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Journal of General Internal Medicine

, Volume 29, Issue 6, pp 961–961 | Cite as

Crystalline Bone Marrow in Systemic Oxalosis

  • Joseph C. ChiovaroEmail author
  • Anuj Gaggar
Clinical Image

Keywords

Oxalate Glyoxylate Nephrolithiasis Calcium Oxalate Urine Oxalate 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
A 43-year-old woman with a history of two failed orthotopic kidney transplants, ventricular tachycardia, and recurrent nephrolithiasis underwent a bone marrow biopsy during an evaluation for refractory anemia. The aspirate revealed extensive crystal deposition with nearly absent residual hematopoiesis (Fig. 1). The crystals were birefringent under polarized light (Fig. 2) suggestive of calcium oxalate. The plasma oxalate level was elevated at 42.8 umol/l (normal < 1.8 umol/l), consistent with a diagnosis of systemic oxalosis from presumed primary hyperoxaluria.
Figure 1

Bone marrow biopsy demonstrating extensive calcium oxalate crystal deposition.

Figure 2

Same view under polarized light.

Primary hyperoxaluria is a rare, autosomal recessive disorder of hepatic glyoxylate metabolism resulting in overproduction of oxalate.1 Oxalate nephropathy results in renal failure, which leads to a further increase in the plasma concentration of oxalate. Calcium oxalate can then deposit into a wide array of tissues including bone, retina, peripheral nerves, arterial media, and the heart.2 For some patients, treatment with pyridoxine to reduce urine oxalate levels may be beneficial, though liver and kidney transplantation is often required.3

Both kidney transplants had taken place overseas, and the patient’s initial renal failure and first transplant failure were attributed to obstructive nephropathy from renal calculi. The second transplant loss was from rejection related to a reduction of immunosuppression, though biopsy revealed deposition of calcium oxalate crystals as well.

Notes

Conflict of Interest

Dr. Gaggar reports stock ownership and current employment with Gilead Sciences.

References

  1. 1.
    Hoppe B. An update on primary hyperoxaluria. Nat Rev Nephrol. 2012;8(8):467–75.PubMedCrossRefGoogle Scholar
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    Hoppe B, Beck BB, Milliner DS. The primary hyperoxalurias. Kidney Int. 2009;75(12):1264–71.PubMedCrossRefGoogle Scholar
  3. 3.
    Bergstralh EJ, Monico CG, Lieske JC, et al. Transplantion outcomes in primary hyperoxaluria. Am J Transplant. 2010;10(11):2493–501.PubMedCentralPubMedCrossRefGoogle Scholar

Copyright information

© Society of General Internal Medicine 2013

Authors and Affiliations

  1. 1.Portland VA Medical Center and Oregon Health and Sciences UniversityPortlandUSA
  2. 2.University of California, San FranciscoSan FranciscoUSA

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