial contractility was

truly reduced during the acute phase of the

disease, but that the measured indices rose in

response to changes in afterload,’4 or in response

to increased sympathetic tone.� This hypothesis

seems unlikely in our patients. First, many

subjects were hypertensive at the time of the first

ultrasonic exam ination ; increased afterload would

tend to depress and not to increase ejection phase

indices. � � Second, five months later, mean heart

rate nieasured during the acute phase of AGN was

significantly lower than during the recovery pen-

od, suggesting that sympathetic tone was notunduly increased at the time of admission to the

hospital. Bradycardia is not uncommon during

the edematous and hypertensive phase of AGN

and has been attributed to increased vagal

tone. �

We think that our findings indicate that left

ventricular function was normal in all the patients

and, therefore, that signs suggesting congestiveheart failure cannot be explained on the basis ofmyocardial dysfunction. Likewise, left ventricularinternal dimension was normal in all subjects

during the edematous phase of the disease andremained unchanged throughout the study. The

mean value for thickness of both the interventnic-

ulan septum and the left ventricular posterior walldecreased slightly but significantly during thestudy, suggesting that the thickness of these walls

might have been slightly increased during the

edematous phase. Diastolic overload of the left

ventricle causing left ventricular hypentrophy orinterstitial infiltration of the myocardmm by fluid

could be responsible for this phenomenon. Since

no significant relationship was noted between

increased thickness of the left ventricular posteni-or wall or of the interventnicular septum and thepresence of hypertension, we are of the opinion

that hypertension was not a causative factor. The

echocardiogram on admission demonstrated in-

creased thickness of the interventricular septumin three children and of the left ventricular

posterior wall in two children, but none of the

children had electrocardiographic evidence ofleft ventricular hypertrophy. In contrast to

patients with chronic glomerulonephritis, chil-

dren with AGN rarely have voltage criteria forleft ventricular hypertrophy and tend to have a

decreased amplitude of the R waves in tracingstaken early in the course of the illness.’ Thisdifference may be related to the transient natureof the hemodynamic and pathologic alterations inmost cases of AGN.

The most consistent echocardiographic finding

in our study was the abnormality noted in the size

of the left atrium. Thus left atnial size wasincreased in all but three children during theedematous phase and returned to normal in all

but one child when measured five months later.

The left atrium-aorta ratio, which is less depen-

dent on body surface area and which has beenproposed as a better indicator of left atrial size,’7

similarly decreased significantly during the study

period. The reason for left atrial enlargement hasnot been directly investigated in this study.However, it has been well documented that leftatnial size can markedly and rapidly change in



ARTICLES 787

response to variations in pulmonary flow’7 or in

response to fluid infusion,” and we think that it is

reasonable to suggest that the enlargement of the

left atriuni noted on admission was secondary to

the increase in blood volume noted during the

edematous phase of acute glomerulonephritis.

The ratio of the right ventricular preejectionperiod to the right ventricular ejection time

(RPEP/RVET) has been used to evaluate seriallythe pulmonary vascular bedl and might haveprovided information on the pulmonary circula-

tioli of our patients. Since pulmonic valve echo-

grams were not routinely obtained, right ventnic-

ular systolic time intervals could not be measured

in this study.

CONCLUSION

This study demonstrates that signs suggesting

heart failure in patients with acute poststrepto-

coccal glomerulonephnitis are not due to myocar-

dial damage but probably reflect fluid overload.

Treatment should aini at reducing the increased

circulating blood volume rather than trying to

1111 prove myocardial function.

REFERENCES1. Murphy TR, Murphy FD: The heart in acute glomeru-

lonephritis. Ann Intern Med 41:510, 1954.

2. Feigenbaum H: Echocardiography, ed 2. Philadelphia,Lea & Febiger, 1976, pp 87-340.

3. Pombo JF, Troy BL, Russel RO: Left ventricularvolumes and ejection fraction by echocardiography.

Circulation 43:14, 1971.4. McDonald IC, Feigenbaum H, Chang S: Analysis of left

ventricular wall motion by reflected ultra sound.

Application to assessment of myocardial function.

Circulation 46:14, 1972.5. Lowe KG: Systemic hypertension in children, in Watson

H (ed): Pediatric Cardiology. London, Lloyd-Luke

Ltd. 1968, pp 844-845.

6. Liebman J: Electrocardiography, in Moss AJ, Adams FH(eds): heart Disease in infants, Children andAdolescents. Baltimore, Williams & Wilkins Co.

1968, pp 183-231.

7. Rubin MI, Rapoport M: Cardiac complication of acutehemorrhagic nephritis. Am I Dis Child 55:244,

1938.8. Gore I, Saphir 0: Myocarditis associated with acute and

subacute glomerulonephritis. Am Heart I 36:300,

1948.

9. Davies CE: Heart failure in acute glomerulonephritis. QI Med 20:163, 1951.

10. De Fazio V, Chrisensen RC, Regan TJ, et al: Circula-

tory changes in acute glomerulonephritis. Circula-‘tion 20:190, 1959.11. Cardozo EL: Hydremia in acute nephritis. Acta �tIed

Scand 125:333, 1946.12. Eisenberg 5: Blood volume in patients with acute

glomerulonephritis as determined by radioactive

chromium tagged red cells. Am I Med 27:241,1959.

13. Ross J Jr. Sobel BE: Regulation of cardiac contraction.Annii Ree Physiol 34:47, 1972.

14. Hirshleifer J, Crawford M, O’Rourke RA, Karliner JS:

Influence of acute alterations in heart rate and

system arterial pressures on echocardiographicmeasures of left ventricular performance in normalhuman subjects. Circulation 54:835, 1975.

15. Anzola J, Rushmer RF: Cardiac responses to sympathet-ic stimulation. Circulation Res 4:312, 1956.

16. Ash R, Mitchell I, Rapaport M: Electrocardiographicvariations in acute glomerulonephritis. Am I Di.s’

Child 67:106, 1944.17. Silverman NH, Lewis AB, Heyman MA, Rudolph AM:

Echocardiographic assessment of ductus arteriosus

shunt in premature infants. Circulation 50:821,

1974.18. Orlando J, Del Vicario M, Aronow \‘iS, Cassidy J:

Correlation of mean pulmonary artery wedge pres-

sure, left atrial dimension and PTF-V in patientswith acute myocardial infarction. Circulation

55:750, 1977.



1979;63;782PediatricsBenderley

Pnina Vardi, Walter Markiewicz, Joseph Levy, Olga Adler, Egon Riss and AbrahamThe Heart in Acute Glomerulonephritis: An Echocardiographic Study

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Pnina Vardi, Walter Markiewicz, Joseph Levy, Olga Adler, Egon Riss and AbrahamThe Heart in Acute Glomerulonephritis: An Echocardiographic Study


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