Calcineurin inhibitor induced thrombotic microangiopathy is a rare but well recognized complication of a renal transplantation that occurs in 1% of the patients who are on tacrolimus immunosuppression. Among the other aetiological factors of the "de-novo" Thrombotic Microangiopathy (TMA), the condition especially has to be differentiated from an antibody mediated rejection, as both have different pathogenesis, therapeutic connotations and outcomes.We report a case of a middle aged female renal transplant recipient treated with tacrolimus, who developed localised thrombotic microangiopathy in the early post transplantation period. Despite the normal trough levels of tacrolimus, a diagnosis of "Tacrolimus induced TMA" was rendered after excluding other causes of the "de-novo" TMA, which included an antibody mediated rejection, a meticulous clinico-pathological correlation and serological studies. The treatment included the substitution of tacrolimus by rapamycin, with the subsequent normalization of the renal function. INTRODUCTIONPost renal transplant thrombotic microangiopathy (PT-TMA) is a "recurrent" or "denovo" ,"localized" or a "systemic" devastating disorder that, as per the USRDS data analysis, occurs with an incidence of 5-6 episodes per 1000 people years [1,2].Among the proposed aetiological factors, Calcineurin inhibitor induced TMA (CNI-TMA) is a rare but well documented cause of acute renal failure [3]. An early allograft biopsy with a prompt diagnosis of the condition, its distinction from an antibody mediated rejection and its management by drug substitution, plays a vital role in the allograft outcome.We report a case of localized tacrolimus associated TMA occurring in the early stage after renal transplantation. CASE REPORTA 52 year-old Caucasian female underwent a living, non-related, donor transplantation for ESRD. After an initial induction with basiliximab, the post transplant immunosuppression consisted of methylprednisolone (10 mg/day), mycophenolate mofetil (1g/ day) and tacrolimus (5 mg/day). A clinical improvement with good diuresis was achieved for 48 hours, following which the renal functions deteriorated, with a reduction in the urine output and peak serum creatinine levels of 3.8 mg/dl. The laboratory investigations (before dialysis) showed the following: haemoglobin -11.1 g/dl, platelets -1.64 lakhs/mm 3 , blood urea nitrogen -62 mg/dl, sodium -136 mEq/l, potassium -5.9 mEq/l, chloride -117 mEq/l, phosphate -4.9 mEq/l, uric acid -8.9 mg/dl, complement C3c-95mgm/dl, C4-25mgm/dl and lactate dehydrogenase -210 u/l. With a clinical suspicion of acute tubular necrosis/acute rejection, a renal biopsy was done, which revealed fibrin thrombi in the glomerular capillaries [Table/ Fig-1 A and B] and arterioles at the glomerular vascular pole with associated fibrinoid necrosis, in a focal and segmental fashion [Table/ Fig-2 A and B]. Some of the glomeruli exhibited tuft collapse and widening of the Bowman space. The proximal tubular epithelial cells showed isometric cytoplasmic vacuoliz...