|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 2 | Page : 125-126
Tubercular constrictive pericarditis after renal transplantation
A Anitha1, V Siddini2, HS Ballal2
1 Department of Nephrology, Manipal Hospital, Salem, Tamil Nadu, India
2 Department of Nephrology, Manipal Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||26-Nov-2014|
Dr. A Anitha
903, 21st Main, 38th Cross, 4th T Block, Jayanagar, Bengaluru - 560 041, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Anitha A, Siddini V, Ballal H S. Tubercular constrictive pericarditis after renal transplantation. Indian J Nephrol 2015;25:125-6
Constrictive pericarditis (CP) is reported in 2.4% of renal recipients.  A 40-year-old teacher, with presumed chronic interstitial nephritis underwent transplantation in 2004 (donor-6 antigen matched brother). Immunosuppression was mycophenolate mofetil (MMF), cyclosporine and steroids till 2012; MMF and steroids later. There were no rejections; serum creatinine was 0.8 mg/dl.
Two months after a febrile illness she noticed exhaustion, pedal edema and 6 kg weight gain. She had no pallor, was afebrile, BP was 100/70 mmHg. Heart sounds were muffled, jugular venous pressure elevated and there was hepatomegaly. Investigations showed creatinine 1.13 mg/dl, trace proteinuria without active sediments, hypoalbuminemia (2.1 g/dl). Clinical suspicion of CP was confirmed by cardiomegaly on X-ray, pericardial thickening on echocardiogram, 6 mm effusion on computed tomography scan with mediastinal lymphadenopathy.
Pericardiectomy tissue was TB - polymerase chain reaction (PCR) positive; histology showed caseating necrosis [Figure 1]. She received anti-tubercular treatment (ATT) (isoniazid, rifampicin, ethambutol, pyrazinamide); MMF was changed to azathioprine. After 3 months, she was asymptomatic with normal graft and liver functions.
|Figure 1: Pericardial tissue showing granuloma with central coagulative necrosis along with langhans' giant cell (x20 H and E stain)|
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Chronic CP, a sequelae of healing pericarditis, obliterates pericardial cavity, interferes with ventricular filling and cardiac output. TB remains common etiology, especially in developing countries.  Clinical features are weakness, cachexia; edema and ascites. Examination findings are feeble apical pulse, muffled heart sounds, distended neck veins, hepatomegaly and jaundice. Electrocardiography displays low voltage complexes, flattened or inverted T-waves and atrial fibrillation. X-ray demonstrates cardiomegaly and pericardial calcification. Echocardiogram shows pericardial thickening and effusion, distended inferior vena cava and hepatic veins, left shift of the ventricular septum during inspiration. Pericardiectomy relieves constriction; operative mortality is 5-10%; histopathology may reveal the etiology.
In patients with chronic kidney disease, uremia or effusion due to under-dialysis, hypoalbuminemia or volume overload contribute to pericarditis. TB remains a differential diagnosis. However, CP is rare.
Tuberculosis occurs in 10-13% of renal recipients.  CP is reported in about 2.4%.  Calcineurin inhibitors/sirolimus and oppurtunistic infections should be considered as etiologies. 
Forty-one cases of CP post renal transplant are reported in the literature. Sever described 34 cases, only one of tubercular etiology.  One Presumed chronic glomerulo nephritis, with exudative pleural effusion, treated with 4 weeks of ATT pre-transplant, developed idiopathic CP while on modified ATT 4 months post-transplant.  Another case from Sri Lanka had pericardial effusion (fluid: Acid-Fast Bacilli negative) and positive tuberculin test while on dialysis; underwent transplantation after 6 months of ATT and developed CP 6 years post-transplant. Five other cases of CP of unknown etiology are reported in the literature.
Our case was the only CP among 466 renal transplants (2004-2014); 8 (1.7%) had TB. She did not have TB pre-transplant, was not on Cyclosporine, cumulative immunosuppression was minimal and TB was confirmed by histopathology and PCR. CP is extremely rare; can occur at any time post-transplant. High degree of suspicion, pericardiectomy along with ATT can prevent graft dysfunction.
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