Brief Reports

Indian Pediatrics 1999;36: 911-913

Cardiac Status in Post-Streptococcal Acute Glomerulonephritis

From the Departments of Pediatrics and Biochemistry⁺ Al Arab Medical University, Benghazi, Libya and *Department of Pediatrics, All India Institute of Medical Sciences, New Delhi 110 029, India.
Reprint requests: Dr. Harjit Singh, P.O. Box 12836, Dubai - UAE.
Manuscript received: November 11, 1997;
Initial review completed: December 16, 1997;
Revision accepted: April 12, 1999

Post-streptococcal acute glomeruloneph-ritis (PSAGN) is still prevalent in the developing countries. A small proportion of children with PSAGN present to the hospital with heart failure(1). This is assumed to be the result of factors such as acutely rising blood pressure, fluid overload and/or electrolyte imbalance. A possible role of primary myocardial dys- function has received scant attention. The few studies that exist have not used modern techniques to evaluate cardiac function. This is because of the fact that PSAGN is uncommon in the developed world. The present study was undertaken to evaluate the left ventricular status in patients with PSAGN using two-dimensional echocardiography.

Subjects and Methods

Thirty-four children with PSAGN in the age group 3 to 11 years, admitted to Al Fatah Children's Hospital, Benghazi, Libya, were investigated. Diagnosis of the disease was based on clinical presentation and evidence of streptococcal infection (positive throat culture and/or ASO titer >200 TU).

Investigations included complete blood counts, erythrocyte sedimentation rate, complete urinanalysis, ASO titer, blood urea and creatinine, creatinine clearance, fractional excretion of sodium (FENa). An electrocardiogram (ECG), and two-dimensional echocardiogram (2D-echo) were done in all patients. Left ventricular ejection fraction (LVEF) was calculated from left ventricular end-diastolic internal diameter (LVIDed) and left ventricular end-systolic internal diameter (LVIDes) using the following formula:

LVEF = (LVIDed³) _ (LVIDes³) / (LVIDed³)

Corrected QT interval (QT_C) in the ECG was derived from the nomogram based on Bazett's formula; 0.425 second was taken as the upper cut-off point(2).

Results

There were 18 boys and 16 girls with a median age of 7.2 years. Twenty-three children presented with hypertension, nine with left heart failure, and one with hypertensive encephalopathy.

Eight of the nine children with left heart failure were hypertensive on presentation (blood pressures: 140/100, 140/110, 150/110, 140/120, 150/100, 150/110, 120/100 and 160/120  mmHg). All had normal serum electrolytes, three had raised blood urea (65, 73 and 90 mg/dl, respectively). FENa was >1.0 in six patients.

Seventeen patients had preceding pharyn-gitis and nine had pyoderma; one child had both. Throat cultures were positive for group A beta-hemolytic streptococcus in seven patients.

Nineteen of 34 patients had a prolonged QT_C on the ECG. The prolonged QT_C had no relation to the biochemical profile (Table I). None of these patients had hypocalcemia and 5/19 were normotensive on admission and remained so till the time of investigation.

Table I^__Biochemical Profile of Children with PSAGN in Relation to QT_C .

Values represent mean ± SD (range).

p >0.05 for all comparisons.

* Number of patients 14 in the group with normal QT_C.

Three of 34 patients had a LVEF less than 50%. Two of these patients were hypertensive on presentation, and two had FENa >1.0. One patient had raised blood urea, hyponatremia and hyperkalemia. All these patients had prolonged QT_C. All the three patients recovered completely.

One of these patients, a nine-years-old girl, was admitted with left heart failure. She was hypertensive, had a QT_C of 0.49 second, and LVEF 11%. This patient was followed for six months during which the left ventricular function recovered completely (LVEF = 51%, QT_C 0.41 second). This patient became normotensive by day 28 but continued to have prolonged QT_C up to day 90.

Discussion

In the present study 3/34 patients with PSAGN had decreased LVEF which provides objective evidence of decreased left ventricular function. In two of these patients dysfunction and prolonged QT_C at onset may be explained by hypertension. However, one patient was normotensive and another one persisted with both abnormalities two months after blood pressure returned to normal range.

Prolonged QT_C recorded in 19/34 patients, including the three with decreased LVEF, may also be an indicator of myocardial dysfunction in some cases since 5/19 children with prolonged QT_C were normotensive.

In a recent study on PSAGN(1), heart failure was recorded in 13/50 patients. One of these

was normotensive at presentation, two had hyponatremia and five hyperkalemia. ECG changes were recorded in 27/42 children with hypertension and 3/8 patients with normal blood pressure. Prolonged QT_C was the most common abnormality, present in 15/42 hypertensive patients and 1/2 normotensive children. Heart failure in normotensive children was ascribed to myocarditis.

Seick et al.(3) in a case report on PSAGN with rheumatic fever occuring together in one patient, recorded an impaired left ventricular systolic function (LVEF = 27%). However, in a study of left ventricular hemodynamics in PSAGN, Kamisago and Hirayama(4) recorded increased left ventricular contractility and afterload, mainly due to preload.

Both acute rheumatic fever and PSAGN share a common pathogenesis and rarely can coexist. Furthermore, a variety of renal pathological changes have been recorded in acute rheumatic fever. These include focal proliferative glomerulonephritis and interstitial neph-ritis(5). These changes provide indirect evidence of existence of pathological changes more widespread than the clinical expression of the disease.

Kaplan and co-workers(6) have demonstrated transient multiorgan vasculitis, including that of the central nervous system in PSAGN. Myocarditis is occasionaly documented in PSAGN(7). It is likely that myocarditis and/or vasculitis may explain depressed left ventricular function in some cases of PSAGN.

References

1. Banapurmath CR, Zacharias TS, Somashekhar KS, Abdul Nazer PU. Congestive cardiac failure and electrocardiographic abnormalities in acute glomerulonephritis. Indian Pediatr 1996; 33: 589-592.

2. Singh H. Pediatric Companion. New Delhi, Interprint, 1996; p 124.

3. Seick JO, Awad M, Saour J, Ali H, Quinibi W, Mercer E. Concurrent post-streptococcal carditis and glomerulonephritis: Serial electrocardiographic diagnosis and follow-up. Eur Heart J 1992; 13: 1720-1723.

4. Kamisago M, Hirayama T. Echocardiographic evaluation of left ventricular hemodynamics in children with post-streptococcal acute glomerulonephritis. Nippon-Ika Diagaku Zasshi 1994; 61: 306-314.

5. Gibney R, Reineck HJ, Bannayan GA, Stein JH. Renal lesions in acute rheumatic fever. Ann Int Med 1981; 94: 322-326.

6. Kaplan RA, Zwick DL, Hellerstein S, Warady BA, Alon U. Cerebral vasculitis in acute post-streptococcal glomerulonephritis. Pediatr Nephrol 1993; 7: 194-195.

7. Gore I, Saphir O.Myocarditis associated with acute and subacute glomerulonephritis. J Pediatr 1996; 69: 390-402.