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Table of Contents
CASE REPORT
Year : 2017  |  Volume : 11  |  Issue : 3  |  Page : 168-170

Esophageal tuberculosis and infected tuberculous lymphocele: Unusual case presentations of tuberculosis in postrenal transplantation


Department of Nephrology, MIOT International, Chennai, Tamil Nadu, India

Date of Web Publication20-Dec-2017

Correspondence Address:
Dr. B Balaji Kirushnan
Departments of Nephrology, MIOT International, 4/112, Mount Poonamallee Road, Manapakkam, Chennai - 600 089, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijot.ijot_8_17

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  Abstract 


Tuberculosis is one of the most common opportunistic infections noted after renal transplantation. It can present in unusual ways making it a diagnostic challenge. Gastrointestinal tuberculosis after renal transplantation is rarely reported. We present 2 rare cases of gastrointestinal tuberculosis that was diagnosed promptly and treated.

Keywords: Tuberculosis, renal transplant, lymphocele, esophageal ulcer


How to cite this article:
Kirushnan B B, Akhil MS, Arumugam K, Ravichandran R. Esophageal tuberculosis and infected tuberculous lymphocele: Unusual case presentations of tuberculosis in postrenal transplantation. Indian J Transplant 2017;11:168-70

How to cite this URL:
Kirushnan B B, Akhil MS, Arumugam K, Ravichandran R. Esophageal tuberculosis and infected tuberculous lymphocele: Unusual case presentations of tuberculosis in postrenal transplantation. Indian J Transplant [serial online] 2017 [cited 2019 Oct 19];11:168-70. Available from: http://www.ijtonline.in/text.asp?2017/11/3/168/221198




  Introduction Top


The incidence of tuberculosis (TB) in solid-organ transplant (SOT) recipients is higher compared with general population but varies by geographical location.[1] In areas with low endemicity of TB, the prevalence among SOT recipients is 0.5%–6.4% while it has been reported to be as high as 15.2% in highly endemic areas.[2],[3] Solid-organ recipients are more vulnerable as they are immunosuppressed.[4] Other infections such as cytomegalovirus (CMV) can downgrade immunity and activate occult TB. The diagnosis of TB in transplant recipient is delayed in view of the atypical presentations, increased likelihood of negative tuberculin skin tests, and interferon-gamma release assay.[5] The multidrug-resistant strains of TB add to the burden and they are associated with high mortality.[6] It accounts for the high morbidity and worsens the economic burden of patients, especially those in lower socioeconomic strata. The incidence of TB in renal allograft recipients is 12.3% as of 2003 in a study from India.[7] However, later reports of TB in postrenal transplant recipients have not been reported probably due to varied atypical presentations where diagnosis was not established.


  Case Reports Top


We report two unusual cases of TB in postrenal transplant patients.

Case 1: Tuberculous esophageal ulcer

A 48-year-old male who was diagnosed to have chronic kidney disease due to hypertension with a solitary kidney underwent deceased donor renal transplantation on September 26, 2014, after a waiting period of 3 years on twice weekly hemodialysis. Blood group of donor and recipient was A positive. Donor was a 43-year-old road traffic accident victim with no comorbidities and serum creatinine of 1.0% mg. Crossmatch testing done by complement-dependent cytotoxicity was negative. B-cell flow crossmatch was positive with median channel shift value of 75; however, T-cell flow crossmatch was negative. Donor-specific antibodies to HLA Class I and II were negative. He received thymoglobulin 1 mg/kg for 3 days as induction regimen. Postoperatively, he had no surgical complications and creatinine was 1.2% mg on postoperative day 6. He had new-onset diabetes mellitus after transplant which was managed with oral hypoglycemic agents. He had no episodes of rejection and was compliant to therapy. He was maintained on prednisolone 7.5 mg/day, tacrolimus 3.5 mg/day, and mycophenolate sodium 720 mg twice daily. Tacrolimus levels were serially monitored and it was around 6 ng/ml. Six months after renal transplant, he had complaints of dyspepsia with heartburn which was not responding to a trial of oral proton-pump inhibitors. Upper gastrointestinal (GI) endoscopy showed esophageal ulcer. CMV viral load was less than lower detectable limit empirical treatment with acyclovir was given for 5 days. Endoscopy ulcer biopsy was suggestive of necrotizing granulomatous inflammation with a possibility of TB. Acid-fast stain (AFB) stain in the endoscopic biopsy was negative. Computed tomography (CT) abdomen and thorax was not done as the patient could not afford for the same. Blood interferon-gamma release assay (TB Quantiferon gold) was positive. C-reactive protein was 11.1. He was initiated on T. Isoniazid 300 mg/day, T. Ethambutol 1000 mg/day, T. Pyrazinamide 1500 mg/day, and T. Ciprofloxacin 1000 mg/day. Rifampicin was avoided contemplating drug interaction with immunosuppressive drugs. The dose of mycophenolate was reduced to 540 mg twice daily. He improved symptomatically and was doing well. In August 2015, he was seen by gastroenterologist for repeat endoscopy which showed partial regression and healing of the ulcer. Repeat C-reactive protein was 5.4. He was on four drugs for 1 year after which he is continued on isoniazid 200 mg/day as prophylaxis. There was no change in the graft function following reduction in the immunosuppression.

Case 2: Lymphocele tuberculosis

A 50-year-old male patient who had chronic kidney disease due to biopsy-proven IgA nephropathy was initiated on weekly thrice hemodialysis in 2006. He underwent live-related renal transplant elsewhere on August 7, 2007, with donor being his brother. There was a haplomatch and crossmatch by CDC was negative. Flow crossmatch and donor-specific antibody were not available. There was no induction agent used. The patient came for follow-up after transplantation to our hospital. Postrenal transplant, his best creatinine was 1.6% mg after 2 months. He was on triple immunosuppression with prednisolone 12.5 mg, cyclosporine 125 mg in the morning and 100 mg at night, and mycophenolate mofetil 500 mg three times a day. He had the right lower limb swelling noticed 21 days after transplant, and ultrasound showed a collection of 500 ml inferoposterior to the transplant kidney. Venous Doppler of the left lower limb did not show evidence of deep vein thrombosis. Collection was aspirated, and drain fluid urea and creatinine were near the same with the serum. Lymphocele was diagnosed. One month later, a repeat ultrasound still showed the persistence of collection of approximately 300 ml. As there were no edema, no hydronephrosis, and azotemia, it was decided to monitor the lymphocele periodically. Three months after transplant, he also had CMV infection for which he was started on valganciclovir 900 mg/day for 21 days and followed by CMV prophylaxis 450 mg/day for 6 months.

In December 2010, he was admitted with fever. Blood and urine culture showed no growth. Ultrasonography abdomen showed transplant kidney hydronephrosis with a cystic collection inferomedial to the transplant kidney. There was no worsening of azotemia. He was treated with empirical intravenous antibiotics cefotaxime 1 g twice daily.

He was having low-grade fever intermittently and was readmitted after 1 month after the previous episode for evaluation. CT abdomen showed complicated thick wall collection inferomedial to the transplant kidney. Midline infraumbilical laparotomy was done and lymphocele drainage was done. Thick-walled lymphocele with brown-colored fluid was aspirated and AFB smear was positive, TB polymerase chain reaction was positive. AFB culture was positive after 2 weeks and was identified as Mycobacterium tuberculosis complex. He was initiated on four drugs; T. Isoniazid 300 mg once daily, T. Ethambutol 800 mg once daily, T. Pyrazinamide 750 mg twice daily, and T. Ciprofloxacin 500 mg twice daily. After 2 months, he was continued on isoniazid and ethambutol for a total of 12 months. He is asymptomatic and doing well. Annual repeat ultrasound done 1 year later showed no collection around the transplant kidney

Diagnosis and treatment of active TB in transplant recipients is challenging due to their diverse pulmonary and nonpulmonary conditions mimicking TB. Transplant patients are also at risk for significant interactions with immunosuppressive drugs. Direct evidence for the management of transplant recipients for the prevention and treatment of TB is lacking, and decisions are largely based on expert opinion and extrapolation from immunocompetent and other immunocompromised populations. Although TB may affect any transplanted patient, recipients of lung transplants have the highest rate of TB relative to other transplanted organs.[8] This is not surprising since the lung is the primary portal of entry for M. tuberculosis. Other factors that may affect the incidence of TB include advanced age, HCV infection in kidney transplant recipients, diabetes mellitus, the use of T-cell depleting antibodies, enhanced immunosuppression in the setting of rejection, and hemodialysis in renal transplant recipients.[8] As per the data in 1998 from the University of Pittsburgh, most transplant patients present with pulmonary TB (51%), 33% have disseminated TB, and 16% have extrapulmonary disease of other organs.[8] TB has been reported to be present from a variable duration of 1 month to 10 years after transplant. Radiographic evidence of past TB and positive tuberculin skin test in the pretransplant period is associated with earlier onset of disease. The use of lymphocyte-depleting antibodies for induction in renal transplants has been shown to have an earlier onset of TB than those who receive other types of induction therapies.[8] Hallmark symptoms of TB, i.e., fever and constitutional symptoms, such as night sweats and weight loss are not universal in transplant patients. Fever, for example, was seen in 64% of transplant recipients with localized disease and in 91% with disseminated disease.[2] In patients with pulmonary disease, a wide range of radiographic manifestations, including focal infiltrate, miliary pattern, nodules, pleural effusions, diffuse interstitial infiltrates, and cavitatory disease has been described.[8] The risk of adverse outcomes following TB among SOT recipients is increased compared to nonimmunocompromised patients. Mortality rates of 19%–40% have been described which represents a 10-fold increase compared to the overall mortality of TB.[9] In addition, complex interactions between the agents used to treat TB and the agents typically used to prevent rejection may result in allograft loss in up to one-third of cases.[10]

Esophageal TB is rare, even in endemic areas. It accounts for 0.3% of all reported GI TB cases.[11] This is probably because of stratified squamous epithelium and peristalsis of the esophagus that prevents stasis of infected mucus if any. Reported cases are due to direct extension from the lungs, mediastinal lymph nodes, and the thoracic spine.[12] Endoscopic features of TB are variable and nonspecific. While TB can affect any segment of the esophagus, it occurs most commonly at the mid-esophagus because of its proximity to the hilar and mediastinal lymph nodes around the bifurcation of the trachea, and the most common macroscopic endoscopic finding is a solitary shallow linear ulcer with smooth edges and a necrotic base.[12] Rarely, it may mimic a neoplasm with a mass lesion or a stricture. Odynophagia and dysphagia are the most common symptom which was there in our patient too.[12] Jarret et al. describe a case of GI TB after renal transplant with fever, abdominal pain, and GI bleeding as the presenting symptom.[13] There was a case report of an esophageal ulcer in a simultaneous pancreas-kidney transplant recipient from the United Kingdom.[14] The same patient received treatment with four primary antitubercular drugs, and there was shrinkage in the ulcer demonstrated in the repeat endoscopy.

Lymphocele TB after transplant has been described in the literature. Tuberculous paranephric abscess which was treated medically was described by Wong et al. in 1999.[15] Recently, tuberculous lymphocele was reported in a 53-year-old woman after live renal transplantation.[16] However, the authors, in this case, pointed out TB to be donor derived in view of very early occurrence after transplant. The late occurrence after transplant rules out donor-derived sources. We hypothesize that lymphocele could have got infected with tubercle bacilli through lymph nodes in the pelvic region.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Baijal R, Agal S, Amarapurkar DN, Kumar HR, Kotli N, Jain M. Esophageal tuberculosis: An analysis of fourteen cases. J Dig Endosc 2010;1:14-18.  Back to cited text no. 12
    
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Jarrett O, Grim SA, Benedetti E, Clark NM. Gastrointestinal tuberculosis in renal transplant recipients: Case report and review of the literature. Transpl Infect Dis 2011;13:52-7.  Back to cited text no. 13
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Rahmatulla S, Marshall A, Bhagani S, Jones GL, Gale DP. Esophageal tuberculosis infection in a simultaneous pancreas and kidney transplant recipient. Gen Med (Los Angel) 2014;2:144.  Back to cited text no. 14
    
15.
Wong TY, Szeto CC, Ho KK, Leung CB, Li PK. Successful medical eradication of tuberculous paranephric abscess in renal transplantation. Nephrol Dial Transplant 1999;14:1288-90.  Back to cited text no. 15
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Al-Nesf MA, Al-Ani OI, Al-Ani AA, Rashed AH. Renal allograft tuberculosis with infected lymphocele transmitted from the donor. Saudi J Kidney Dis Transpl 2014;25:370-5.  Back to cited text no. 16
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