Renal Siderosis in Donor Allograft: Pathologic and Clinical Sequelae

Abstract

Transplantation of a cadaver kidney with marked siderosis and its outcome has not been reported. Increasing use of marginal kidneys has become common practice to expand the donor pool to meet the growing demand and will lead to increased recognition of kidney disease in cadaver donors with an unknown effect on graft outcome. This is a case report of a recipient of a cadaver kidney with marked siderosis monitored by surveillance biopsies and evaluated by clinico-pathological correlation. The recipient continued to have transplant kidney function, and a surveillance biopsy shows the natural course of the pathologic resolution of renal siderosis. Case ReportA 73-year-old woman with end stage renal disease, diabetes and hypertension presented for renal transplantation. Available organ was from a 63-year-old man with a medical history of mechanical heart valve replacement for many years (mitral and aortic) and an embolic stroke. The organ had been rejected for transplantation at other centers. Final donor BUN and creatinine values were 27 mg/dL and 1.0 mg/dL, respectively.The kidney was brown in color to the naked eye examination and flushed well with cold University of Wisconsin solution before transplantation. Pathologic evaluation of the graft was performed before transplantation, using Banff 97 (1) schema. An approximate hemosiderin quantitation was performed on Prussian blue-stained sections using the same method originally described by Scheuer et al. (1,2) for the quantitation of hemosiderin in liver biopsies, with grade 0 being negative and grades 1, 2, 3 and 4 representing increasing amounts of stainable hemosiderin. Microscopically, chronic changes of global glomerulosclerosis (10%), fibrosis and arterial sclerosis were noted [ci1, cv1, Banff 97 (1)]. The tubular epithelium showed severe iron overload (4+/4+) ( Figure 1A). The iron was distributed predominantly in the proximal tubular epithelial cells and the absolute level was quantified from paraffin-embedded tissue at 3985 lg/g of dry weight. The organ was utilized for transplantation. Cold ischemic time was 15 h and warm ischemic time was 25 min. The clinical assumption was that the kidney would function in the recipient because it was functioning well in the donor and the iron would slowly be removed from the graft in a recipient who did not have iron overload. The immunosuppression was basiliximab induction, and maintenance with cyclosporine, mycophenolate mofetil and prednisone. The kidney functioned immediately and the recipient did not require dialysis support in the post transplant period. Two months post transplant a biopsy for clinical rejection showed 1A rejection (Banff 97) and decreased iron (3+/4+). The chronic fibrosis, vascular and tubular grades were unchanged since transplantation ( Figure 1B). One-year protocol biopsy showed quantitatively decreased tubular epithelial iron (2+/4), occasional interstitial macrophages containing iron pigment and no rejection. The chronic fibrosis, vascular and tubular grades were unchanged since transplan...