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Abstract: FR-PO947

Renal Dysfunction due to Mitral Valve Repair-Induced Hemosiderosis With Partial Recovery After Corrective Surgery

Session Information

Category: Anemia and Iron Metabolism

  • 200 Anemia and Iron Metabolism


  • Fernandez, Nicole, LewisGale Medical Center, Salem, Virginia, United States
  • Guez, Gilad S., LewisGale Medical Center, Salem, Virginia, United States
  • Elsanjak, Abdelaziz A., LewisGale Medical Center, Salem, Virginia, United States
  • Vanbeek, Christine A., AmeriPath Inc, Oklahoma City, Oklahoma, United States

Renal hemosiderosis (RH) occurs when free hemoglobin is filtered by glomeruli and reabsorbed by proximal tubular cells (PTC). Hemosiderin subsequently accumulates within PTC lysosomes. Various conditions associated with intravascular hemolysis may lead to RH. Mechanical hemolysis is a known complication of severe heart valve disease and heart valve replacement. However, biopsy-proven RH is rarely reported following mitral valve (MV) repair. Here, we describe a case of renal dysfunction due to RH after MV repair with follow-up after corrective surgery.

Case Description

77 year-old male with history of severe MV regurgitation and atrial fibrillation. He underwent a MV repair that included triangular resection, primary leaflet repair, and cosgrove posterior annuloplasty ring. This resulted in significant improvement in cardiac function. Baseline serum Cr was 0.9 mg/dL.
3 months post-procedure, he developed gross hematuria. U/A showed 3+ blood, 1+ protein, and 2-5 RBCs. Macrocytic anemia (Hb 7.6 g/dL, MCV 117 fL) and hemolysis (LDH 2,043 U/L,haptoglobin < 20 mg/dL) were also noted. Peripheral smear was negative for shistocytes. Platelet count was normal. Serum Cr was elevated at 2.1 mg/dL.
Renal biopsy showed abundant golden refractile granules within PTC cytoplasm on the H&E stain (Fig. 1A), which were confirmed to be hemosiderin on the Prussian Blue stain (Fig. 1B). Arteriosclerosis and mild interstitial fibrosis (~20%) were present. Glomeruli were normal.
Transesophageal echo showed new mild MV regurgitation with a posteriorly directed annuloplasty ring and new small ventricular septal defect. He then underwent a corrective surgery. His hemolytic anemia and hemoglobinuria resolved within 2 months and serum Cr improved to 1.3 mg/dL.


The few prior case reports of MV repair-induced RH had clinical manifestations ranging from asymptomatic urinary abnormalities to renal dysfunction and did not describe repeat surgery. This case demonstrates that corrective surgery can lead to resolution of hemolysis and at least partial recovery of renal dysfunction.