3 mg/dL on 9 October 2012. He was admitted to our hospital for an episode biopsy on 16 October. On admission, he was in good condition, and the results BAY 80-6946 mouse of physical examination were normal. The clinical course is shown in Figure 1. Laboratory findings indicated allograft dysfunction (S-Cr, 3.7 mg/dL) with mild proteinuria (500 mg/day), and the serum trough

TAC level was 1.8 ng/dL. An abdominal CT revealed swelling of the transplanted kidney. On scintigraphy, the transplanted kidney took up a great deal of gallium. Histologically, kidney infiltration by diffuse aggressive tubulointerstitial inflammatory cells was evident, and both severe tubulitis and mild intimal arteritis were observed (Fig. 2A–C). Also, the peritubular capillaries showed evidence of infiltration by inflammatory cells (including neutrophils) (Fig. 2D). No medial arteriolar hyalinosis or interstitial fibrosis/tubular atrophy was observed. Detailed laboratory examination detected neither donor-specific antibody in serum nor C4d immunoreactivity of the peritubular capillaries. We thus diagnosed our patient with acute vascular rejection corresponding to Class ACR IIA of the Banff 2007 criteria. We treated him with 3 consecutive days of intravenous steroid pulse therapy (methylprednisolone, 500 mg/day) twice weekly and the

TAC dose was increased to 12 mg/day from 8 mg/day. The S-Cr level decreased gradually from 3.7 to 2.8 mg/dL, but did not fall further. BAY 73-4506 in vivo We performed a second biopsy on 1 April 2013 and found no evidence of rejection but mild glomerular collapse. The angiotensin II receptor blocker (olmesartan, 10 mg/day) was stopped and the S-Cr level steadied at 2.7 mg/dL. Antituberculosis agents were continued for 9 months and the lung tuberculosis resolved completely. We report a case of acute vascular rejection occurring during antituberculosis therapy in a patient with a kidney transplant. Our data are relevant to two distinct issues. First, how can tuberculosis (TB) infection Fluorouracil manufacturer of kidney transplant patients

be avoided? Second, how can the target trough TAC level be maintained when patients with kidney transplants are prescribed RFP? The incidence of TB infection of kidney transplant recipients is 1–15% (thus 100-fold greater than in the general population). TB in transplant patients most commonly involves the lung, as is true of TB cases in general populations, but the frequency of disseminated disease is much higher in kidney recipients. TB may present at any time, but 67% of TB infections occur within the first year after transplantation.[2] Subclinical infection is the most frequent cause of TB in kidney transplant recipients, and TB may be reactivated after administration of immunosuppressive agents. To prevent TB in such patients, both adequate evaluation of the patient and prescription of medication targeting latent TB infection (LTBI) are required during the pre-transplant period.