Kidney Week

Abstract: TH-PO783

Unique Case of Hemosiderosis-Induced Ascites in Kidney Transplant Recipient

Session Information

• Transplantation: Clinical - 1
  October 24, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

• 2102 Transplantation: Clinical

Authors

• Ahmed, Mansoor, Stony Brook University, Stony Brook, New York, United States

Mansoor Ahmed, MD

• Bhuiyan, Sakil Amin, Stony Brook University, Stony Brook, New York, United States

Sakil Amin Bhuiyan, MBBS

• Kaur, Navdeep, Stony Brook University, Stony Brook, New York, United States

Navdeep Kaur, MD

• Abdulrahman, Rula A., Stony Brook University, Stony Brook, New York, United States

Rula A. Abdulrahman, MD

• Daccueil, Farah, Stony Brook University, Stony Brook, New York, United States

Farah Daccueil, MD

Introduction

Iron overload or hemosiderosis is often a frequent complication from intermittent blood transfusions. Anemia of end stage kidney disease (ESKD) is managed with IV iron and erythropoietin stimulating agents (ESAs) and these patients are at risk of iron overload, especially those with increased dialysis vintage. Here we describe a unique case of recurrent ascites caused by secondary hemosiderosis in a kidney transplant recipient who was on Peritoneal Dialysis (PD) for 12 years.

Case Description

A 61-year-old female with ESKD secondary to presumed Hypertension underwent 2nd deceased donor renal transplant(DDRT) in 2023. She was on PD from 2011 to 2023. She required 8 units of PRBC’s peri-operatively. Nadir creatinine 0.77 mg/dl. Post-transplant course complicated with COVID PNA, transplant renal artery stenosis requiring stent placement. She developed ascites three months post-transplant requiring frequent large volume paracentesis which was contributed to hepatic congestion in setting of heart failure with preserved ejection fraction (HFpEF). Seven months post-transplant she developed AKI in setting of E.coli bacteremia, CMV viremia and a transplant renal biopsy was performed showing focal endothelialitis, suggesting T cell mediated rejection, CMV nephritis and renal hemosiderosis and about 40% IFTA. Labs also showed iron levels of 15, Ferritin of 1400, TSAT 27%, AST/ALT normal, with elevated ALP 130. MRI liver was done which showed mild diffuse gain of signal in liver and spleen. A liver Biopsy was also performed which showed nodular regenerative hyperplasia and 1-2+ iron staining in Kupffer’s cells + hepatocytes and no evidence of fibrosis. Given liver biopsy findings and multiple transfusion history, it can be hypothesized that recurrent ascites was likely to secondary hemosiderosis rather than HFpEF. Patient’s AKI recovered with treatment of underlying infection. Of recent, she has not required paracentesis.

Discussion

Here we describe an interesting case of a transplant patient with high dialysis vintage who developed recurrent ascites due to renal hemosiderosis. It is possible that long term IV iron exposure and multiple transfusions immediately post-transplant lead to secondary hemosiderosis. Long term PD could be contributing to development of ascites as well.