Background: Acute rejection affects 5-9% grafts in first year post kidney 
transplantation. It is usually associated with renal dysfunction and occasionally 
subnephrotic proteinuria. Nephrotic syndrome presentation of acute rejection is rare 
with only few case reports reported in literature. 3-13% of patients develop nephrotic 
syndrome post kidney transplantation. Nephrotic syndrome post kidney transplantation can happen early (<1 year) or late (>1 year). Here we report a case of nephrotic syndrome immediate post kidney transplantation. 
Case: 38 years old male K/C/O hypertension, gout and ESRD on MHD for 2 years 
underwent ABO compatible living kidney transplantation with immunosupression being tacrolimus, mycophenolate sodium, steroids and induction being ATG (3mg/kg).Preoperatively HLA typing revealed 2/6 match. CDC, Flowcytometry and DSA Class 1 and 2 were negative. Patient had gradual decline of creatinine to 1.5mg/dl on POD7 which rose to 2mg/dl on POD8. Tac level was 6.5 and graft doppler showed normal flow pattern. Patient was started on pulse 500mg for 3 days after kidney biopsy. Kidney biopsy was suggestive of acute cellular rejection, c4d being negative with no significant glomerular changes. Despite therapy patient developed anasarca and ascites. Serum albumin decreased from 4.2 to 2.4 gm/L, urine routine revealed 2+ proteinuria and 24 hour protein was 13gm/day. There was no prior history suggestive of nephrotic syndrome in either recipient or donor ruling out recurrence. Electron microscopy showed podocyte effacement and no deposits. No evidence of TMA or viral infection was present on biopsy. Patient was treated with 5 sessions of plasma exchange andRituximab 500mg suspecting podocytopathy associated with acute rejection. Gradually over 2 weeks anasarca resolved and proteinuria declined to 0.5gm/day and creatinine stable at 1.3mg/dl. There has not been any recurrence of proteinuria 2 years post transplantation and creatinine stable at 1.4mg/dl. 
Discussion: In various studies nephrotic syndrome is present in 3-13% of patients post kidney transplantation. Denovo and recurrent GN accounts for 46% of cases whereas 40% are due to chronic allograft nephropathy. Early nephrotic syndrome post kidney transplantation can be due to recurrent, or donor derived glomerulonephritis. Other causes bein rejection, viral infection and drug toxicity. In our patient a final diagnosis of denovo minimal change disease with acute cellular rejection was made. Only few cases of podocytopathy associated with rejection are reported.  De novo MCD is associated with good response and remission rates. It is postulated that these features are due to T cell dysregulation and release of cytokines leading to podocytopathy and nephrotic syndrome. 
Conclusion: Our case report highlights that early detection and treatment of rejection are helpful in good clinical response and long term outcomes. Role of PLEX and Rituximab need to be defined.