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Kidney Week

Abstract: TH-PO1048

When Delayed Graft Function Isn't Acute Tubular Necrosis (ATN): De Novo Kappa Light Chain Cast Nephropathy in a Living Donor Kidney Transplant Recipient

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Nouman, Muhammad Khuram, University of Louisville, Louisville, Kentucky, United States
  • Pujari, Ashwini S., University of Louisville, Louisville, Kentucky, United States
Introduction

Delayed graft function (DGF) after living donor kidney transplantation is uncommon and should not be presumed ischemic. Persistent DGF warrants prompt allograft biopsy and evaluation for alternative etiologies, including recurrence of native disease, thrombotic microangiopathy, rejection, and rare causes such as plasma cell dyscrasia.

Case Description

A 61-year-old man with ESRD due to diabetes underwent living unrelated kidney transplantation complicated by DGF requiring ongoing hemodialysis. Initial imaging showed preserved perfusion with delayed excretion, consistent with acute tubular injury. Despite supportive care, he remained oliguric without graft recovery.

Follow-up imaging revealed perinephric fluid collections requiring drainage without improvement. Due to persistent DGF, allograft biopsy demonstrated kappa light chain cast nephropathy with acute tubular injury and no evidence of rejection. Immunofluorescence showed strong kappa-restricted staining in tubular casts and along tubular and glomerular basement membranes; electron microscopy showed no immune-type deposits.

Serum studies revealed markedly elevated free kappa light chains (2373.40 mg/L), lambda 23.54 mg/L, with a kappa/lambda ratio of 100.82. Urine free light chains were also elevated (kappa 16723 mg/L, lambda 85.17 mg/L; ratio 196.35). Bone marrow biopsy demonstrated 40–55% monoclonal plasma cells, confirming kappa light chain multiple myeloma.

The patient received high-dose dexamethasone and limited plasma exchange (discontinued due to intolerance) and was initiated on daratumumab-based therapy. Immunosuppression was modified with discontinuation of mycophenolate and continuation of tacrolimus.

Discussion

This case highlights a rare cause of persistent DGF due to de novo multiple myeloma with light chain–mediated allograft injury. It underscores the importance of comprehensive CKD evaluation prior to transplantation, including screening for monoclonal gammopathy in patients with atypical features. Failure to identify plasma cell dyscrasia pre-transplant may lead to early allograft dysfunction. Persistent DGF—particularly in living donor transplants—should not be presumed ischemic and warrants early allograft biopsy and evaluation for systemic causes. Prompt recognition and targeted hematologic therapy are essential to optimize graft outcomes.