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CLINICAL BRIEF

Pericardial Tamponade in Nephrotic Syndrome:

An Uncommon Complication

Sunita Namdev   &  Sriram Krishnamurthy   &

Niranjan Biswal   &  Barath Jagadisan

Received: 22 March 2012 /Accepted: 3 July 2012 /Published online: 20 July 2012# Dr. K C Chaudhuri Foundation 2012

Abstract  An 11 y   – old boy with steroid resistant nephrotic

syndrome (SRNS) secondary to focal segmental glomerulo-

sclerosis (FSGS) developed pericardial tamponade duringthe course of illness. He was promptly managed with peri-

cardiocentesis. Pericardial tamponade is an extremely rare

complication in childhood nephrotic syndrome and very few

cases have been reported in literature. Recognition of this

rare, yet serious and life threatening complication in child-

hood nephrotic syndrome (NS) is emphasized to prevent 

fatalities in children with nephrotic syndrome.

Keywords  Pericardial tamponade . Nephrotic syndrome .

Steroid resistance . Focal segmental glomerulosclerosis

Introduction

Fluid retention in nephrotic syndrome (NS) often leads to

 peripheral edema, ascites, and pleural effusions. Intuitively,

 pericardial effusions could be anticipated as well, but liter-

ature is scarce regarding this complication in NS [1, 2]. The

authors herein describe an 11 y-old boy with NS who

developed pericardial tamponade.

Case Report

An 11 y-old boy presented to the authors’ hospital in August 

2011 with anasarca and oliguria. There was no hematuria,

rash, joint swelling, fever or jaundice. His blood pressure

was 130/90 mm Hg (>95th centile). Cardiovascular and

chest examination were normal. Investigations showed mas-sive proteinuria (urine protein 3+, urinary protein/creatinine

ratio03.1), hypoalbuminemia (1.8 g/dl) and hypercholester-

olemia (780 mg/dl). Blood urea, serum creatinine and T3,

T4, TSH levels were normal. He was treated with prednis-

olone (2 mg/kg) and amlodipine. However, proteinuria (4+)

 persisted even after 4 wk. In view of steroid resistance, he

underwent a renal biopsy, which revealed focal segmental

glomerulosclerosis (FSGS), with immunofluorescence

showing IgM and C3 deposits. He was then treated with

cyclosporine, prednisolone and enalapril. Due to uncon-

trolled hypertension, he required additional treatment with

 prazosin and atenolol.

After completion of 3 mo of cyclosporine therapy, he

continued to have hypoalbuminemia (1.9 g/dl) and massive

 proteinuria (4+). He was admitted for edema control with

diuretics (frusemide and spironolactone), without much suc-

cess. Albumin infusion could not be given due to persistent 

hypertension.

On the seventh day of admission, he developed tachyp-

nea (respiratory rate of 40/min), pulse rate 100/min with

 pulsus paradoxus. Heart sounds were muffled. Chest radio-

graph showed massive cardiac enlargement (Fig.   1); elec-

trocardiogram showed low QRS voltages. Echocardiogram

confirmed pericardial tamponade with right atrium and right 

ventricular collapse (Fig.   2). Blood urea and serum creati-

nine were normal. Pericardiocentesis was done and 400 ml

of fluid drained. Pericardial fluid was clear with no cells;

 protein was 150 mg/dl, glucose was 90 mg/dl; Gram stain

and polymerase chain reaction (PCR) for tuberculosis were

negative. The pericardial fluid protein: serum protein was

0.3, while pericardial fluid LDH: serum LDH was 0.4,

suggestive of a transudate. Pericardial fluid culture was

sterile. He had significant clinical improvement and the

S. Namdev : S. Krishnamurthy : N. Biswal (*) : B. Jagadisan

Department of Pediatrics, Jawaharlal Institute of Postgraduate

Medical Education and Research (JIPMER),

Pondicherry 605006, India 

e-mail: drnbiswal@yahoo.com

Indian J Pediatr (July 2013) 80(7):598 – 600

DOI 10.1007/s12098-012-0858-x

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 pigtail catheter was removed. Repeat echocardiogram 1 wk 

later showed no effusion. Anti-nuclear antibody (ANA),

dsDNA and anti-neutrophil cytoplasmic antibody (ANCA),

C3 levels, HBsAg and HIV serology were negative. Ultra-

sonogram showed normal size, shape and echotexture of the

kidneys and ureters.

Proteinuria (4+) continued to persist despite cyclosporine

therapy. Thereafter he demonstrated worsening urea and

creatinine over a period of 2 wk (blood urea 108 mg/dl,

creatinine 3.6 mg/dl) with oliguria. In view of nephrotoxicity,

cyclosporine and enalapril were discontinued. Treatment with

mycophenolate mofetil and plasmapheresis were initiated

which led to improvement in edema and partial remission of 

 proteinuria (2+) on follow up with a weight loss of 3 kg andserum albumin 2.6 g/dL.

Discussion

Edema, one of the major clinical manifestations of the

 NS, results from hypoalbuminemia which diminishes the

colloid osmotic pressure of plasma leading to seepage

of fluid from intravascular into interstitial compartment,

with contraction of plasma volume causing salt and

water retention [3,   4]. Large pericardial effusions are

very rare in childhood idiopathic nephrotic syndrome.Pericardial effusion has been also described to occur in

idiopathic NS as well as systemic lupus erythematosus

(SLE)- associated NS [2,   5 – 7]. The index patient did

not satisfy biochemical, histopathological or clinical criteria 

for the diagnosis of SLE. Investigations for secondary

etiology (ANA, dsDNA, ANCA, C3 levels, HBsAg and

HIV serology) were also negative.

Pericardial tamponade is an even rarer complication in

 NS. On MEDLINE search, the authors could find only two

reports of pericardial tamponade in association with child-

hood NS. The first was an 8 y- old Turkish girl with

idiopathic steroid resistant NS (due to FSGS) on cyclospor-

ine therapy, similar to the present case, who developed life

threatening pericardial tamponade, attributed to fluid over-

load, diminished glomerular filtration rate and hypoalbumi-

nemia; managed with pericardiocentesis [1]. The other 

report describes a 4 y-old Indian girl with steroid-resistant 

 NS (Minimal change disease) who developed chylopericar-

dial tamponade secondary to superior vena cava thrombosis

[8]. In the index case , pericardial tamponade was transuda-

tive, non-chylous, and occurred possibly due to hypoalbu-

minemia and fluid overload [7]. There are anecdotal reports

of cyclosporine in association with pericardial effusion in

 patients undergoing cardiac transplantation; this could also

have been contributory in the index patient [9]. Other causes

such as hypothyroidism, tuberculosis and SLE were ruled

out by appropriate investigations. Since the renal function

tests at the time of detection of pericardial effusion were

normal, it is unlikely that pericardial effusion was a 

manifestation of uremia. Similarly, pericardial effusions

due to viral infections   e.g.,   echovirus or coxsackievirus

were unlikely since the nature of the pericardial effusion

was transudative.

Fig. 1   Chest x-ray of the patient showing massive cardiac enlargement 

a  before and  b   after pericardiocentesis

Fig. 2   Echocardiogram showing pericardial tamponade with right 

atrium and ventricular collapse.  PE   Pericardial tamponade;  RA   Right 

atrium;  RV   Right ventricle;  LA  Left atrium;  LV   Left ventricle

Indian J Pediatr (July 2013) 80(7):598 – 600 599

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In conclusion, the authors emphasize that although

 pericardial tamponade is exceedingly rare in childhood

 NS, recognition of this serious complication in children

with NS complicated by respiratory distress, is essential

to initiate a prompt and life saving pericardiocentesis.

Conflict of Interest   None.

Role of Funding Source   None.

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