To the editor

In their recent article published in Polish Archives of Internal Medicine, Siek et al1 described an interesting case of tuberculosis (TB) in a kidney allograft. Although the findings reported have considerable clinical value, there are certain issues that require clarification.

Tuberculosis is caused by a number of Mycobacterium species, collectively referred to as the Mycobacterium tuberculosis complex (MTBC), which includes M. tuberculosis, M. africanum, M. canettii, M. bovis, M. bovis BCG, M. microti, M. caprae, M. pinnipedii, M. suricatta, M. mungi, and M. orygis.2 The most commonly encountered and important agent of TB in humans is M. tuberculosis. MTBC constitutes a notably genetically homogeneous group. Nontuberculous mycobacterial (NTM) species play pathological roles in development of chronic inflammatory lung damage, which is classified as a particularly complex group of NTM pulmonary diseases. Consequently, simply indicating that TB is caused by Mycobacterium species is insufficient.

In addition, the authors do not mention imaging tests for detecting pulmonary TB, such as chest X-ray or chest computed tomography (CT). It might have been worth investigating TB by searching for more disseminated disease. Of note, post-transplant TB affects the respiratory system in 50% of patients, with subsequent progress to disseminated disease in 30% of cases.3 Pulmonary TB can develop as a consequence of hematogenous TB spread from transplanted kidneys. Given that chest X-rays are routinely performed prior to conducting transplant procedures, it would thus be interesting to compare X-ray images obtained before and after transplantation. Chest CT is more sensitive than chest radiography in detection and characterization of both subtle localized or disseminated parenchymal disease and mediastinal lymphadenopathy.4

In the case described by Siek et al,1 TB was apparently confirmed on the basis of a positive acid-fast bacillus smear from material collected using ultrasound-guided percutaneous puncture. Nonetheless, there is no information on results of molecular analyses (polymerase chain reaction), which can rapidly confirm MTBC infection and identify a mutation associated with rifampicin resistance. In this regard, rapid molecular diagnostic tests, such as Xpert MTB/RIF (Cepheid, Sunnyvale, California, United States), are widely recommended by the World Health Organization as an initial investigation for diagnosis of pulmonary and extrapulmonary TB, as well as resistance to anti-TB agents.5 Ideally, such tests should be performed prior to initiating appropriate therapy in all TB patients. What is more, Siek et al1 do not present results regarding the culture of MTBC and drug sensitivity tests. Culturing using available liquid media remains the gold standard method for bacteriological confirmation of TB, and still plays a key role in the diagnosis of TB from paucibacillary samples and in the differential diagnosis of NTM infection. It would have been interesting to know if any sputum was available and whether smear tests were performed or bronchial washings collected. Additionally, it would have been reasonable to obtain urine samples for the Xpert MTB/RIF test and culture.

Finally, assuming a diagnosis of drug-susceptible TB, the duration of antituberculous treatment (ATT) appears to have been exceptionally long in this case. The patient was treated for 2 years, on account of persistent focal lesions in the transplanted kidney. The authors provide no clear explanation for this seemingly excessively long treatment. With the exception of instances of central nervous system, bone, or joint involvement, a traditional 6-month regimen is recommended in the cases of both pulmonary and extrapulmonary TB. Moreover, it was not confirmed whether the intensive and continuation phases of the therapy were followed. It would be interesting to learn whether such prolonged treatment was tolerated well by the patient. Also, it would be worthwhile to show information pertaining to any side effects during this long ATT, such as drug-induced liver injury, the risk of which has been established to range from 5% to as high as 33%.6

Although it is appreciated that given strict word limitations it might be difficult to present details relating to all these issues, a consideration of these points would undoubtedly make this case report more complete.