In this case kidney biopsy is essential in making the correct diagnosis. Therefore, a high index of suspicion for this disorder should be maintained in the presence of unexplained metabolic acidosis, hyperosmolality, unexplained AKI, and neurologic dysfunction.
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Thiamine and pyridoxine are essential cofactors in the glyoxylate pathway, and a deficiency results in increased oxalate formation [ 22 ]. The third mechanism occurs in the setting of significantly decreased fluid intake. Lower fluid intake leads to lower urine output, hence promoting the formation of oxalate stones through increased concentration of urine oxalate.
The fourth mechanism is decreased oxalate excretion. In chronic kidney disease, lower GFR is associated with elevated plasma oxalate levels [ 23 ].
The degree of kidney function impairment is often correlated with the serum oxalate concentration [ 24 ]. This is because oxalate is removed from the body almost entirely by glomerular filtration and by secretion at the level of the proximal tubule [ 25 , 26 , 27 , 28 , 29 , 30 ].
Finally, increased dietary oxalate may lead to secondary hyperoxaluria, particularly in patients with underlying CKD. Oxalate is present in a wide variety of leafy green vegetables and fruits. Table 3 includes a list of common foods high in oxalate. In addition, vitamin C and ethylene glycol are important sources of oxalate precursors.
Dietary oxalate is absorbed in the intestines by SLC26 family of transporters, via both paracellular and transcellular pathways [ 33 ]. The intestinal absorption of oxalate is affected by the bioavailability of the ingested oxalate [ 34 ]. The disease spectrum of hyperoxaluria ranges from nephrocalcinosis, nephrolithiasis to oxalate nephropathy.
Nephrocalcinosis and nephrolithiasis may remain asymptomatic, with slow CKD progression, often discovered incidentally on radiographic imaging. In such event, renal replacement therapy may be required and if concern for primary hyperoxaluria is present, combined liver and kidney transplantations may need to be considered [ 5 , 36 , 37 ].
In summary, our patient with underlying CKD stage G3B developed acute oxalate nephropathy leading to ESKD from secondary oxalosis due to excessive consumption of oxalate-rich foods and likely decreased fluid intake. Patients with predisposing conditions such as CKD have a higher risk of developing oxalate-induced nephropathy.
In addition, our case illustrates the importance of a kidney biopsy in determining the etiology of AKI when the etiology remains elusive. Therefore, in addition to the typical work-up, special attention should be warranted to the dietary habits of patients at high risk, such as those with underlying CKD. Williams HE. Oxalic acid and the hyperoxaluric syndromes.
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The biosynthesis and turnover of oxalate in normal and hyperoxaluric subjects. J Clin Invest. For commercial re-use, please contact journals. Issue Section:. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions. Add comment Cancel. Submit a comment. Comment title. You have entered an invalid code. Submit Cancel. Thank you for submitting a comment on this article. Your comment will be reviewed and published at the journal's discretion.
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