Abstract: FR-PO010

Renal Hemosiderosis as a Complication of Total Artificial Heart Therapy

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Baig, Mirza Shahrukh, VCU Medical Centre, Richmond, Virginia, United States
  • Gupta, Gaurav, Medical College of Virginia/Virginia Commonwealth University, Richmond, Virginia, United States
  • Kumar, Dhiren, Medical College of Virginia/Virginia Commonwealth University, Richmond, Virginia, United States
Background

Mechanical circulatory support with a total artificial heart (TAH) is approved as a bridge to heart transplantation. Hemolysis is a common complication after implantation of a TAH. The incidence of renal failure requiring dialysis after TAH has been estimated at 12-15%. Kidney biopsy findings in patients with TAH and chronic hemolysis with renal failure have not been described.

Methods

A 57-year-old male with a history of non-ischemic cardiomyopathy underwent implantation of TAH. Post-TAH he developed progressive renal dysfunction (GFR decline= 70ml/min to 40 ml/min) presumed secondary to cardio-renal syndrome. He was also noted to have chronic hemolysis confirmed by evidence of fragmented RBC’s on smear, elevated LDH and undetectable haptoglobin concentration. Due to this, he required blood transfusions for the next seven months till the time he underwent an orthotopic heart transplant (OHT). Post-OHT he developed worsening acute kidney injury requiring hemodialysis (HD). After being maintained on HD for 8 weeks, a kidney biopsy was performed. In addition to moderate interstitial fibrosis, his biopsy was remarkable for extensive intracytoplasmic and luminal iron deposition in tubular epithelial cells. His renal function recovered partially over the next 4 weeks with a most recent recorded GFR of 20 and dialysis was withdrawn. He was listed pre-emptively for a kidney transplant.

Conclusion

We posit that the TAH-induced hemolysis and subsequent hemosiderosis contributed to the renal dysfunction seen in this patient. This pre-transplant injury could predispose OHT patients to further acute kidney injury in the setting of hemodynamic peri-operative insults and calcineurin inhibitor therapy. We propose that assessment of renal histology might shed further light on the etiopathogenesis of renal failure and to assess the potential for renal recovery in patients with artificial heart devices and/or heart transplant.

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