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Abstract: FR-PO546

Secondary Hyperoxalemia Causing Cardiac Failure in an ESRD Patient

Session Information

Category: Trainee Case Report

  • 1602 Pathology and Lab Medicine: Clinical

Authors

  • Peeples, Samuel Jefferson, University of North Carolina Health Systems, Chapel Hill, North Carolina, United States
  • Saha, Manish K., UNC Kidney Center, Chapel Hill, North Carolina, United States
  • Derebail, Vimal K., University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
  • Balos, Lucia, Jacobs School of Medicine, Buffalo, New York, United States
  • Hinderliter, Alan L., University of North Carolina Health Systems, Chapel Hill, North Carolina, United States
  • Venuto, Rocco C., Erie County Medical Center, Buffalo, New York, United States

Group or Team Name

  • University of North Carolina Kidney Center
Introduction

Secondary hyperoxaluria is a known complication of bariatric surgery due to impaired fat absorption. Oxalate deposition leading to organ dysfunction is poorly defined outside of primary oxalosis. We describe a case of cardiac and renal oxalosis with end-organ failure secondary to gastric bypass surgery.

Case Description

A 65-year-old male on hemodialysis for 3 years with history of heart failure with preserved ejection fraction (EF), jejunoileal bypass at age 18 and right nephrectomy due to cystic mass presented for exertional dyspnea and orthopnea after newly establishing care with us. His ESRD was presumed due to chronic nephrolithiasis after his jejunoileal bypass surgery. Electrocardiogram demonstrated atrial fibrillation and low QRS voltage. Transthoracic echocardiography (TTE) showed mildly thickened left ventricular wall with granular, sparkling texture to the myocardium,preserved EF, and biatrial enlargement concerning for cardiac amyloid. Serum immunofixation revealed an IgA lambda spike of 0.9 g/dL with kappa and lambda serum free light chains of 19mg/dL and 28mg/dL (ratio 0.67). Bone marrow aspiration showed 5-10% plasmacytosis, a lambda predominance and negative Congo red stain. Fat pad biopsy was negative for amyloid. Myocardial biopsy demonstrated diffuse cardiac oxalosis and interstitial fibrosis; Congo red stain was negative. Retrieval and staining of frozen tissue from prior nephrectomy revealed diffuse oxalosis with interstitial fibrosis. Serum oxalate levels before and after dialysis were 27 and 8 mcmol/L (normal <1.6), respectively, with an oxalate reduction ratio of 67%.

Discussion

Cardiac and renal oxalosis may have resulted from jejunoileal bypass, a now uncommon surgery. Oxalate is well cleared by HD, but long-standing hyperoxalemia prior to ESRD and between dialysis sessions likely led to myocardial deposition. Patients with ESRD due to secondary hyperoxalemia should continue to adhere to a low oxalate diet and regular dialysis sessions to prevent extra-renal oxalate deposition. Our case also illustrates that low QRS voltage in association with increased left ventricular wall thickness and a sparkling, granular appearance of the myocardium on TTE is not specific for cardiac amyloid, but may suggest cardiac oxalosis in the appropriate setting.