A Life-Threatening Condition Caused by Accumulation of Oxalate in the Body
Systemic oxalosis is a potentially life-threatening condition that results from the progression of primary or enteric hyperoxaluria. Excess oxalate that cannot be eliminated by the kidneys begins to accumulate in tissue throughout the body, including the blood, bones, joints, skin, eyes, heart, and kidneys.
With systemic oxalosis, the uncontrolled deposition of oxalate crystals can increase the risk of kidney inflammation, fibrosis and progressive kidney failure that can be fatal.1 This damage to the kidney further reduces the kidney’s ability to eliminate oxalate, causing a vicious cycle that can accelerate the loss of renal function.
Systemic oxalosis can also cause a range of serious health issues outside the kidneys, including bone disease, anemia, skin ulcers, heart and vision problems, and growth deficiencies in children. A common sign of systemic oxalosis is recurrent kidney stones that are painful and even debilitating. Because of this, patients who present with recurrent kidney stones, or those who have even a single episode of kidney stones at a young age, should be evaluated for systemic oxalosis and hyperoxaluria.
Currently there is no approved pharmacologic therapy for the reduction of oxalate in patients with systemic oxalosis. Existing treatment options generally are non-specific and have varying degrees of success. Damage to the kidney associated with hyperoxaluria and systemic oxalosis may require patients to be treated with kidney transplantation. In one European study, 3% of patients being evaluated for a kidney transplant were found to have enteric hyperoxaluria.2
Retrospective and observational studies suggest that patients with systemic oxalosis are likely to have a poor outcome in kidney transplant procedures.2-6 Kidney transplantation can be challenging because of the risk of recurrent calcium-oxalate deposition and nephrolithiasis. There is also an association between high systemic levels of oxalate crystals and poor long-term graft survival, declining kidney function and recurrent need for dialysis.2-9
1. Ermer T et al. Curr Opin Nephrol Hypertens. 2016; 25(4): 363–37.
2. Roodnat JI et al. Transplant Direct. 2017;3(12):e331.
3. Health Advances interviews and analysis, OPTN.
4. Pinheiro HS et al. Am J Transplant. 2005;5(2):323-9.
5. Bagnasco SM et al. Nephrol Dial Translant. 2009;24(4):1319-25.
6. Palsson RJ et al. [abstract.] J Am Soc Nephrol 28, 2017:356.
7. Nazzal L et al. Nephrol Dial Transplant. 2016;31(3):375-82.
8. Elgstoen KB et al. Nephrol Dial Transplant. 2010;25(7):2341-5.
9. Perinpam M et al. Clin Biochem. 2017;50(18):1014-9.