Primary Kidney Allograft Dysfunction Due to Myeloma-Cast Nephropathy: A Case Report A. Perkowska-Ptasinska, M. Glyda, M. Paczkowski, and M. Durlik ABSTRACT Cast nephropathy is a rare event among renal transplants, usually associated with multiple myleoma or light chain nephropathy. Herein we have reported primary graft dysfunction early posttransplantation due to cast nephropathy, associated with thrombotic microangiopathy. INTRODUCTION T HERE IS AN INCREASING number of patients with multiple mycloma/light chain deposition disease who have undergone renal transplantation. In the majority of them, the monoclonal protein-associated nephropathy oc- curs or recurs in the transplant. 1–4 Thrombotic microangi- opathy (TMA) is a common complication among kidney transplant patients. It may accompany an acute transplant rejection, or a manifestation of cyclosporine, CsA or Pro- graf toxicity. 5,6 CASE REPORT This 55-year-old man developed cast nephropathy early posttrans- plant. The patient had been dialyzed for 1 year due to end-stage native kidney insufficiency of unknown reason. On August 2003, he received a kidney allograft from a three HLA-mismatched, cadav- eric, 57-year-old female donor, who died due to intracranial hemorrhage. The donor and recipient were negative for HIV, hepatitis C virus, and hepatitis B virus infections. Apart from mild anemia, no changes in recipient peripheral blood morphology were observed at the time of transplantation. The initial immunosuppression consisted of CsA, azathioprine (AZA), and prednisolone (Pred) in typical doses. On day 16 there was conversion of AZA to mycophenolate mofetil with subsequent withdrawal of CsA on day 21, followed by the introduction of Rapamune. There were no clinical signs of CsA toxicity during its administration, and the drug dosage was controlled by the trough and C 2 blood level measurements. Three weeks after transplant the patient was still oliguric and dialysis-dependent. The lowest post- transplant serum creatinine concentration was 8.9 mg/dL. There was no erythrocyturia on urinalysis. The urine protein content was 25 mg/dL. The patient displayed good blood pressure control (140/80 mm Hg), a heart rate of 70 beats per minute. The lipid profile analysis revealed triglyceride of 90 mg/dL and total choles- terol of 210 mg/dL (high-density lipoprotein: 84 mg/dL, low-density lipoprotein: 79 mg/dL). The graft biopsy revealed scattered acido- philic, PAS-positive casts engulfed by multinucleated giant cells, marked reduction in arterial lumine caused by the proliferative, and focally myxoid changes within the intima, as well as fine, acidophilic granular arteriolar wall thickenings associated with the presence of a few scattered intrawall fragmented erythrocytes. The immunomorphologic testing showed positive staining for light chains lambda, and only weak staining for immunoglobulin 6 and Clq within the casts. There were no C4d deposits in the graft. On the basis of microscopic and immunomorphologic evaluations, we rendered an initial diagnosis of cast nephropathy due to light chain gammopathy in possible association with mild thrombotic micro- angiopathy within the graft. Trepanobiopsy as well as blood and urine immunofixation tests revealed changes consistent with mul- tiple myeloma IIB. During the post-transplantation period INR and activated partial thromboplastin time remained within normal limits, as well as serum LDH and bilirubin concentration. At 6 weeks after transplantation the patient was still dialysis-dependent, despite the urine volume of 2.5 L/d. On posttransplant day 51 the graft was removed due to its constant dysfunction. DISCUSSION We do not know the reason for the native kidney insuffi- ciency in this case. Considering the early, posttransplanta- tion occurrence of cast nephropathy, an association be- tween unrecognized lymphoproliferative disease and native kidney insufficiency seems probable. The reported litera- ture incidence of thromboembolic events among patients with multiple myeloma is high. It has been attributed to impaired fibrinolysis, mostly secondary to increased PAI-1 activity, the influence of monoclonal proteins with fibrin structure, procoagulant autoantibody production, and ef- fects of inflammatory cytokines on endothelium. 7–9 More- over, injury to the endothelium, either by neoplastic cells or From the Department of Transplantation Medicine and Ne- phrology (A.P.-P., M.D.), Transplantation Institute, Warsaw Med- ical University, Warsaw, Poland, and Department of Transplan- tology (M.G., M.P.), District Hospital, Poznan, Poland. Address reprint requests to Agnieszka Perkowska-Ptasinska, Transplantation Institute, Warsaw Medical University, Nowogrodzka 59, 02-006 Warsaw, Poland. E-mail: aggape@poczta.onet.pl © 2007 by Elsevier Inc. All rights reserved. 0041-1345/07/$–see front matter 360 Park Avenue South, New York, NY 10010-1710 doi:10.1016/j.transproceed.2007.01.089 Transplantation Proceedings, 39, 1683–1684 (2007) 1683