ObjectiveThe standard anti-tuberculosis (TB) regimen occasionally causes acute kidney injury (AKI). The major etiology is rifampicin-induced acute interstitial nephritis. However, the standard management of AKI induced by anti-TB drugs has yet to be established. Methods We retrospectively reviewed patients with TB who developed AKI after starting standard anti-TB treatment between 2006 and 2016 at a single TB center. The clinical characteristics and the management are described. Results Among 1,430 patients with active TB, 15 (1.01%) developed AKI. The mean age (standard deviation) was 61 years (18). The median (interquartile range) time to AKI development was 45 days (21-54 days). The median serum creatinine level before anti-TB treatment was 0.7 mg/dL (0.5-1.4 mg/dL), whereas the median peak serum creatinine level after AKI onset was 4.0 mg/dL (3.08-5.12 mg/dL). Five patients (33.3%) were pathologically confirmed as having acute interstitial nephritis (AIN), and 7 patients (46.7%) had a clinical diagnosis of the disease. All anti-TB drugs were stopped, and steroids were administered to 5 (100%) patients with pathologically confirmed AIN and 3 (42.8%) patients with clinically diagnosed AIN. The renal function was normalized in 12 patients (80.0%) after restarting anti-TB treatment without rifampicin (n=12) or isoniazid (n=1). Two patients died due to severe renal failure after restarting rifampicin. Conclusion Rifampicin is the leading cause of AKI. Levofloxacin may be an alternative to rifampicin thanks to its safety and potency. Restarting anti-TB treatment without rifampicin and short-term steroid administration may be a feasible management for AKI.

This study examined Mycobacterium tuberculosis (MTB)-secreted MPT64 as a surrogate of bacterial viability for the diagnosis of active pulmonary TB (PTB) and for follow-up treatment. Methods: In this proof-of-concept prospective study, 50 PTB patients in the Tokyo metropolitan region, between 2017 and 2018, were consecutively included and 30 healthy individuals were also included. Each PTB patient submitted sputum on days 0, 14 and 28 for diagnosis and follow-up, and each healthy individual submitted one sputum sample. The following were performed: smear microscopy, Xpert MTB/RIF, MGIT and solid culture, and MPT64 detection on the sputum samples. Ultrasensitive ELISA (usELISA) was used to detect MPT64. The receiver operating characteristic analyses for diagnosis and follow-up revealed the optimal cut-off value of MPT64 absorbance for detecting culture positivity at multiple intervals. Results: The sensitivity of MPT64 for diagnosing PTB was 88.0% (95% CI 75.7-95.5) and the specificity was 96.7% (95% CI 82.8-99.9). The specificity of MPT64 for predicting negative culture results on day 14 was 89.5% (95% CI 66.9-98.7). The sensitivity of MPT64 for predicting positive culture results on day 28 was 81.0% (95% CI 58.1-94.6). Conclusions: This study revealed that MPT64 is useful for diagnosing active PTB in patients and predicting treatment efficacy at follow-up.

The Author Replies We appreciate Dr. Fukuchi and colleagues for their prompt comment on our article. We describe the details of the two patients who died. One patient was referred to our hospital because his acute kidney injury (AKI) relapsed after Rifampicin (RIF) desensitization in a previous hospital. His renal function did not improve despite stopping all anti-tuberculosis (TB) drugs and administering steroids. When the patient was transferred to our hospital, his blood pressure was <80 mmHg, and he had severe delirium. We sedated him and started continuous renal replacement therapy (CRRT). However, the patient could not tolerate CRRT due to his unstable vital signs and continuing delirium. In addition, he developed massive pleural effusion and generalized edema. The patient finally developed severe bacterial pneumonia and died of respiratory failure three days after his referral to our hospital. Therefore, we were unable to restart the anti-TB drugs. The other patient was over 80 years old and developed AKI after Isoniazid, RIF and Ethambutol administration. The patient had severe malnutrition when diagnosed with active pulmonary TB. We stopped all anti-TB drugs and administered steroids. After his renal function improved, we started RIF desensitization. However, his AKI relapsed only a short while later. The patient's general condition did not recover, and he became continuously bedridden. He finally developed aspiration pneumonia and acute respiratory distress syndrome. His ultimate cause of death was respiratory failure. The author states that he has no Conflict of Interest (COI).

The hemolytic titer of cynomolgus monkeys was greater than the titer measured in human serum. However, human DAF showed nearly the same complement regulatory function in both human and cynomolgus monkey sera.

The bronchoscopy, though usually safe, is occasionally associated with complications, such as pneumonia. However, the use of prophylactic antibiotics is not recommended by the guidelines of the British Thoracic Society. Thus far there are few reports of the risk factors for post-bronchoscopy pneumonia; the purpose of this study was to evaluate these risk factors. We retrospectively collected data on patients in whom post-bronchoscopy pneumonia developed from the medical records of 2,265 patients who received 2666 diagnostic bronchoscopies at our institution between April 2006 and November 2011. Twice as many patients were enrolled in the control group as in the pneumonia group. The patients were matched for age and sex. In total, 37 patients (1.4%) had post-bronchoscopy pneumonia. Univariate analysis showed that a significantly larger proportion of patients in the pneumonia group had tracheobronchial stenosis (75.7% vs 18.9%, p < 0.01) and a final diagnosis of primary lung cancer (75.7% vs 43.2%, p < 0.01) than in the control group. The pneumonia group tended to have more patients with a history of smoking (83.8% vs 67.1%, p = 0.06) or bronchoalveolar lavage (BAL) (4.3% vs 14.9%, p = 0.14) than the control group. In multivariate analysis, we found that tracheobronchial stenosis remained an independent risk factor for post-bronchoscopy pneumonia (odds ratio: 7.8, 95%CI: 2.5–24.2). In conclusion, tracheobronchial stenosis was identified as an independent risk factor for post-bronchoscopy pneumonia by multivariate analysis in this age- and sex- matched case control study.