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| LETTER TO EDITOR |
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| Year : 2015 | Volume
: 25
| Issue : 2 | Page : 125-126 |
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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 |
Correspondence Address:
Dr. A Anitha
903, 21st Main, 38th Cross, 4th T Block, Jayanagar, Bengaluru - 560 041, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0971-4065.145098
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 |
Sir,
Constrictive pericarditis (CP) is reported in 2.4% of renal recipients. [1] 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)
Click here to view |
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. [2] 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. [3] CP is reported in about 2.4%. [1] Calcineurin inhibitors/sirolimus and oppurtunistic infections should be considered as etiologies. [4]
Forty-one cases of CP post renal transplant are reported in the literature. Sever described 34 cases, only one of tubercular etiology. [1] 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. [5] 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.
| References | |  |
| 1. | Sever MS, Steinmuller DR, Hayes JM, Sreem SB, Novick AC. Pericarditis following renal transplantation. Transplantation 1991;51:1229-32.  |
| 2. | Bashi VV, John S, Ravikumar E, Jairaj PS, Shyamsunder K, Krishnaswami S. Early and late results of pericardiectomy in 118 cases of constrictive pericarditis. Thorax 1988;43:637-41. |
| 3. | Jha V, Kohli HS, Sud K, Gupta KL, Minz M, Joshi K, et al. Laryngeal tuberculosis in renal transplant recipients. Transplantation 1999;68:153-5. |
| 4. | Steele GH, Adamkovic AB, Demopoulos LA, Rothrock LC, Caulfield ME, Blum MD, et al. Pericardial effusion coincident with sirolimus therapy: A review of Wyeth's safety database. Transplantation 2008;85:645-7. |
| 5. | Sreejith P, Kuthe S, Jha V, Kohli HS, Rathi M, Gupta KL, et al. Constrictive pericarditis in a renal transplant recipient with tuberculosis. Indian J Nephrol 2010;20:156-8. [ PUBMED]  |
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