LAUSR

Some kidney transplantation recipients with negative donor specific antibodies can develop acute rejection episodes which are difficult to treat, associated with non-HLA antibodies like angiotensin 2 type 1 receptor antibodies (AT1R Ab). The mechanism of rejection by AT1R ab involves vascular injury. Our cases are unique as the first patient got mineralocorticoid deficiency like picture unexpectedly. For the second case, hyperacute rejection cause in the first allograft was not identified and but hyperacute rejection episodes involving antibodies against endothelial cells are reported in literature. 2 patients received renal transplantation from life related donors in out institute developed acute rejection episodes. As part of investigations, we did non -HLA antibodies testing which came positive . Case 1 30 years old male, with end stage renal disease on hemodialysis . The patient had a live related renal transplant with Mismatch 1-1-1 and negative DSA. Induction with Basiliximab was initiated but changed to ATG due to delayed graft function. Kidney biopsy on day 6 post operatively showed diffuse moderate to severe acute tubular injury (up to necrosis) with glomerular intracapillary fibrin microthrombi, focal minimal peritubular capillaritis and mild glomerulitis and focal weak C4d positivity, highly suspicious for active antibody mediated rejection. The patient was treated with pulse steroids, ATG total of 7.5mg/kg, 3 sessions of Plasma exchange and IVIG 2 g/kg and 2 doses of Rituximab for his hyperacute rejection. AT1R antibodies titer was 11U/ml. MICA was negative. Losartan was initiated as a maintenance therapy.