Laboratory data revealed that our patient did not express donor-specific antibody and the peritubular capillaries did not exhibit C4d immunoreactivity. Upon consideration of both histological and laboratory findings, we diagnosed acute vascular rejection of Banff 2007 class ACR IIA. We commenced 3-day sessions of intravenous steroid

pulse therapy twice weekly and adjusted the trough TAC level to 5–8 ng/mL by varying the TAC dose. We next performed an allograft biopsy and found no evidence of rejection (the S-Cr level was 2.7 mg/dL on April 1 2013). The present case report demonstrates the difficulties associated with management of TAC-based regimens in kidney transplant patients undergoing antituberculosis therapy. We also review the relevant literature. The proportion of selleck compound kidney allografts that is not rejected has improved dramatically in the era of the calcineurin inhibitor (CNI), but the use of such a strong immunosuppressant increases the risk of infection. Of the various possible infections, tuberculosis is particularly problematic because infection of transplant patients is associated with a higher incidence of mortality than noted click here in the general population. The same antituberculosis agents are recommended for use in both transplant patients and the general population.[1] Rifampicin (RFP) plays a key role in antituberculosis therapy, but the

trough CNI level requires close attention because it is frequently decreased by RFP use. A 29-year-old man was admitted to our hospital in June 2013 for a scheduled biopsy 1 year after primary kidney transplantation. He had been diagnosed with IgA nephropathy at the age of 17 years. He underwent peritoneal dialysis in June 2011. In June 2012, he received a live-donor kidney transplant from his father. The ABO blood types of donor and recipient were compatible, and the HLA alleles were haplo-identical. The standard complement-dependent cytotoxicity cross-match test was negative. Immunosuppressive therapy consisted of tacrolimus (TAC), mycophenolate

mofetil, methylprednisolone and basiliximab. The allograft exhibited excellent early function, associated with an S-Cr selleck kinase inhibitor level of 1.2 mg/dL. The 1 year protocol biopsy revealed no evidence of rejection. However, our patient was diagnosed with lung tuberculosis. The QFT was positive and the chest CT findings typical of tuberculosis. Standard therapy with antituberculosis agents, consisting of isoniazid (INH) 300 mg, rifampin (RFP) 450 mg, ethambutol (EB) 500 mg and pyrazinamide (PZA) 1500 mg daily, commenced on 9 June 2012. Despite increasing the TAC dose (512 mg, daily) and frequent monitoring of the serum TAC trough level, the serum TAC level decreased gradually from 3.1 ng/dL on 7 July 2012 to 1.6 ng/dL on 1 October 2012.