r rejection (ACR) accounted for 7.5% of the cases which is comparable to other published studies from India\[[@ref1]\] but less when compared to the western studies.\[[@ref2]\] The discrepancy is attributable to the biopsy policies; ACR being higher in centers doing protocol biopsies. ACR is common in first two weeks post-transplant, but it ranged from 1 month to 16 years in our study.

Borderline rejection was seen in four of our biopsies (5%); three were done beyond the routine time for acute rejection. Some of the studies showed that borderline changes can progress to early Chronic allograft nephropathy (CAN) if left untreated.\[[@ref3]\]

The morphologic features of acute humoral rejection (AHR) were identified in 9 biopsies (11.2%), two were C4d-positive. Donor-specific antibodies (DSA) were not available for these patients. All the patients showed dramatic response to anti-rejection treatment with mean follow-up creatinine level of 1.3 mg/dl. The incidence of AHR with analysis of morphologic features, C4d, and DSA ranges 0-8%.\[[@ref4]\] Tubulitis or arterial fibrinoid necrosis was not seen in any of the biopsies. Some of the recent studies have also emphasized the existence of C4d-negative AHR.\[[@ref5]\]

The causes of renal cortical necrosis (RCN) in transplant settings include technical problems related to the surgery, ABO incompatibility, hyperacute rejection, Hendytic Uremic Syndrome (HUS), and thrombotic microangiopathies.\[[@ref6]\] All the three cases (3.8%) of RCN were seen in association of AHR. There was no evidence of renal artery thrombosis in any of these cases. Cortical necrosis in the setting of AHR is seen to be associated with positive DSA and negative C4d.\[[@ref7]\] Cortical necrosis is an indicator of early graft loss and these patients need to be followed-up for changes of CAN.

The urine culture showed growth of *Pseudomonas* and *E. coli* in two of four patients reported as acute pyelonephritis (5%). Two of the patients responded to antibiotic treatment.

Six patients of calcinuric 